Is Cancer Contagious?
By Alan Cantwell, M.D.
Jackie Kennedy's rapid death from "Non-Hodgkin's lymphoma" cancer
in May I994 shocked and saddened the world. Now officials of the American Cancer
Society are hinting that some lymphomas may be caused by viruses. If so, are
these viruses contagious? And how can we protect ourselves from them? What do
we really know about the origin and cause of cancer? Are these new cancer viruses
related to cancer-causing retroviruses like HIV (the AIDS virus)?
As a rich woman, Mrs. Kennedy-Onassis received the best treatment for her disease
at one of the most prestigious cancer hospitals in New York. Yet, within 5 months
of the discovery of her lymphoma, she was dead. Even in my most paranoid state
I cannot conceive of any sinister aspect of her demise. However, it is a well
kept secret in medical circles that the required treatment for cancer, particularly
chemotherapy and radiation, can sometimes hasten the death of cancer patients.
For example, one of my patients had "routine" treatment for Hodgkin's
disease, which consisted of extensive surgery followed by radiation to the chest
and abdomen. After he re covered from this, he was given an intensive course
of chemotherapy. Within a year of his diagnosis, and less than four months after
chemotherapy, he died. At autopsy, there was no evidence of cancer. His death
was caused by fatal damage to his heart and lungs by the radiation treatment
he received. How much of Jackie's death can be attributed to the treatment she
underwent for cancer will never be known.
Cancer Mysteries
Cancer kills more American women than any other disease. Cancer of the breast
is the No1 killer in Anglo, Black, Latina, Chinese and Japanese-American women.
No one knows the reason for this. Jackie's cancer, Non-Hodgkin's lymphoma, is
among the top 10 most common forms of cancer in all races, except for Blacks.
Again, no one knows why. Why do Chinese-American men have a high risk of liver
cancer, when the disease is decidedly uncommon in other Americans? Why is the
prostate cancer rate among Blacks in Los Angeles county 60% higher than in Anglos;
and 80% higher than Asians? Why do Anglo men have a bladder cancer rate twice
that of other groups? No one has an adequate explanation for these cancer occurrences.
Lymphoma Cancer
There are three major types of lymphoma cancer: Hodgkin's disease, Non-Hodgkin's
lymphoma, and a type of lymphoma which affects the skin called mycosis fungoides.
All lymphoma patients may experience similar symptoms. The exact type of lymphoma
requires diagnosis by a pathologist, and depends on the microscopic appearance
of the cancerous cells and tissue. The "classification" of lymphoma
types is in constant flux and reappraisal. Strangely, the cancer cells of Jackie's
Non-Hodgkin's lymphoma were reported as a new type called "Ki-1."
Hodgkin's disease is one of the very few forms of cancer that has long been
considered as having a possible infectious origin. For decades, epidemiologists
have recognized "cluster cases' of Hodgkin's. The actual number of cases
was so high in certain communities that it was highly unlikely to be due to
statistical chance. Even so, definite proof of a Hodgkin's disease agent has
not been forthcoming. Some scientists are now suspecting a possible cancer causing
retrovirus.
The Cancer Microbe
All this would not surprise my mentor, the late Virginia Livingston MD, who
for 40 years claimed that various bacterial and viral forms of "the cancer
microbe" were responsible for the infectiousness and possible contagiousness
of cancer. Long before the discovery of the AIDS virus, she stressed care in
the sexual arena, as well as the importance of hygiene, diet and supplements
in the treatment of cancer. Her use of vaccines made from the patient's own
cancer bacteria ultimately resulted in the condemnation of her cancer research
and her treatment methods for cancer. Robert Gallo MD, the co-discoverer of
the AIDS virus, denounced her scientific work as insanity.
Over the past century physicians have refused to believe that an infectious
agent could cause cancer. In the 1970s, scientists proved that animal cancer
viruses were capable of causing cancer, but there was no proof that viruses
caused human cancer. Now with the discovery of cancer-causing retroviruses,
such as the AIDS virus, doctors are reconsidering the idea. The history of modem
medicine seems to prove Cantwell's law that "Most physicians are wrong
in their understanding of most diseases, most of the time."
Why is Non-Hodgkin's lymphoma one of the fastest rising cancers in the U.S.?
Is the rise related to drug use (legal and illegal), immunosuppression from
environmental sources, or radiation effects? No one knows. My own published
research into the cause of all three types of lymphoma indicates that "cancer
microbes" are the infectious agent. My studies confirm Livingston's research,
as well as the cancer microbe research of dozens of other scientists throughout
the world who have implicated bacteria in various forms of cancer. This work
is documented in my book The Cancer Microbe (1990). Over thirty of my published
papers on AIDS, cancer, and other immunologic diseases, are available in medical
libraries. And anyone hooked into a computer network can get abstracts of these
papers through "Medlars 11," the National Library of Medicine's computer
retrieval service.
The startling cancer microbe discoveries are ignored by the cancer establishment.
Undoubtedly the recognition of a heretofore unnoticed infectious agent in cancer
and AIDS would provoke havoc in medical science. Thus, cancer bacteria remain
"in the closet" and the research "politically incorrect."
Death by Cancer
So many people have been done in by cancer at a convenient time in history
that conspiracy buffs wonder if you can "give" people cancer. I recall
the propitious cancer deaths of Jack Ruby, William Casey, Martha Mitchell, the
Shah of Iran, Mae Brussell, and others. (Even O.J. Simpson was tested for lymphoma
cancer in a swollen lymph node while imprisoned awaiting trial for murder.)
Can you kill people by injecting them with cancer viruses and bacteria? Of course!
No one in their right mind would want blood from a dying cancer or AIDS patient.
Can you give a person cancer? If cancer in animals can be caused by injecting
them with cancer viruses and bacteria, it would certainly be possible to do
the same with human beings!
Cancer: One Disease or Many?
The American Cancer Society constantly reminds us that there are many "different"
kinds of cancer. This concept is highly effective in raising money for each
type of cancer that the ACS promotes. But in reality there is a close relationship
between certain forms of cancer, particularly lymphoma and leukemia (cancer
of the blood). In the 1970s, virologists discovered that animal retrovirus infection
(similar to the AIDS virus) could cause an increase in lymphoma and leukemia
in the animals, as well as immunosuppression. In 1983, a year before the official
discovery of HIV, Harvard veterinarian Myron Essex found that 25% of gay AIDS
patients had viral antibodies to blood from a case of "human T-cell leukemia,"
caused by a new retrovirus called "human T-cell leukemia virus-1."
When Robert Gallo announced his discovery of the AIDS virus in 1984, he believed
the virus was related to this new family of leukemia viruses. Thus, he first
named the AIDS virus "Human T-cell leukemia virus-3." Later, the virus
was renamed HIV: the human immunodeficiency virus.
When the AIDS virus (HIV) was introduced into the gay community in the late
1970s, the incidence of Kaposi's sarcoma (a previously rare form of cancer),
as well as the incidence of Non-Hodgkin's disease, began to skyrocket in HIV-infected
gay men. Both types of cancer had previously been associated with immunosuppression.
For example, in the mid-1970s the normal incidence of Kaposi's sarcoma increased
400 to 500 times in transplant patients who were routinely immunosuppressed
with prescribed drugs as part of the procedure. In 1981, the year the AIDS epidemic
became official, Bijan Safai and Robert Good, scientists at Memorial Sloan Kettering
Cancer Center in New York City, declared a close association between Kaposi's
sarcoma, leukemia and lymphoma. They proposed all three cancers be considered
"as part of a spectrum of disease affecting the lymphoreticular system."
The American Cancer Society is unlikely to remind its contributors that treatment
for one form of cancer can cause the formation of another "different"
cancer. For instance, after chemotherapy about three percent of Hodgkin's disease
patients go on to develop Non-Hodgkin's lymphoma, or leukemia. Officially, the
reason for these "second cancers" is unknown. Surprisingly, most cancer
experts assume two different diseases are involved. They theorize that chemotherapeutic
drugs depress the immune system, resulting in the development of "new"
cancers.
Is Cancer Contagious?
Physicians now understand that sexually transmitted retroviruses, such as HIV,
can cause cancer and immunosuppression. Nevertheless, doctors continue to tell
patients (unless they are gay) that cancer is
neither infectious or contagious. What about the transmissibility of new retroviruses
that have been identified in certain human leukemia cases? So far, the cancer
establishment is not commenting. Do cancer viruses and the increasing rates
of certain forms of cancer, such as Non-Hodgkin's lymphoma, have a relationship
to the AIDS epidemic? In the absence of a positive HIV test, I would say no.
(Both Jackie Kennedy and O.J. Simpson tested negative for HIV.) In my book,
Queer Blood: The Secret AIDS Genocide Plot (1993), I describe the genetic engineering
of animal cancer viruses in the early 1970s that, in my opinion, resulted in
the creation the AIDS virus. (Are there any PARANOIA readers who actually believe
AIDS comes from African green monkeys?)
Man-Made Viruses
Whether one agrees with the idea that AIDS is a man-made epidemic, it is a
fact that we now deal with viruses that are "natural" (so-called endogenous
viruses); and viruses that are genetically manipulated, man-made, and "unnatural"
(exogenous viruses). These laboratory-created viruses are now used as an integral
part of the new gene splicing technology. Engineered and altered animal cancer
viruses, such as the mouse leukemia virus, have already been used in human genetic
experiments. If cancer viruses can be injected into people to make them well,
they certainly can be injected into people to make them sick! Can genetically
engineered viruses be covertly seeded into select populations for political
and genocidal purposes? Was the "introduction" of the AIDS virus into
the Black African population, and into the U.S. gay male population, a deliberate
attempt to eliminate these groups? Goverment AIDS experts repeatedly tell us
that AIDS began as a Black African disease when an African green monkey "jumped
species." The U.S. public was initially told AIDS is a "gay"
disease, caused by anal sex and drugs. But who can conceive of a Black heterosexual
epidemic in Africa that transformed itself into an exclusively young white gay
male epidemic in New York, Los Angeles, and San Francisco?
Recently a physician colleague referred a patient to me with a written diagnosis
of "AIDS caused by homosexuality." This indicates how powerful and
effective the governments disinformation program has been in convincing
the public (and some physicians) that AIDS is a gay disease. Now that 4 million
men and women are infected with HIV worldwide, do people really think most were
sodomized?
Coping with Cancer
Jacqueline Kennedy-Onassis's death from cancer, despite access to the best
treatments and doctors that money could buy, certainly justifies a degree of
cancerophobia. Her rapid demise makes us wonder if her treatment killed her
quicker that her lymphoma. (Some lymphoma patients live for many years.) But
did she have any treatment options? If you had cancer, would you go against
the advice and wisdom of a cancer expert? Who would turn down chemotherapy and
radiation if they thought it would save their life? How do doctors separate
the toxic effects of cancer from the toxic effects of treatment with chemotherapeutic
drugs, surgery, radiation and steroids? Will doctors be able to save us if we
are diagnosed with cancer? Can we catch cancer-causing viruses from our family,
our friends, our lovers? Is this reason for paranoia? You bet it is!"
Doctor Cantwell is the author of The Cancer Microbe, Queer Blood: The Secret
AIDS Genocide Plot ($12.95), and AIDS: The Mystery & The Solution ($9.95).
All books are available from Aries Rising Press, P0 Box 29532, Los Angeles,
CA 90029. (213) 462 6458. Enclose $2.00 s&h for one book; $3.00 s&h
for two or more. CA residents must add sales tax.
Source: Paranoia, winter 1994/95
THE ROLE OF VIRUSES
Objective: The students will learn how viruses contribute to the development
of Cancer.
The students will learn how viruses may be used to cure cancer.
Background: Viruses are a unique group of organisms that grow only in the cells
of bacteria, fungi ,protists, plants and animals. A typical virus is made of
a protein shell or a capsid , which surrounds a nucleic acid core. The genome
may be DNA or RNA. The function of the capsid is to protect the viral genome
while the virus is outside of living host cells. They range in size between
10 to 200 microns. In order to replicate they infect and take over the host
cell.
Whole viruses never arise directly from preexisting viruses.
They develop and reproduce only within cells of specific hosts. Since viruses
do not have many of the necessary structures like ribosomes to produce proteins,
they must redirect the genome of the host cell in order to reproduce themselves.
Cancer : A disease of genetic change. Some viruses cause cancer by mutating
the genome of the host cell. These mutations cause the host cells to lose control
over cell division, which leads to uncontrolled cell division, ultimately forming
malignant tumors.
Viruses
In addition to chemicals and radiation, a few viruses also can trigger the development
of cancer. In general, viruses are small infectious agents that cannot reproduce
on their own, but instead enter into living cells and cause the infected cell
to produce more copies of the virus. Like cells, viruses store their genetic
instructions in large molecules called nucleic acids. In the case of cancer
viruses, some of the viral genetic information carried in these nucleic acids
is inserted into the chromosomes of the infected cell, and this causes the cell
to become malignant.
Examples of Human Cancer Viruses
Only a few viruses that infect human cells actually cause cancer. Included in
this category are viruses implicated in cervical cancer, liver cancer, and certain
lymphomas, leukemias, and sarcomas. These cancers can sometimes be spread from
person to person by infectious viruses, although such events account for only
a very small fraction of human cancers. For example, the risk of cervical cancer
is increased in women with multiple sexual partners and is especially high in
women who marry men whose previous wives had this disease. Transmission of human
papilloma virus (HPV) during sexual relations appears to be involved
AIDS and Kaposi's Sarcoma
People who develop AIDS after being infected with the human immunodeficiency
virus (HIV) are at high risk for developing a specific type of cancer called
Kaposi's sarcoma. Kaposi's sarcoma is a malignant tumor of blood vessels located
in the skin. This type of cancer is not directly caused by HIV infection. Instead,
HIV causes an immune deficiency that makes people more susceptible to viral
infection. Infection by a virus called KSHV (Kaposi's sarcoma-associated herpesvirus)
then appears to stimulate the development of Kaposi's sarcoma.
Bacteria and Stomach Cancer
Viruses are not the only infectious agents that have been implicated in human
cancer. The bacterium H. pylori, which can cause stomach ulcers, has been associated
with the development of stomach cancer. People infected with H. pylori are at
increased risk of developing stomach cancer. Research is under way to define
the genetic interactions between infectious agents and their hosts that may
explain why cancer develops.
Click
here to see how a papilloma virus contributes to the development of cervical
cancer
http://press2.nci.nih.gov/science behind/cancer/cancer32.htm
http://www-ermm.cbcu.cam.ac.uk/9900040Xh.htm
How Cancer Viruses Hit Their Mark
Researchers have identified the role of a protein segment that allows some
cancer-causing viruses to latch onto and infect cells.
The scientists at Purdue University in West Lafayette, Ind., said the protein
segment resembles bee venom. If they can understand the protein and its mechanisms,
they can get a clearer picture of how retroviruses and some other viruses enter
cells.
This may lead to new therapies that target these viruses.
http://www.applesforhealth.com/howcancer1.html
Viruses, Variations and Environment-Studies on
Oral Cancer Etiology
For many years the human papilloma virus (HPV) has been suspected as a possible
culprit in the etiology of oral cancer. Two types of the virus, HPV-16 and HPV-18,
are found in oral cancer tissues more frequently than in normal tissues. Scientists
are still not sure, though, how HPV might contribute to the development of oral
cancer.
http://quitsmoking.about.com/library/blorcanc5.htm
Viruses and Cancer Viruses and Cancer
http://syllabus.syr.edu/bio/tpfondy/bio501/CxVirus/CxVirus.pdf
Viruses
and Cancer, 1962: What They Knew
http://ourworld.compuserve.com/
Yes,
Virginia, Viruses Do Cause Cancer
http://www.mcn.org/c/irapilgrim/toc12.html
Cancer Viruses
Molecular Virology Program
Patrick S. Moore, MD, MPH, Director
--------------------------------------------------------------------------------
The Molecular Virology Program (MVP) is devoted to basic science research on
the viral causes of cancer, the use of viruses in understanding fundamental
aspects of cancer cell biology, and the potential use of viral vectors to treat
malignancies. Over the past two decades, eight viruses have been found to cause
human cancers. It is estimated that approximately 20% of malignancies world-wide
are caused by infectious agents and additional human tumor viruses are likely
to be discovered. A number of common human cancers including Kaposi's sarcoma
(the most common malignancy in AIDS patients), cervical carcinoma, and some
forms of lymphoma, hepatocellular carcinoma, nasopharyngeal carcinoma, and adult
T cell leukemias are now known to be caused by viruses. Cancers occurring among
immunosuppressed persons, particularly AIDS and transplant patients, are frequently
caused by viruses. Because these cancers are caused by a foreign agent, unique
treatment opportunities exist to exploit immunologic or virus-specific therapeutics
The MVP program consists of core facilities and resources at the Hillman Cancer
Center that will include five laboratory faculty members by the time of it is
fully staffed in 2004. Approximately 30 associate MVP faculty members in the
University of Pittsburgh system make use of UPCI core resources and collaborate
on individual projects.
http://www.upci.upmc.edu/internet/research/Mol_Virology/
CancerPath - Internet Links to Cancer Sites & Cancer and Viruses
http://www.geocities.com/abettica/cancervirus.html
. Cancer is a disease of aging. It is caused by
heritable changes in the cell's genetic material. Cancer cells divide to produce
daughter cancer cells. Much of what we now know about the genes involved in
the development of cancer is attributable to research into RNA and DNA tumor
viruses. There are 7 families of viruses associated with tumors (1 RNA and 6
DNA families). The DNA viruses include the hepadnaviruses, the polyoma virus,
the papilloma viruses, the adenoviruses, the herpesviruses and the poxviruses.
The RNA virus family is the retroviruses (sub group oncoviruses). It is important
to note that in humans the association of viruses and cancer is not causal and
is often correlative or ambiguous. At best viruses are thought to be cofactors
or co-carcinogens in the development of human tumors. This underscores the fact
that cancer is a multistep process. It is the relative simplicity of the viral
genome (compared to the enormous complexity of the cellular genetic material)
that has permitted the identification of genes involved in the genesis of human
cancer.
http://iain.umsmed.edu/~micro/oncs.html
SV-40, a pro-cancer virus in vaccines
In 1955, Jonas Salk performed a medical miracle when he discovered how to mass
produce polio vaccine by growing it on the kidneys of rhesus monkeys. While
there is no question that thousands were saved from the ravages of polio by
the Salk vaccine, by 1960 a problem had surfaced -- researchers had isolated
a viral contaminate in the vaccine, Simian (monkey) Virus # 40. It seems that
when the live polio virus grown on monkey tissues was extracted for vaccine
production this SV-40 virus was extracted as well.
When SV-40 was injected into research animals it produced brain cancer. It
appears our government didn't wish to create a public panic or discredit the
public health service, because instead of recalling the tainted vaccines, it
quietly ordered the manufacturers to find a monkey free of SV-40 and continue
production. As of 1963, the rhesus monkey had been replaced with the African
green monkey for production of a safer polio vaccine, but between the years
of 1955 and 1963 as many as 98 million Americans had received doses of live
polio virus vaccines tainted with SV-40.
Nowadays SV-40 has appeared in 61% of all new cancer patients -- patients too
young to have received the contaminated vaccine being administered forty years
ago who are now believed to have been infected by human to human transmission.
Being a blood born organism, it is also suspected that SV-40 is transmissible
from mother to child during pregnancy. The more this matter is researched the
more startling the evidence. Senior epidemiologist at the National Institutes
of Health, Dr. Howard Strickler, has plotted a geographic pattern to the cancers
associated with SV-40 helping to confirm its link to the tainted vaccine. People
who lived in Massachusetts and Illinois who received identified lot numbers
of the contaminated vaccine administered in the 1950s are now demonstrating
ten times the rate of the osteosarcoma bone tumors as those who received vaccine
free of the SV-40 contaminate in other parts of the country.
DNA Polyoma Viruses
In 1964, studies were conducted on a polyoma virus (a tumor-producing DNA virus).
It was discovered that the persistent genetic DNA material in the polyoma virus
brought about malignant transformations in hamster embryo cell cultures. This
was reported in the November 23, 1964 issue of the Journal of the American Medical
Association.
SV-40 is one example of a DNA polyoma virus. Polyoma (many tumor-causing) viruses
cause prolonged infection where tissue is destroyed, integrate into the hosts
genetic material, are capable of mutating a cell, may reproduce after coming
into contact with a 'helper' virus, enable the separate replication of the viral
genome, can generate immune responses, and they can induce malignancy. Scientists
are amazed at how little genetic information these viruses carry in proportion
to the damage they can cause.
The 'D' in DNA and the 'R' in RNA have characteristics which are dependent
on the kind of sugar molecule associated with it. DNA exists predominantly in
the nucleus, but is also represented in the cytoplasm and in the mitochondria.
RNA is also present in the cytoplasm. When viral RNA or DNA combines with the
genetic material in the cell itself, the viral genetic material can become part
of the host cell genetic code, altering the genetic structure of the cell. When
the altered cell duplicates, the encoded viral genetic material may affect cellular
processes in such a way as to produce abnormal cells, which sometimes become
malignant or cancerous.
Cancer-Causing RNA Viruses and DNA proviruses
The discovery in 1975 that viruses causing cancer in animals had a special
enzyme called reverse transcriptase makes the problem even more interesting.
These kind of viruses are called RNA viruses. When an RNA virus has the reverse
transcriptase enzyme within its structure, it allows the virus to actually form
strands of DNA which easily integrate with the DNA of the host cell which it
infects. Studies by Dr. Robert Simpson of Rutgers University indicate that RNA
viruses which do not cause cancer can also form DNA, even without the presence
of reverse transcriptase. DNA formed in this way from an RNA virus is called
a provirus. It is known that some non-cancerous viruses have a tendency to exist
as proviruses for long periods of time in cells without causing any apparent
disease. In other words, they remain latent. Some examples of common RNA viruses
that do not cause cancer, per se, but have the capacity to form proviruses are
influenza, measles, mumps and polio viruses.
Viruses as Catalysts for Cancer
An article in the January 6, 1962 Science Newsletter indicated that 'common
human viruses act as carriers in causing cancer by interacting with cancer-causing
chemicals; this has been indicated by experiments which show that cancer-causing
substances that are present in too small a quantity by itself will become active
and create tumors when combined with single doses of virus. Malignant tumors
appeared in five type of injected mice.' The viruses mentioned were ECHO9, B-4,
Coxsackie, and Polio virus 2. The article further indicated that 'viruses may
also activate other cancer causing substances besides chemicals in the environment,
such as DMBA, AF, and DBA.'
Even common non-tumor viruses, including those in smallpox vaccine and polio
virus 2, can act as carcinogens. It was reported in Science on December 15,
1961 that these common viruses acted as catalysts in producing cancer when given
to mice in combination with known organic carcinogens in amounts too small to
induce tumors themselves. This means that some vaccinations will induce cancer,
when combined with the growing problem of environmental pollution from toxic
by-products of agriculture (pesticides on and in food) and industry.
A Listing of Cancer Causing Microbes
The July 14th 1997 issue of Business Week has an article in it about how many
cancers are being linked to various viruses, and bacteria ,and parasites. Among
the organisms now linked to cancer are as follows
Microbe Type of Cancer
------- --------------
Hepatitis B Virus Liver Cancer
Human Papiloma Virus ( HPV ) Cervical Cancer
Helicobacter Pylori Stomach Cancer
HTLV-1 A type of Leukemia in Japan
Epstein- Barr virus (EBV) Burketts Lymphoma, naso pharyngeal
cancer
Kaposi's Sarcoma Herpes Virus (KSHV) Kaposi's Sarcoma, and 100 % of
Myeloma cases.
Schistosomiasis Bladder Cancer
Liver Flukes Liver and biliary cancer
Helicobacter hepaticus Liver cancer
Hepatitis C Virus Liver cancer
Papilloma viruses (HPV-5,HPV-8,HPV-17) Skin cancer
Polyoma virus (BK and JC) Neural tumors? and insulinomas?
Retrovirus (HTLV-2) Hairy-cell leukemia
Lyme Disease bacteria B. Burgdorferi Skin and Breast cancer
Epstein-Barr Virus Majority of Non-Hogkins lymphoma (sp)
Granuloma type Virus Skin Cancer (Not confirmed)
References
Fisher, B. L. (1997). Workshop on Simian Virus 40: A Possible Human Polyoma virus.
National Vaccine Information Center, January 27, On-line at http://www.909shot.com/polio197.html
Carbone, M., et al. (1996). SV-40 Like Sequences in Human Bone Tumors. Oncogene,
13(3), 527-535.
Elswood, B. F., & Stricker, R. B. (1995). Polio Vaccines and the Origin
of AIDS. Medical Hypotheses, 42(6), 347-354.
Krieg, P., Amtmann E, Jonas, D., Fischer, H., Zang, K., & Sauer G. (1981).
Episomal Simian Virus 40 Genomes in Human Brain Tumors. Proceedings of the National
Academy of Sciences of the United States of America, 78(10), 6446-6450.
Lednicky, J. A., Garcea, R. L., Bergsagel, D. J., & Butel, J. S. (1995).
Natural Simian Virus 40 Strains are Present in Human choroid Plexus and Ependymoma
tumors. Virology, 212(2), 710-717.
Martini, F., et al. (1995). Human Brain Tumors and Simian Virus 40. Journal
of the National Cancer Institute, 87(17), 1331.
Martini, F., et al. (1996). SV-40 Early Region and Large T Antigen in Human
Brain Tumors, Peripheral Blood Cells, and Sperm Fluids From Healthy Individuals.
Cancer Research, 56(20), 4820-4825.
Pass, H. I., Kennedy, R. C., & Carbone, M. (1996). Evidence for and Implications
of SV-40 Like Sequences in Human Mesotheliomas. Important Advances in Oncology,
89-108.
Rock, A. (1996). The Lethal Dangers of the Billion Dollar Vaccine Business.
Money, December, pages 148-163.
Tognon, M., et al. (1996). Large T Antigen Coding Sequences of Two DNA Tumor
Viruses, BK and SV-40, and Nonrandom Chromosome Changes in Two Glioblastoma
Cell Lines. Cancer Genetics and Cytogenics, 90(1), 17-23.
Inherited virus may play role in breast cancer
NEW YORK, Aug 12 (Reuters Health) -- An inherited virus may be one of the factors
that triggers breast cancer in humans, researchers report. Scientists say that
a primitive retrovirus, human mammary tumor virus (HMTV), has been identified
in human breast cancer tissues.
'If a definitive link to this retrovirus is established, HMTV may become a target
for a vaccine to prevent breast cancer and a target for new treatments for breast
cancer,' explained study lead author Dr. Robert Garry of Tulane University in
New Orleans, Louisiana.
A retrovirus similar to HMTV has already been linked to malignant breast tumors
in mice. Speaking to attendees at the 11th International Congress of Virology
in Sydney, Australia, Garry explained that vertebrate species other than mice
-- including some humans -- carry similar viruses.
He said that his team had identified the virus, dubbed HMTV, in breast cancer
tissue and other organ issue from breast cancer patients, and also in tissues
from individuals who did not have breast cancer.
The virus, he said, is likely to be 'a cofactor' for triggering breast cancer,
along with other factors such as an individual's genetic makeup. Dr. Orli Etingin,
an oncologist and assistant professor of medicine at New York Hospital/Cornell
Medical Center in New York City, called the finding 'a very interesting new
piece of the (cancer) puzzle.'
Speaking with Reuters Health, she noted that 'retroviruses have (already) been
implicated in certain kinds of lymphomas.' But she believes that 'a lot more
research really has to be done in order to confirm the finding and also to establish
what the relationship of the virus is to the development of tumors in humans.'
Subcellular Life Forms
John Baez
September 3, 1998
Also available in Postscript and LaTeX, thanks to Stephen Mulraney.
I like biology, but as a mathematician, I am drawn to the elegance of the very
simplest forms of life: the subcellular life forms. They are so simple, in fact,
that even calling them "alive" can be controversial. They lack many
of the usual features of life. They don't have cell walls, most of them don't
metabolize, and they are all parasitic, depending on other organisms for their
ability to reproduce! Some of them even have no genetic code! Many of them cause
diseases, but others are crucial to the well-being of their host, and many are
so well integrated with their host that it becomes difficult to decide whether
they are part of the host or a separate entity.
Indeed, besides my love of elegance and my morbid fascination with parasites,
the main reason subcellular life forms appeal to me is that they challenge our
naive notion of organisms as entities with clear, well-defined boundaries. It's
clear by now that life doesn't respect this simple picture. Whenever a pattern
of any sort, however abstract, is able to replicate itself, it does! Typically
these patterns overlap and interact in subtle ways, so one can't easily say
where one ends and the other begins.
These are the main kinds of subcellular life forms that I know about so far:
Viruses
Viroids
Virusoids
Plasmids
Transposons
and
Prions
I'll say a little about each kind. If you know any more fascinating facts about
subcellular life forms - especially if you know kinds that aren't on this list
- please email me!
Some of the above terms are defined in an essay by Diener and Prusiner called
"The Recognition of Subviral Pathogens" [MM]. But beware! People argue
quite a bit about the correct classification of these life forms. That's part
of what's interesting about them: they really stretch our ideas in biology to
the breaking point.
One thing to keep in mind: these life forms are small. Remember that DNA is
a double helix containing information in the form of AT and CG "base pairs"
(paired molecules of adenosine and thymine, or cytosine and guanine), while
single-stranded RNA is a single helix containing information in the form of
A, U, C, and G "bases" (molecules of adenosine, uracil, cytosine and
guanine). The human genome is made of DNA and contains about 5 billion base
pairs. The genome of a bacterium is also made of DNA but has less than 10 million
bases. The potato spindle tuber viroid, on the other hand, is nothing but a
circular loop of RNA consisting of 359 bases! Small, simple - but effective!
--------------------------------------------------------------------------------
Viruses
Diener and Prusiner define a virus to be a "small infectious pathogen composed
of one or more nucleic acid molecules usually surrounded by a protein coat."
They typically reproduce by latching onto the wall of a cell and inserting their
genetic material - i.e., the nucleic acids - into the cell. This genetic material
then uses the cell's machinery to make more copies of the virus. Typically,
these copies overrun the cell until it bursts. However, the actual life cycle
of a virus is often more complicated than this thumbnail sketch! Viruses use
a large number of sneaky tricks to overcome the defense mechanisms of the cell.
Apart from their intrinsic interest, viruses are important because they cause
many diseases among humans, such as:
the common cold
influenza (the flu)
measles
rubella
mumps
warts
chickenpox
smallpox
acquired immunodeficiency syndrome (AIDS)
herpes
hepatitis
rabies
poliomyelitis (polio)
encephalomyelitis
encephalitis
yellow fever
dengue fever
as well as diseases of domesticated animals and plants.
There is standard taxonomy of viruses [CT] [Ma2], [F], but I will content myself
with a rough classification into the following 3 sorts:
DNA viruses
RNA viruses
and
Retroviruses
DNA viruses
The genome of a DNA virus is a single molecule of DNA, either linear or circular,
and usually double-stranded. Outside the host cell, this DNA is surrounded by
a protein coat. There are 5 known families of DNA viruses affecting humans.
The size and structure of the DNA viruses varies widely, from the small hepatitis
B virus (HBV), whose round shell contains a circular DNA molecule with about
2,400 base pairs, to the large brick-shaped or ovoid pox viruses, which have
a lipid coating and whose DNA has between 120,000 and 360,000 base pairs.
Like retroviruses, some DNA viruses work their way into the nucleus of their
host cell and then copy themselves into the host's DNA. An example is the he pat it us
B virus, which occupies liver cells. This can cause tumors.
RNA viruses
The genome of an RNA virus is usually a single molecule of RNA, either linear
or circular, but some contain up to a dozen molecules of RNA. Outside the host
cell, this RNA is protected by a protein coat. Most viruses are RNA viruses.
There are 13 known families of RNA viruses affecting humans. RNA virus range
widely in morphology and size, with their genome containing anywhere from 1,700
to 60,000 nucleotides.
(Actually the smallest one, the hepatitis delta agent (HDV), is quite different
from all the rest. Like a virusoid, it is a circular loop of RNA that can only
reproduce in cells infected by a helper virus, the hepatitis B virus. But unlike
a virusoid, it affects animals rather than plants, it has its own protein coat,
and its genome is bigger than that of a virusoid, having 1,700 nucleotides instead
of a mere 350 or so. However, its genome is much smaller than that of any other
virus.)
One can broadly classify RNA viruses into:
positive-strand RNA viruses
negative-strand RNA viruses
double-stranded RNA viruses
A "positive-strand" RNA virus consists of single-stranded RNA that
functions directly as messenger RNA in the host cell, so that ribosomes in the
host cell synthesize various proteins needed by the virus when encountering
this RNA. A "negative-strand" RNA virus consists of single-stranded
RNA that does not function as messenger RNA, since it contains the complementary
base pairs. Negative-strand RNA viruses carry enzymes with them into the host
cell to synthesize messenger RNA from the RNA in the virus. "Double-stranded"
RNA viruses have both positive and negative strands. For some reason these are
more likely to consist of several separate pieces of RNA.
Retroviruses
Retroviruses are like RNA viruses when outside the host cell, but once inside
the cell's nucleus, they can copy themselves into the DNA of the host cell using
an enzyme called "reverse transcriptase", which translates RNA into
DNA. They are thus intermediate between RNA viruses and nuclear DNA viruses.
Once they are integrated into the DNA of the host cell, they may take a long
time to reemerge. In fact, so-called "endogenous retroviruses" can
be passed down from generation to generation, indistinguishable from any other
cellular gene, and evolving with their hosts! The very distinction between host
and parasite becomes somewhat blurry in this case. In fact, once an endogenous
retrovirus lost the genes that coat for its protein coat, it would become indistinguishable
from an LTR retrotransposon - one of the many kinds of "junk DNA"
cluttering up our chromosomes.
It has been estimated that between .01% and .1% of the genome of wild and laboratory
mice consists of endogenous retroviruses. The same is probably true for humans.
to form protein coats - since most mammalian DNA serves no known purpose, the
above figures may be drastic underestimates. Indeed, 97% of human DNA is so-called
"junk" DNA of this sort!
Retroviruses are important in genetic engineering because they raised for the
first time the possibility that RNA could be transcribed into DNA, rather than
the reverse. In fact, some of them are currently being deliberately used by
scientists to add new genes to mammalian cells.
In addition, retroviruses are important because AIDS is caused by a retrovirus:
the human immunodeficiency virus (HIV). This is part of why AIDS is so difficult
to treat. Most usual ways of killing viruses have no effect on retroviruses
when they are latent in the DNA of the host cell.
Many retroviruses cause tumors in animals. These viruses contain host-derived
genetic information.
--------------------------------------------------------------------------------
Viroids
A viroid is defined to be a "small infectious pathogen composed entirely
of a low molecular weight RNA molecule". Thus, unlike a virus, a viroid
has no protein coat. It is nothing but a single-stranded circular loop of RNA!
Most viroids consist of about 250 to 575 nucleotides, much smaller than a typical
virus. Also, viroids don't function as messenger RNAs, so they don't make the
cell synthesize enzymes: they rely completely on pre-existing enzymes in the
host for their reproduction.
Most known viroids cause diseases in plants. The first viroid was discovered
in 1971, by Diener. It's called the potato spindle tuber virus (PSTV), since
it causes a disease that makes potatoes abnormally long and sometimes cracked.
At the time, Diener's isolation of the viroid causing this disease met with
some skepticism, since it was so much smaller than any known virus. By 1991,
however, at least 15 plant diseases had been traced to viroids. There are also
2 viroids known, the hop latent viroid (HLV) and a viroid living in grapevines,
that cause no known symptoms! This raises the fascinating possibility that there
could be more such viroids lurking around.
The complete molecular structure of many viroids has been worked out, which
has allowed a classification of viroids on the basis of their RNA sequences.
Roughly speaking, there are a large family of viroids that share many features
with PSTV, together with one viroid that seems very different: the avocado sun blotch
viroid (ASBV). McInnes and Simons have proposed a further classification of
the PSTV-type viroids into three kinds [Ma1].
It is clear from these RNA sequences that viroids are not "degenerate
viruses", as had once been thought. They are quite different from any known
viruses. One interesting theory is that they arose from RNA that escaped from
cell nuclei.
It's also interesting that all viroid diseases have been detected in the 20th
century, some quite recently - in contrast to diseases caused by viruses. Also,
many viroid diseases have been spreading after their discovery, often due to
human activity. A fascinating example is the coconut cadang-cadang viroid (CCCV),
a disease of coconuts which has been spreading throughout the Phillipines. On
the island of Luzon, a puzzling feature of this disease was that it only affected
crops owned by speakers of Bicalano, while adjacent crops owned by speakers
of Tagalog went unharmed! Eventually people realized that the viroids were spread
by workers cutting the palms. Tagalog owners prefer to hire Tagalog workers,
while Bicalanos hire Bicalanos, some of whom came from an area where the disease
was prevalent. (See the article by Maramarosch entitled "The Cadang-Cadang
Viroid Disease of Palms" [D].)
Because of this sort of epidemiology, Diener has suggested that viroids may
be latent to their native host plants (like HLV), becoming pathogenic only when
transferred to other species thanks to agriculture. Indeed, the viroid causing
tomato "planta macho" disease in Mexico, TPMV, has also been found
in wild plants there, where it seems sometimes "recover" from ASBV
by sending up a new shoot. This new shoot is still infected with the viroid,
but it shows no symptoms other than reduced fruit yield. Descendents of such
a "recovered" tree are also infected with the viroid, and also symptomless,
except for reduced fruit yield. Thus the avocado appears able to "come
to terms" with the viroid in some way. Personally, I'd like to raise this
possibility: that some viroids actually play a beneficial role in their native
host plants! This may seem surprising, but when we compare the behavior of plasmids,
it may seem less so.
--------------------------------------------------------------------------------
Virusoids
A virusoid is a "viroid-like RNA encapsidated in a virus shell that also
contains viral RNA". In other words, like viroids, they are circular loops
of RNA, usually containing about 350 nucleotides. But unlike viroids, they reside
inside the protein coat of a "helper virus". They can only reproduce
in cells that have been infected by this helper virus, because they use some
of the RNA of the helper virus to reproduce. The helper virus is typically an
RNA virus consisting of about 4500 nucleotides.
In short, a virusoid is a parasite of its helper virus. But it's not always
so simple. Sometimes the helper virus is unable to reproduce unless the virusoid
is present! Then we have symbiosis rather than parasitism.
The first virusoids were discovered in the early 1980s in Australia, associated
with viruses causing plant diseases such as velevet tobacco mottle (VTMoV),
solanum nodiflorum mottle (SNMV), lucerne transient streak (LTSV), and subterranean
clover mottle (SCMoV).
An interesting theory about the origin of virsoids is that in plants infected
with both viruses and viroids, the viroids got encapsidated in the viruses and
later lost their ability to reproduce independently.
At this point, I should admit that the terminology concerning virusoids is
quite confusing to me. People sometime use "satellite RNA" as a synonym
for "virusoid", but I'm not always sure when it's supposed to be an
exact synonym. Diener and Prusiner define a "satellite RNA" to be
a "small RNA that does becomes packaged in protein shell made from coat
proteins of another, unrelated, helper virus, on which the satellite RNA depends
for its reproduction". The similar-sounding term "satellite virus"
appears to be reserved for an RNA virus that depends for its reproduction on
an unrelated helper virus, but whose genome codes for its own protein coat.
--------------------------------------------------------------------------------
Plasmids
A plasmid is a "small autonomously replicating circular molecule of DNA
that is devoid of protein and not essential for the survival of its host".
Plasmids range in size greatly, from about 4350 to 240,000 base pairs. Most
known plasmids infect bacteria, but some infect plant and animal cells. They
often copy themselves into the DNA of the host cell, and many carry genetic
traits from one cell to another. Most plasmids keep a limit on the number of
copies of themselves they keep in each host - the so-called "copy number",
which ranges from 1 to about 40. Many plasmids are "conjugative".
This means they can transfer copies of themselves from one host to another by
forcing the host to undergo "conjugation" - a form of sex in which
genetic material is exchanged between bacteria.
People tend not to speak of plasmids as "life forms" quite as often
as they do with viruses. In part this may be because plasmids are sometimes
beneficial to their host cells, rather than pathogenic.
However, is difficult for me to resist the impression that plasmids are just
as "alive" as viruses. Indeed, some viruses become plasmids when parts
of them are missing! For example, the "lambda bacteriophage" is a
virus that infects the intestinal bacterium E. coli, but "lambda dv particles",
which arise from the lambda phage simply by deleting some DNA, are plasmids.
The lambda phage multiplies inside its host and then kills it by "lysis",
which destroys the cell membrane and releases lots of copies. The lambda dv
particles, on the other hand, stays in the cell in a fairly stable number of
copies and does not kill its host. The difference is that while the lambda dv
particles contain genes for replication, they lack genes for lysis and the protein
coat.
If we think of plasmids as life forms, we must admit that they are very successful.
Many plasmids spread so thoroughly in cultures of bacteria that less than one
cell in 100,000 lacks a copy! Some kinds of plasmids contain genes that help
make sure copies are efficiently passed on to both daughter cells when the host
cell divides. F plasmids have a particularly clever mechanism - they temporarily
inhibit cell division when they have not yet replicated inside the host!
Plasmids are diverse and very interesting. Some important kinds are:
R Plasmids
F Plasmids
Colicin Plasmids
Virulence Plasmids
Metabolic Plasmids
Tumor-Causing Plasmids
and
Cryptic Plasmids
While they don't quite fit under this heading, I can't resist also mentioning
Cosmids
and
Phasmids
These are man-made entities based on plasmids, used in biotechnology. Are they
alive? You judge.
Some good books on plasmids include "Plasmids" by Paul Broda [B],
"Bacterial Plasmids" by Kimber Hardy [H], and "Plasmids of Eukaryotes:
Fundamentals and Applications" by K. Esser et al [E].
R Plasmids
R plasmids were first discovered in Japan in 1957. In Japan, dysentary was treated
with sulphonamide until about 1950. Then, more and more strains of the bacteria
causing dysentary became resistant to this antibiotic, rapidly rendering it
ineffective. Doctors then began using tetracycline, streptomycin and chloramphenicol.
By 1957, 2% of the bacteria causing dysentary were resistant to one of more
of these drugs, and by 1960, 13% were resistant. It turned out that R plasmids
were the culprit!
R plasmids contain genes that give their bacterial hosts resistance to antibiotics
as well as to poisonous metal ions such as arsenic, silver, copper, mercury,
lead, zinc and so on. Because many R plasmids are conjugative, this resistance
can spread from one bacterium to another. Because they can live in more than
one species of bacteria, R plasmids can also spread resistance between bacteria
of different species!
Spread of resistance to antibiotics is now a major problem in medicine. Drugs
which were used for many years to control bacterial diseases are now becoming
helpless against new resistant strains. The problem has been made worse by the
tendency for doctors and veterinarians to use antibiotics when they aren't strictly
necessary, for example as part of livestock food. As a result an environment
is created where bacteria with resistance have a great competitive advantage,
so they spread rapidly.
It has also recently been found that weeds growing near crops that were genetically
engineered to resist herbicides can acquire this trait. I'm not sure, but I
suspect that this happens via plasmids as well.
R plasmids make it clear that the idea of evolution as a battle between species
with separately evolving genomes is a great oversimplification. Instead, genetic
communication and cooperation between different species can be very important.
F Plasmids
F plasmids live in the bacterium E. coli and were discovered in the 1920s. An
F plasmid contains genes that make the cell membrane of its host form long tubes.
These tubes, called "sex pili", attach themselves to other E. coli
and puncture their cell membranes. The F plasmid then duplicates and a copy
passes from the original host to the new host. A clever system has evolved to
ensure that the sex pili of a given bacterium never attach to itself.
F plasmids give their hosts no known traits besides these sex pili. The evolutionary
origins of sex are much debated these days; we see here the fascinating possibility
that sex can originate as a kind of disease whose sole function is to spread
a parasite!
Colicin Plasmids
Colicin plasmids contain genes that give their host bacterium a certain small
probability of bursting open and releasing chemicals called "colicins".
These chemicals kill other bacteria by rendering their cell membranes permeable
to important ions. There are many strains of colicin plasmid. Each one confers
immunity only to the particular sort of colicin it produces. Different strains
of colicin plasmid are "incompatible", meaning that a given strain
bacterium cannot stably contain both.
In short, different strains of colicin plasmid compete with each other using
the resources of their hosts. A colicin plasmid will confer an advantage to
its host bacteria if the other strains of bacteria nearby do not have a colicin
plasmid. However, when there are many different strains of colicin plasmid present,
all strains of host bacteria suffer. Thus there is a certain similarity between
colicin plasmids and "protection rackets" run by Mafia-like gangs.
Colicin plasmids are not the only sort of plasmids that exhibit incompatibility.
Similar plasmids tend to be incompatible with each other, while drastically
different plasmids are usually compatible. One theory is that incompatible plasmids
use the same mechanisms to maintain their copy number. In a cell containing
two incompatible sorts of plasmid, their reproduction is blocked until the total
number of copies of the two together drops to the copy number of each one. This
is an unstable situation, especially for plasmids with a low copy number, so
eventually descendants of the host cell contain only one or the other plasmid.
Virulence Plasmids
Virulence plasmids contain genes that make their bacterial hosts more virulent
to their hosts. A familiar example involves the bacterium E. coli, which inhabits
the human large intestine. Certain strains of E. coli contain plasmids whose
genes make the E. coli synthesize toxins that cause diarrhea. These "enterotoxigenic
strains" of E. coli are probably an important cause of diarrhea among travellers.
More seriously, in developing countries, diarrhea is one of the principal causes
of death among those under five.
"Vibrio cholerae", the cause of cholera, is a bacterium whose genes
code for a diarrhea-causing toxin. The DNA of these genes is closely related
to the DNA of certain virulence plasmids infecting E. coli - so closely that
there is almost certainly a common ancestor. For example, Vibrio cholerae could
have evolved from an earlier bacterium by permanently integrating the DNA from
a virulence plasmid into its genome.
Strains of bacteria and viruses often become less virulent as they coevolve
with their hosts. Thus one may wonder what evolutionary advantage a virulence
plasmid could confer to the bacteria containing it. In the case of bacteria
causing diarrhea, there is an obvious possibility: diarrhea can serve as a mechanism
for spreading the bacteria - and their plasmids - that cause it!
Metabolic Plasmids
Metabolic plasmids contain genes that let their bacterial hosts metabolize or
degrade otherwise indigestible or toxic chemicals. For example, the bacterium
Pseudomonas putida is able to grow on a wide range of organic compounds that
are toxic to most bacteria, including toluene, octane, camphor, napthalene and
nicotinic acid! It does this with the help of genes contained by metabolic plasmids
called TOL, OCT, CAM, NAH and NIC plasmids.
It's worth noting that some of these chemicals are secreted by plants as part
of a defense against bacteria. Thus we probably have a kind of natural chemical
arms race going on here. Other metabolic plasmids allow bacteria to degrade
herbicides like 2,4-D, as well as certain detergents! People are investigating
the use of such plasmids to help biodegrade pollution.
Tumor-Causing Plasmids
"Crown gall" is a cancer of plants caused by a bacterium known as
Agrobacterium tumefaciens. But actually, the disease is caused by a plasmid
having this bacterium as its host! When the plasmid passes from the bacterium
to the cells of infected fruit trees, some of the genes contained in the plasmid
cause tumors. Do these tumors help spread the bacteria to other trees?
Cryptic Plasmids
Cryptic plasmids are plasmids that have no known effect on their hosts. How
much of this is our ignorance, and to what extent is being truly "cryptic"
a successful strategy?
Cosmids
Cosmids are man-made circular loops of DNA containing plasmid DNA together with
an arbitrary sequence of up to 45,000 base pairs of DNA. They are constructed
by recombinant DNA techniques and then packaged in lambda phage protein coats.
They are used to transfer genes to bacteria.
The lambda phage is a virus that specializes in invading bacteria such as E.
coli. In nature, its protein coat latches onto the bacterial cell membrane and
injects the phage DNA into the bacterium. Biotechnologists have taken advantage
of this by using the lambda phage protein coat to inject a cosmid into the bacterium!
Once inside, the cosmid replicates like a plasmid and, like a plasmid, integrates
its DNA into the genome of the bacterium.
Phasmids
Phasmids are man-made linear DNA molecules whose ends are sequences taken from
the lambda phage, while the middle is a sequence taken from a plasmid, together
with a sequence of whatever DNA one wants. Like cosmids, they are constructed
by recombinant DNA techniques and packaged in lambda phage protein coats, and
used to transfer genes to bacteria. However, both the lambda phage and plasmid
replication functions are intact. In particular, they contain the lambda phage
genes for "lysis", the process whereby a virus dissolves the cell
membrane of its host. Depending on the conditions, the phasmid can act either
like a phage or a plasmid - hence its name.
--------------------------------------------------------------------------------
Transposons
Transposons, or "transposable elements", are sequences of DNA that
move within their host's genome from one position to another. They were first
discovered in the 1940s by Barbara McClintock, who later won the Nobel prize
for this work. They exist in all known organisms, often in large quantities.
Their main "function" appears to be simply their own self-replication,
rather than any benefit to the host, or even any direct effect whatsoever on
the host phenotype. For this reason, people sometimes refer to transposons as
"selfish DNA".
In addition to transposons, there is plenty of other DNA in our chromosomes
that doesn't seem to code for proteins. This is sometimes called "junk
DNA". It comes in various distinct forms, such as "introns",
"satellite DNA", and "pseudogenes". In fact, junk DNA makes
up about 97% of the human genome! Clearly despite its derogatory name, it's
worth understanding and potentially very important. However, since transposons
are the most "organism-like" of junk DNA, I will only talk about them
here.
There is a fair amount of genetic evidence that transposons spread "horizontally"
between sexually isolated species in addition to being "vertically"
passed down the evolutionary tree. However, the mechanisms of this horizontal
transmission are poorly understood. One interesting fact is that certain viruses,
the baculoviruses, can pick up and accomodate transposons from their hosts.
They have been proposed as a possible mechanism for horizontal transmission
of transposons.
The two main classes of transposons are:
Retrotransposons
and
DNA Transposons
The best book on transposons seems to be "Dynamics and Evolution of Transposable
Elements", by Pierre Capy, Claude Bazin, Dominique Higuet, and Thierry
Langin [CBHL]. In this book, retrotransposons are called "Class I elements",
while DNA transposons are called "Class II elements". They also discuss
"Class III elements". This seems to be a grab-bag consisting of transposons
that don't clearly fit into the other two categories. Examples include the "Foldback"
elements in fruit flies, the "Tu" elements in sea urchins, and "MITEs",
or "miniature inverted repeat transposable elements", which are found
mainly in plants and fungi.
Retrotransposons
Retrotransposons copy themselves from one location in the host genome to another
using an RNA intermediate, with the help of reverse transcription from RNA to
DNA.
A rough classification of retrotransposons divides them as follows:
LTR (long terminal repeat) retrotransposons
non-LTR retrotransposons
LINEs (long interspersed nuclear elements)
SINEs (short interspersed nuclear elements)
LTR retrotransposons are are 5000-9000 base pairs long and have "long terminal
direct repeats" - repeating sequences of base pairs at both ends. Between
these are the genes needed for transposition, which code for enzymes like reverse
transcriptase (which copies RNA into DNA), integrase (which integrates the DNA
into the host chromosome), and so on. In all these respects, LTR retrotransposons
are very similar to retroviruses. The most important difference is that retrotransposons
do not code for the proteins forming the viral protein coat. There seems to
be some debate as to whether retrotransposons are retroviruses that have somehow
lost their ability to code for a protein coat, or whether retroviruses are retrotransposons
that have somehow gained this ability. Of course, the two possibilities aren't
mutually exclusive!
As the name suggests, non-LTR retrotransposons lack terminal repeats. They
have been divided into LINEs and SINEs. LINEs have a characteristic adenosine-rich
sequence at one end, and are generally 5000-8000 base pairs long, though truncated
versions are common. They code for various enzymes such as reverse transcriptase
and RNase. The genomes of higher animals and plants may have over 10,000 copies
of LINEs. In fact, at least 15 percent of the human genome consists of LINEs!
SINEs are usually shorter than 500 base pairs. The source of the enzymes needed
for the mobility of SINEs is not yet known - but perhaps it is LINEs! Higher
animals and plants may have over 100,000 copies of SINEs.
DNA transposons
DNA transposons mainly move using a cut-and-paste mechanism: they code for an
enzyme called a "transposase" that catalyzes a process in which the
transposon DNA is excised and reinserted elsewhere in the host genome. Thus
RNA and reverse transcriptase plays no role in their life cycle.
--------------------------------------------------------------------------------
Prions
Prions are small, proteinaceous infectious particles that contain no detectable
nucleic acid of any form, but are transmissible among certain animals, where
they cause fatal brain diseases. These particles are rod-shaped, about 165 nanometers
long and about 11 nanometers in diameter, and they consist largely of a protein
called PrPSc, having molecular weight 33,000-35,000. They are able to resist
inactivation by boiling, acid (pH 3-7), ultraviolet radiation (254 nm), formaldehyde,
and nucleases! They can be inactivated by boiling in detergents, alkali (pH
> 10), autoclaving at 132 degrees centigrade for over 2 hours, and denaturing
organic solvents such as phenol.
Stanley Prusiner won the Nobel prize for medicine in 1997 for his work on prions.
His theory is that prions are a modified form of a protein naturally occuring
in the brain (PrP), and that this modified form can arise from a cell mutation,
but then spread by means of a kind of autocatalyzed chain reaction. This theory
was initially very controversial, because all other self-reproducing biological
entities appear to contain RNA or DNA. There are still many doubters. In the
earlier literature prions are sometimes called "slow viruses", because
of their slow effect. However, no virus has ever been associated with prion
diseases.
Prions have recently received a lot of publicity as the cause of "mad
cow disease", technically known as bovine spongiform encephalopathy. Starting
in the mid-1980s, this disease infected thousands of cattle in England, in part
because they were being fed offal containing nerve tissue from sheep infected
with a prion-caused disease called "scrapie". People got worried that
eating meat from cows with bovine spongiform encephalopathy could cause a prion-induced
brain disease in people. This caused an enormous uproar.
There are already a number of prion-induced brain diseases in people, such
as Creutzfeldt-Jakob disease (which occurs spontaneously in about one in a million
people) and kuru (transmitted by means of cannibalism among the Fore tribe in
New Guinea). There are also prion-induced brain diseases in mink, cats, deer
and moose.
--------------------------------------------------------------------------------
References
Here are some good books to read about this stuff:
[B] Plasmids, by Paul Broda, W. H. Freeman, San Francisco, 1979.
[CBHL] Dynamics and Evolution of Transposable Elements, by Pierre Capy, Claude
Bazin, Dominique Higuet, and Thierry Langin, Landes Bioscience, 1998.
[CT] Principles of Bacteriology, Virology and Immunity, vol. 4: Virology, edited
by L. H. Collier and M. C. Timbury, 8th edition, Decker, 1990.
[D] The Viroids, edited by Theodore Otto Diener, Academic Press, 1985.
[E] Plasmids of Eukaryotes: Fundamental and Applications, K. Esser et al, Springer-Verlag,
New York, 1986.
[F] Virology, 2 volumes, edited by Bernard N. Fields, David M. Knipe and Peter
M. Howley, Lippincott-Raven Publishers, 3rd edition, 1996.
[H] Bacterial Plasmids, Kimber Hardy, American Society for Microbiology, Washington
D.C., 1986.
[MM] Subviral Pathogens of Plants and Animals: Viroids and Prions, edited by
K. Maramorosch and J. J. McKelvey, Jr.., Plenum Press, 1987.
[Ma1] Viroids and Satellites: Molecular Parasites at the Frontier of Life,
edited by Karl Maramarosch, CRC Press, 1991.
[Ma2] The Atlas of Insect and Plant Viruses: Including Mycoplasmaviruses and
Viroids, edited by Karl Maramorosch, Academic Press, 1977.
[Mo] The Evolutionary Biology of Viruses, edited by Stephen S. Morse, Raven
Press, 1994.
[R] Plant Infectious Agents: Viruses, Viroids, Virusoids, and Satellites, edited
by Hugh D. Robertson et al., Cold Spring Harbor Laboratory, 1983.
THE ROBERT CATHEY RESEARCH SOURCE
http://www.navi.net/~rsc
--------------------------------------------------------------------------------
[Originally Published in: U.S. Psychotronics Proceedings, 1993; republished
by permission]
Royal Rife Revisited:
Reconstruction of the Original Rife Ray Tube
by
David M. Tumey and William H. Sheline
Abstract -- In this paper the authors relate information obtained from over
three years of work spent researching and reconstructing a working replica of
Royal Rife's original Ray Tube apparatus. A description of Rife's discovery
of the pleomorphic nature of microorganisms is given along with details of how
this led him to invent a revolutionary non-invasive pathogen devitilization
technique. Also discussed with limited detail was Rife's development of his
extraordinary microscopes. The authors attempt to give the reader new insights
into this exciting, readily available technology. Finally, the authors describe
the design and fabrication of a complete and working beam tube system, constructed
with antique and surplus electronic components. This paper attempts to provide
enough information so that all can understand what it was Rife was attempting
to accomplish, how Rife's machines worked, and how similar machines might be
manufactured today. Also, a list of the original known Mortal Oscillatory Rates
(MORs) is provided. No claims for the use of this device in healing human subjects
are made.
Introduction -- Royal Raymond Rife (1888 - 1971) was an accomplished scientist
and microbiologist who developed an optical microscope that could provide magnifications
and resolutions heretofore unheard of. He was able, through special quartz optics
and a creative optical heterodyning technique, to obtain these resolutions even
though they surpassed the theoretical limits of ordinary visible light microscopy.
Theoretically, the wavelength of the source illumination is the limiting factor
in achievable resolution. It is not possible to image something smaller than
the wavelength of the microscope's light source. That is why electron microscopes
(with far shorter wavelength) can be used today to image extremely small objects.
The major difference between visible light and electron microscopy is that,
by its nature, electron microscopes destroy the microorganisms while viewing
them. Rife's major advantage was that he could observe them in their natural
state. His most powerful instrument is said to be the Universal Microscope which
had a magnification of 61,000X and a resolution of 30,000 diameters. Compare
this with today's state-of-the-art light source microscopes which are limited
to approximately 5,000 diameters.
Rife began his work with the microscopes in the early 1920's and it was from
these original developments that he would make many of his revolutionary discoveries.
It is argued that Rife was the first person to empirically prove that virus
and bacteria are pleomorphic forms. Pleomorphism is the phenomenon by which
one distinct life form mutates into another. Rife basically classified pathogenic
bacteria into 10 individual groups. Rife demonstrated that any organism within
its group could be transformed morphologically into any other organism within
the 10 groups by carefully altering the media in which it was cultured. Of course
this discovery contradicts modern microbiology which teaches that a bacteria's
morphology is fixed and unchangeable.
Rife also discovered techniques for successfully culturing cancer virus. This
virus he identified as BX and it was noted that the viruses refracted a purplish
red color with a monochromatic beam under his microscope. In fact, Rife discovered
that each organism depending on its state would refract unique spectra and have
distinct coloration. By the late 1920's and early 30's, Rife had discovered
that by irradiating these pathogenic microorganisms with specific frequencies
known as MORs for Mortal Oscillatory Rates, he could cause them to devitalize
either by interrupting normal cytologic function or by inducing them to mutate
into a non-pathogenic form.
The instrumentation involved in this irradiation process has been the subject
of a great deal of controversy over the past 50 years. After researching books,
films, articles and notes, the authors have concluded that Rife irradiated his
pathogenic entities with a modulated radio frequency produced by a sophisticated
RF plasma discharge. Rife utilized a radio frequency generator that produced
between 100 and 150 Watts of power with a carrier frequency between 3.1 Mhz
and 35 Mhz. The output from the generator was connected through suitable impedance
matching circuitry to a plasma discharge tube with one or more noble gases.
It is believed that Helium was the primary gas used although many researchers
cite Argon or an Argon mix as the choice ingredient. Further, Rife utilized
a standard dial-type vacuum tube audio frequency generator as the modulation
source for his radio frequency transmitter. The modulation signal was a square
wave and it is assumed he chose this waveform because of its high harmonic content
and broad spectral contributions.
Rife obtained the original MORs through a painstaking method of tuning the
dial of the audio frequency generator while observing the sample pathogen under
his microscope. When a frequency was discovered that demonstrated the ability
to devitilize a particular microorganism, its dial position was duly noted and
marked. The actual frequencies were determined later after the experimental
trials. By the mid 1950s the verified original MOR frequency list included 15
different bacteria and viruses. Regardless of what other researchers have said,
the authors believe that these 15 frequencies represented the complete list.
The following is a listing of these known MORs as compiled by Dr. Robert P.
Stafford, M.D. a physician who worked with an original Rife machine from 1957
to 1963:
Microorganism Frequency in Hertz
------------- ------------------
Tetanus 120
Treponema 660
Gonorrhea 712
Staphlococci 728
Pneumococci 776
Streptothrix (fungus) 784
Streptococci 880
Typhoid Bacteria 712
Typhoid Virus 1862
Bacillus Coli Rod Form 800
Bacillus Coli Virus 1552
Tuberculosis Rod Form 803
Tuberculosis Virus 1552 (same as B-Coli)
Sarcoma (all forms) 2008
Carcinoma (all forms) 2128
Dr. Stafford who is still living in Dayton, Ohio, independently verified some
of Rife's work. Dr. Stafford conducted a rat study with the assistance of Dr.
Robert Zipf, M.D., who at the time was the Director of Medical Research at Miami
Valley Hospital and in addition, the Montgomery County Coroner. Chloroleukemic
Sprague-Dawley rats were utilized in the experiment. Although it is beyond the
scope of this paper to discuss the study results in detail, the encapsulated
summary is as follows: Ten suckling rats were injected with standard doses of
rat leukemic whole blood. Of the seven rats which were inoculated and treated
with the Rife equipment, three survived without symptom. Four of these rats
died. However, the average time to death was 50.5 days as compared to the group
of three non-treated rats which had an average death time of 43.6 days. In addition,
all the non-treated rats died. Clearly, even with the four 'failed-cures', in
the group of treated rats the Chloroma was favorably impressed.
Details of the Original Tube -- In the "Cancer Cure that Worked",
Barry Lynes includes a quote penned by Rife himself, which describes the principles
of the original Ray Tubes. Also, photographs of original tubes can be found
in "The Rife Way III" by Mark Simpson. Figure 1 details the component
arrangement of the early units (prior to the formation of Beam Ray Corp.). As
described in the introduction, a standard frequency generator (a) was utilized
as the square wave modulation source. The individual MORs were selected for
broadcast via this instrument. The function generator was connected to the radio
frequency generator (b). The square wave signal from the frequency generator
was employed in a screen-grid modulation arrangement with the final amplifier
of the radio frequency generator. The RF generator incorporated circuitry bearing
resemblance to a standard radio transmitter and had a single stage crystal controlled
oscillator connected to a class-C amplifier stage. Most likely, the oscillator
used either a 6AG7 or 6V6 vacuum tube, while the output was obtained from a
pair of standard RF transmitter tubes. RCA designed 807's were introduced in
the later models (1940's).
The output from the amplifier was connected to an impedance matching network
(c) designed to maximize the transfer of RF power from the generator to the
gas plasma. As with any transmitter, maximum power transfer occurs when the
impedance of the generator is the same as the impedance of the load. The major
problem with matching to a plasma is that the plasma's impedance is dynamic
and highly non-linear. Rife must have been faced with a formidable challenge
having to address the many variables involved in controlling an RF plasma. The
original plasma tubes were modified X-ray tubes (d). The tube elements were
left intact, however, he tube was refilled with one or more noble gases. When
the plasma discharge occurred, the tube glowed purplish blue as attested to
by Dr. Stafford, John Crane (Rife's research assistant from 1950 - 1971) and
others. Later, Rife had several tubes fabricated from scratch. It is not known
precisely how many of this genus of tube were manufactured.
Although records are difficult to accurately verify, it is generally
thought that patients were treated every third day by exposing them to each
frequency on the list for three to four minutes. Normally, only a subset of
frequencies were used, a popular list being 728, 784, 880, 2008, and 2128 Hertz.
While the modulation frequencies were being broadcast to the patient, the discharge
tube was moved over the body of the subject. It was determined that this kind
of motion greatly enhanced the experimental effects. Also, an additional improvement
was obtained when the MOR frequencies were dithered +/- 10 Hertz. Some believe
that in combination with the MOR rates, the RF generator was gated on and off
at a 4 hertz rate. Early film footage of the Rife tube in operation does tend
to support this conclusion as the tube is seen to flash repetitively.
Building a working Beam Tube -- To date, the authors have constructed a total
of four Rife units. Two units were fabricated around modified Heathkit transmitters
and delivered 100 and 250 Watts respectively. Two additional units were designed
from scratch, one utilizing a single 6DQ6 tube as both an oscillator and amplifier.
This unit produces approximately 50 Watts of input power. The second and favorite
system utilizes a 6AG7 crystal controlled oscillator stage driving a single
807 amplifier. This unit produces about 75 Watts and is ideal for work with
RF plasmas. The 807 is an excellent RF amplifier tube in that it is extremely
forgiving and will deliver the full rated 75 Watts output with only 220 milliwatts
of grid drive. Each of the units employs a solid state modulator in the cathode
circuit of the amplifier stage. This cathode arrangement acheives 100% modulation
more readily than the screen-grid type originally employed by Rife. The schematic
for this unit can be seen in Figure 2.
RF Driver
The most difficult part of the reconstruction effort was obtaining the glasswork
for the plasma discharge tube. Several models were constructed using estimates
obtained from descriptions and photographs of original tubes. In addition, physical
dimensions were taken from several X-ray tubes designed in the 1940's. Tube
fabrication was fabulously expensive and required many tedious hours spent measuring
the effective impedance of various gases under varying pressures and power levels.
A tremendous amount of time was spent researching plasma chemistry in an attempt
to understand the physics behind radio frequency plasma formation and control.
If fabricating a replica tube sounds cost prohibitive, please note that a suitable
discharge tube can be obtained from a neon sign manufacturer. This less expensive
option is highly recommended for a novice experimenter. Have a local glass shop
make a 16-19" straight tube and ask them to fill it with argon or helium.
This type or discharge tube will operate quite reliably and require no periodic
maintenance. Detailed discussions on RF plasmas are beyond the scope of this
paper, so it shall be left to the reader to pursue further information on the
subject. Most technical libraries will have several informative selections pertaining
to RF plasma chemistry.
Referring to Figure 2, starting with the oscillator stage, a 6AG7 tube was
chosen because its plate load resistance is close to the input impedance of
the grid of the 807. This serves to maximize power transfer from the oscillator
to the amplifier stage. These impedances can be calculated by using equations
and tube data found in older Amateur Radio Handbooks. The 807 requires -45 volts
on the grid along with 3.5 milliamps of grid drive for proper excitation. The
screen voltage nominally is 300 and the plate can be run at 600 d.c. volts.
The driving characteristics of the 807 present an input impedance of approximately
11,000 ohms. A standard tuned-plate tuned-grid crystal oscillator circuit was
taken from the handbook along with the recommended component values. The crystal
used was cut for 16.0 Mhz. The screen grid of the 6AG7 was fed through a variable
20,000 ohm potentiometer so that the necessary 3.5 milliamps of the grid drive
could be carefully adjusted. This control prevents the oscillator from overdriving
the amplifier tube. The output from this stage was coupled to the 807 with a
simple series capacitor. A fixed regulated supply was chosen over a grid-leak
configuration for the grid bias circuit because if the oscillator were to fail,
the 807 could be severely damaged. The fixed supply serves as a protective bias
for the amplifier.
The plasma discharge tube presents an approximate impedance of 2000 ohms at
16.0 Mhz. With the 807 operating with 600 volts on the plate and 150 miliamps
of plate current, the output impedance is 4000 ohms, therefore, the discharge
tube is tapped down on the output tank coil enabling it to present a higher
impedance to the amplifier tube via the transformer action of the circuit. Since
the load impedance is matched at 4000 ohms, and the desired loaded Q of the
circuit is approximately 15, the tank inductor should exhibit a reactance of
266 ohms at the carrier frequency. This equates to an inductance of 2.65 microhenrys
at the 16.0 Mhz operating frequency. A variable capacitor with a range of 5
to 50 picofarads was chosen to resonate with this coil.
Since the discharge tube is highly non-linear and has reactive components contributing
to its overall impedance, proper adjustment of the variable capacitor allows
almost complete cancellation of these reactive components. When the tank circuit
is tuned to resonance, the load impedance appears to be purely resistive. This
enables the power to be completely transferred from the amplifier to the discharge
and be dissipated as radiant energy.
Operation and adjustment of the RF driver is fairly simple. Power is first
applied to the filaments of the tubes and the tubes are allowed to warm up for
several minutes. After the tubes have reached nominal operating temperature,
with the amplifier cathode circuit open, high voltage is applied. The drive
tuning and drive level of the oscillator stage are adjusted to produce 3.5 milliamps
of grid drive for the 807. Next, the cathode circuit is closed and the plate
tank capacitor is adjusted to obtain the brightest discharge, which should also
require the least amount of plate current, since the circuit will be at resonance
with all reactances cancelled. The tap for the discharge tube on the tank coil
is adjusted to produce the desired 150 milliamps of d.c. plate current. Modulation
can now be accomplished by connecting a suitable square wave function generator
to the modulation input. The square waves should have a peak to peak level between
10 and 15 volts. A model B&K-3011 function generator will serve nicely in
this capacity.
Conclusion -- Now that the Rife Beam Tube technology is fairly well understood
and can be duplicated with a high degree of confidence, the next logical step
might be to repeat the laboratory studies originally performed by Dr. Stafford
et al. Also, a concerted effort should be undertaken towards recreating a working
Rife type microscope. Much has been written recently about dark-field microscopy
and advances made in Canada by Gaston Naessens and others. Their efforts need
to be supported if this technology is ever to be fully realized.
This paper did not discuss the "Rife Machines" recently popularized
by a number of commercial equipment manufactures. This type of unit normally
incorporates either hand-held electrodes or foot plates. It is believed that
these devices emerged in the 1950s and are more a product of John Crane than
Royal Rife. Rife's involvement in the development of this genre of machine is
at best unclear. Although the authors have heard of positive experimental results
obtained with the electrode units, they feel that the original Beam Tube system
invented by Rife himself offers the best hope as a viable treatment modality.
The authors would raise a caution to any individual utilizing any device like
this as part of a therapeutic regimen.
For additional information on reconstructing a working Rife Beam Tube, contact
the authors through the Phoenix chapter of the USPA.
[Update: The authors are preparing a second paper, and may be contacted at]:
Open Sesame
601 W. Leffels Lane, Suite J
Springfield, Ohio 45506
937-290-6758 voice mail
References:
"The Cancer Cure that Worked", Lynes, Barry, (1987), pp. 72-73.
"The Rife Way III", Simpson, Mark A., (1991), pp. 2-13.
"The New Microscopes", Seidel, R.E. and Winter, M. Elizabeth, Journal
of the Franklin Institute, February, 1944.
"Observations on Bacillus and Typhosus in its Filtrable State", Kendall,
Arthur and Rife, Royal, California and Western Medicine, December 1931.
"Observations with the Rife Microscope of Filter-Passing Forms of Microorganisms",
Science, August 26, 1932.
"Techniques and Applications of Plasma Chemistry", Hollahan and Bell,
(1974), pp. 393-399.
"The Radio Amateur's Handbook", American Radio Relay League, Newington,
Conn.
"RCA Power Circuits -- D.C. to Microwave", Radio Corporation of America,
Harrison, N.J.
"Care and Feeding of Power Grid Tubes", Eimac Division of Varian,
San Carlos, Ca., (1967).
"RCA Transmitting Tubes", Radio Corporation of America, Harrison,
N.J.
"The Semiconductor Data Library", Motorola Semiconductor Products,
Inc., Pheonix, Ariz.
--------------------------------------------------------------------------------
(Current Document Location: http://www.navi.net/~rsc/riferev.htm)
RETURN TO INDEX
The following is a listing of known MORs (mortal oscillatory rates) as compiled
by Dr. Robert P. Stafford, M.D. a physician who worked with an original Rife
machine from 1957 to 1963. They are believed to be the killing frequencies Royal
Rife himself discovered and verified with his microscope. (from http://www.alteredspace.com/~rsc/riferev.htm)
Original Rife frequencies
Tetanus 120 (An acute, often fatal infectious disease caused by the anaerobic,
spore forming bacillus Clostridium tetani.)
Syphilis 660 (Caused by Treponema pallidum, a helical, tightly coiled, motile
spirochete, a helical to sinusoidal bacterium. Mechanisms of T. pallidum pathogenesis
are poorly understood. Existing diagnostic tests for syphilus are sub-optimal,
and no vaccine against T. pallidum is available. The subspecies of T. pallidum
cause syphilis, yaws, nonvenereal endemic syphilis or pinta.)
Gonorrhoea 712 (A gram-negative bacteria, Neisseria gonorrhoea, causes this
sexual disease and primarily affects columnar epithelium in genital mucosal
surfaces of the urethra, accessory ducts and gland, as well as endocervix. If
contaminated fingers rub the eye then conjunctivitis can result.)
Staphlococcus 728 (Genus of nonmotile gram-positive bacteria that are found
in clusters and that produce important exotoxins. Staphylococcus aureus (Staphylococcus
pyogenes) is pyogenic, an opportunistic pathogen and responsible for a range
of infections including severe sepsis, pneumonia, endocarditis and soft tissue
infections.)
Pneumococcus 776 (Gram-positive pyogenic organisms about 1m diameter, usually
encapsulated, closely related to streptococcus, associated with diseases of
the lung. Pneumococcus is an important cause of serious infections in the first
three months of life. These infections are unlikely to be prevented by the currently
available infant immunization strategies. One potential approach to prevention
of pneumococcal disease in early infancy is immunization of pregnant women.)
Streptococcus 880 (A genus of bacteria that are gram-positive cocci, often
occurring in chains of varying length. Some pathogenic species produce exotoxins.
In man, streptococcal species are responsible for numerous infections such as
scarlet fever, tonsillitis, erysipelas (skin infection), endocarditis, rheumatic
fever, glomerulonephritis, impetigo, pneumonia, meningitis, pharyngitis, lymphadenitis
and wound infections. Streptococcus pneumoniae is the main culprit in lobar-pneumonia
and broncho-pneumonia. Streptococcus pneumoniae has been known for more than
100 years as the most important bacterial pathogen of the respiratory tract
in adults and children. In recent years, the pneumococcus has begun to exhibit
increasing resistance to antimicrobial agents.)
Typhoid Bacteria 712 (Typhoid is an infectious febrile illness usually spread
by contamination of food, milk or water supplies with bacteria Salmonella typhi.
This is not to be confused with Salmonella typhimurium which is the cause of
salmonella food poisoning.)
Typhoid Virus 1862
Bacillus Coli Rod Form 800 (Most probably Escherichia coli, the archetypal
bacterium for biochemists, used very extensively in experimental work. A rod
shaped gram-negative bacillus (0.5 x 3-5 m) abundant in the large intestine
(colon) of mammals at about .1% of the total. E. coli, along with other species
of bacteria, provide us with Vitamin K and B-complex vitamins. But a rare strain
of this bacteria, E. coli O157:H7, is responsible for food poisoning which causes
bleeding of the intestines which can be fatal.)
Bacillus Coli Virus 1552
Tuberculosis Rod Form 803 (Tuberculosis, an infectious bacterial disease caused
by Mycobacterium tuberculosis, is characterized by inflammatory infiltrations,
formation of tubercles (solid elevations of skin or mucous membranes), tissue
death, abscesses, formation of fibrous tissue, and calcification of tissue.
Infection is transmitted from infected people, cows, or contaminated milk. Presently
the worlds leading killer. It usually occurs as pneumonia, but TB can also occur
in the brain, back, knee, lymph nodes, or other organs and bones.)
Tuberculosis Virus 1552
Sarcoma cancer (all forms) 2008 (A form of cancer that arises in the supportive
tissues such as bone, cartilage, fat or muscle.)
Carcinoma cancer (all forms) 2128 (A malignant new growth that arises from
epithelium, found in skin or, more commonly, the lining of body organs, for
example: breast, prostate, lung, stomach or bowel. Carcinomas tend to infiltrate
into adjacent tissue and spread (metastasize) to distant organs, for example:
to bone, liver, lung or the brain.)
Streptothrix 784 (A genus of bacilli occurring of the form of long, smooth
and apparently branched threads, either straight or twisted. Streptothrix is
a synonym for Actinomyces israelii. This species is a gram-positive, cast-forming,
nonacid-fast, nonspore-forming anaerobic bacillus that is difficult
to isolate and identify. Its filamentous growth and mycelialike colonies have
a striking resemblance to fungi. They are soil organisms. It can cause the eye
diseases Canaliculitis and Keratitis.)
Also, frequencies for leprosy, polio, cholera, actinomycosis, glanders, bubonic
plague, anthrax, influenza, herpes, cataracts, glaucoma, colitis, sinus, ulcers
were discovered by Rife but we don't have any direct records from him on these
frequencies.
--------------------------------------------------------------------------------
(Definitions in parentheses are mostly from the on-line medical dictionary
at http://cancerweb.ncl.ac.uk/omd/index.html and other medical web sites.)
Rife stated they had narrowed the actual distinct number of groups of pathogenic
bacteria to 10. In his 1953 book, Rife commented on this:
"We have classified the entire category of pathogenic bacteria into 10
individual groups. Any organism within its group can be readily changed to any
other organism within the ten groups depending upon the media with which it
is fed and grown. For example, with a pure culture of bacillus coli, by altering
the media as little as two parts per million by volume, we can change that micro-organism
in 36 hours to a bacillus typhosis showing every known laboratory test even
to the Widal reaction. Further controlled alterations of the media will end
up with the virus of poliomyelitis or tuberculosis or cancer as desired, and
then, if you please, alter the media again and change the micro-organism back
to bacillus coli."
Rife contended certain conclusions escaped earlier researchers simply because
they lacked the evidence of their eyes in seeing these forms develop from a
single entity: pleomorphism. They require a power of magnification and resolution
beyond the typical 2,000 power instrument.
Rife's work suggested that the wide array of disease bacterium were merely
differentiation phases in a life-cyle of an as of yet undetermined entity. Researcher
Gaston Naessens has verified many of Rife's findings, and has delineated 16
phases of change of what Rife called the premodal identity, which Naessens calls
"somatids".
The Rife frequency instrument kills the "normal" carcinoma cancer
cell by rupturing the thousands of BX cancer viruses they contain and thereby
dumping the BX cancer virus contents into the cancer cell cytoplasm. This BX
cancer virus as Rife named it in 1931 is not a virus by the normal standard
usage of the term today. Rife based his definition on the fact that the BX cancer
virus could pass through the finest Berkefeld porcelain filter of the time (000
filter). The BX cancer virus is ovoid in shape, .066 microns along the major
axis and .05 microns along the minor axis. It is motile, driven by a proton
transport flagella the same as its bacterial parent, the E-coli bacteria. When
the BX cancer virus is ruptured it spills out its genome, ribosomes, RNA, enzymes,
and various proteins. When thousands of these ruptures occur all at once in
a carcinoma cancer cell the results are fatal to the cancer cell. A similar
situation occurs in the sarcoma cancer cell when the BY cancer viruses are all
disintegrated at once. The BY cancer virus is another form of the BX cancer
virus which Rife found caused sarcoma cancer after it had been exposed to prolonged
ultraviolet light exposure.
Royal Rife's Laboratory Research on Bacillus "X" cancer virus
The BX was isolated from ten different cases of breast carcinoma by Dr. Royal
Raymond Rife at the Rife Research Laboratory in SanDiego (Point Loma), California.
It was carried through forty-four transplants on "K" media in all
ten instances.
The technique used in the isolation of this organism is in brief as follows;
blocks of tissue, taken under the most sterile
conditions, were transferred into "K" media (previously examined for
sterility). These were then placed under the direct
influence of an argon filled gas tube working under five thousand volts for
twenty four hours, then were placed in water baths
with two inches of vacuum, and incubated at 37.5°C. At this time the delicate
shine of growth is noticeable. From this point on
as many as desired transplants can be made without repeating the foregoing operations.
The BX is a filterable virus, which filters through the W Berkfeld filter.
It is a small ovoid granule, highly plastic, and visible only
with monochromatic light. The angle of refraction is 12 3/10°, and the color
by chemical refraction is purple red. The length of
the organism is 1/15 u, and its breadth 1/20 u. It carries an attraction to
the cathode pole. Its death rate in milliamperes is 175
DC. The X-ray and Infrared have no influence on the organism, but the Ultraviolet
ray slows up its motility. The thermal death
point is 42°C for 24 hours, the filament voltage is 10, and the filament
amperage is 86. The plate voltage is 928, and its
unmodulated electronic oscillatory rate is 11,780,000 cycles per second. The
wavelength of super regeneration of Audion tube is 17 6/10 meters.
An inoculating serum was prepared by combining in a mixture, the transplants
from the ten original growths with a (?) to 1 dilution of normal saline solution.
(The symbol (?) indicates that the text was cropped out in the photocopy.)
On Aug. 3, 1933 1/10 cc of the above serum was inoculated into the breasts
of two sets of white rats; one set consisting of
two pregnant females with one control, and the other of two young females and
one control. The animals had been kept in
quarantine for a period of ninety days and were normal in every respect at time
of inoculation. Seven days later the inoculated
rats developed lesions (superficial) in the thyroid region and on the shoulders.
These lesions varied in size and severity on
succeeding days. The controls remained normal. On Aug. 21, the control of the
pregnant female set gave birth to two young;
one died. The delivery of the inoculated pregnant females was still delayed,
and the temperatures of all the inoculated animals
rose from 1 to 1 1/2° F. The lesions increased in area and density, and
one in particular was decidedly elevated. On Aug. 22,
one of the infected rats presented 5 young, and the other until this day has
remained barren, the swelling of the abdomen which
evidently was occupied by the young having gone down and returned to normal.
In the offspring of the infected mother, two
developed the identical type of lesions on the surface of the thyroid region.
One of these grew otherwise normally and in the
other the growth was stunted. The latter developed a severe growth on the upper
portion of the right side of the jaw, which
consumed most of the normal tissue. The teeth were badly malformed, and grew
very long, curving down and deep into the
throat. These were shortened by surgical operation. During this entire period
the controls remained normal.
On Aug. 28, a set of male rats consisting of the same number was inoculated
as in the females. The same type of epidermal foci
developed, the control remaining normal. On Sept. 5, one of the males was posted
and revealed no pathology. A lesion was
excised from the shoulder of the other inoculated male. (*) On Sept. 14, the
Bacillus X was recovered and identified in the
media. The lesions on all the inoculated rats vary in size and density from
day to day and in some cases clear up and break out
in other portions of the epidermis.
(*) Tissue placed in "K" media and run through the original method
of technique.
It has been demonstrated by experiment that the BX exists in two cycles, which
may be classified as forms A and B. Form A
applies to BX in its ultra filterable cycle. In this stage the organisms theoretically
exist in malignant tissue. Examination of the
fresh filtrate preparation of malignant tissue under 20,000X magnification,
using any known system of illumination, fails to reveal
the presence of living bodies. However, after a special method of cultivation,
involving the use of the argon ray and vacuum
conditions, the aforementioned filtrate in "K" medium contains a swarming
myriad of the visible cycle, form B. The BX in this
form may be seen under 8-11,000X magnification, (using monochromatic illumination)
as a highly plastic ovoid granule, purple
red in color.
Since experiments show that the Bacillus X in form A exists in malignant tissue,
it is theoretically possible to change its cycle to
form B by application of the argon ray and vacuum conditions. After the cycle
change has been accomplished (in theory), the
application of the oscillative ray at a cycles per second vibration of 11,780,000
should completely destroy the BX in the
malignant tissue.
(note: the frequency listed here is the base frequency that undergoes modification
by the audio frequency that isn't listed here which is believed to be 2127 or
2008.)
The Forty Year Legacy of Tainted Polio Vaccine
by
Harold Stearley
In the late 1940's and early 1950's the polio virus was taking a savage toll
on the American public. Thousands of children and adults were crippled or killed.
In 1955, Jonas Salk performed a medical miracle when he discovered how to mass
produce polio vaccine by growing it on the kidneys of rhesus monkeys. While
there is no question that thousands were saved from the ravages of polio by
the Salk vaccine, by 1960 a problem had surfaced -- a problem which would come
back to haunt the nation some forty years later.
The complication researchers had isolated in 1960 was a viral contaminate.
It seems that when the live polio virus grown on monkey tissues was extracted
for vaccine production another virus was extracted as well, SV-40. When this
monkey virus was injected into research animals it produced brain cancer. It
appears our government didn't wish to create a public panic or discredit the
public health service, because instead of recalling the tainted vaccines, it
quietly ordered the manufacturers to find a monkey free of SV-40 and continue
production. As of 1963, the rhesus monkey had been replaced with the African
green monkey for production of a safer polio vaccine, but between the years
of 1955 and 1963 as many as 98 million Americans had received doses of live
polio virus vaccines tainted with SV-40.
Jumping to the early 1990's, Michele Carbone, Assistant Professor of Pathology
at Loyola University in Chicago, isolated fragments of the SV-40 virus in human
bone cancers and in a particularly nasty form of lung cancer called mesotheliomas.
The viral contaminate from the 50s was back to haunt us, and appeared in 33%
of the osteosarcoma bone cancers studied, in 40% of other bone cancers, and
in 60% of the mesotheliomas lung cancers. Dr. Carbone believed this study could
explain why 50% of the current mesotheliomas being treated were no longer occurring
in association with their traditional cause of asbestos exposure.
Already sounding like a bad science fiction story, the worse news was yet to
follow. An Italian team of researchers from the Institute of Histology and General
Embryology of the University of Ferrara lead by Dr. Fernanda Martini discovered
SV-40's presence in various other tumors.
To be specific they found the monkey virus in 83% of choriod plexus papillomas,
in 73% of ependymomas, in 47% of astrocytomas, in 50% of glioblastomas, and
in 14% of meningiomas.
While the virus's appearance in all of these types of brain tumors is mortifying,
even more so is the fact that it materialized in 23% of blood samples and 45%
of sperm fluids taken from normal individuals -- normal meaning free of disease
at the time of testing. The researchers determined the virus could be transmitted
sexually and through blood transfusions. As if to drive this point home, SV-40
has appeared in 61% of all new cancer patients -- patients too young to have
received the contaminated vaccine being administered forty years ago who are
now believed to have been infected by human to human transmission. Being a blood
born organism, it is also suspected that SV-40 is transmissible from mother
to child during pregnancy.
The more this matter is researched the more startling the evidence. Senior
epidemiologist at the National Institutes of Health, Dr. Howard Strickler, has
plotted a geographic pattern to the cancers associated with SV-40 helping to
confirm its link to the tainted vaccine. People who lived in Massachusetts and
Illinois who received identified lot numbers of the contaminated vaccine administered
in the 1950s are now demonstrating ten times the rate of the osteosarcoma bone
tumors as those who received vaccine free of the SV-40 contaminate in other
parts of the country.
The Food and Drug Administration (FDA) mandates that every American infant
and child receive polio vaccinations. While public health officials continue
to emphasize how current supplies of the vaccine are safe, Peter Reeve, FDA
Virologist, has acknowledged that the administration abandoned independent testing
of vaccine purity some fifteen years ago. The job of ensuring safety and purity
rests squarely on the shoulders of those manufacturing the vaccines with no
federal oversight. Wyeth-Lederle controls the supply of all the oral polio vaccine
in this country, and last year's sales totaled some $230 million dollars. Surely
there would be no conflict of interest in allowing this corporation to be the
sole agent of quality oversight of their own pocketbook?
The government may not have paid attention to the quality of these vaccines,
but they had formulated a plan for their distribution. Federal vaccination policy
advocated the use of live-virus oral polio vaccine (OPV) based on the belief
the live virus shed in the body fluids of infants immunized with OPV could immunize
others through contact exposure. The Centers for Disease Control (CDC) insisted
this was a safe practice, and emphasized that no one previously vaccinated could
contract the disease in this manner. The public was never informed of this strategy,
however, and no consent was ever obtained from the unknowing participants in
this vaccination scheme. One hundred and twenty people, many previously vaccinated,
contracted polio as a result of this practice. To add insult to injury in 1994
the World Health Organization proclaimed polio was eliminated from the Western
Hemisphere. Insult because for the past seventeen years the only cases of polio
occurring in the United States have been caused by the vaccine itself, and injury
because this victory will be paid for in blood from the cancers produced by
the monkey virus spread with the vaccine.
One might ask just how such a thing could happen considering the injectable
form of the vaccine (IPV) does not use a live virus and doesn't transmit the
disease it is designed to shield us from? Well, Wyeth-Lederle's leading competitor
Connaught produces IVP which could explain why Wyeth lobbied so hard against
the CDC recommending increased use of IVP. In 1996 the CDC revised its recommendation
from four doses of OPV to two doses of IVP followed by two doses of OPV, however,
physicians have been instructed to give all four doses as OPV if they desire.
The cost of IVP vaccine is $5.40 per dose, whereas OPV costs $2.32 per dose.
With the difference in cost favoring the use of OPV, and the current climate
of regulating health care costs, clearer guidelines must come from the government
if they truly expect to increase the use of the safer IVP vaccine.
Well the story of contaminated polio vaccine is not over yet. Microbiologist
Howard Urnovitz, Ph.D. provided significant evidence at the Eighth Annual Houston
Conference on AIDS that human immunodeficiency virus type 1 (HIV-1) is a monkey
hybrid virus which was produced when 320,000 Africans were injected with polio
virus contaminated with live simian immunodeficiency virus (SIV) in the late
1950's. Apparently, viral fragments combine easily with other viruses to produce
these hybrids called "chimeras." This theory was confirmed by another
research team headed by Dr. B. F. Elswood at the University of California in
San Francisco. Interestingly enough, when researchers Cecil H. Fox and John
Martin applied to the National Institutes of Health for grants to confirm the
presence of SIV and simian cyto-megalovirus (SCMV) contaminates in polio vaccines
their requests were denied. Dr. Urnovitz may have an explanation as he stated
in the Boston Globe, "that almost 100 million Americans were exposed (to
SV-40) through a government sponsored program, but for over 30 years, there
has been virtually no government effort to see if anyone's been harmed by the
exposure." He added, "The government will not fund science that makes
it look culpable."
Could it be our government, once again, is attempting to avoid a public panic
while ignoring the great potential for harm these viruses could inflict. Time
will tell. Harvard Medical School professor, Dr. Ronald Desroier points out
that taking all known scientific evidence into account that the medical experts'
knowledge is limited to "perhaps 2% of existing monkey viruses." Who
knows what lethal virus may be discovered in our blood streams forty years from
now as a result of good intentions....
References
Berleur, M. P., & Cordier, S. (1995). The Role of Chemical, Physical, or
Viral Exposures and Health Factors in Neurocarcinogenesis: Implications for
Epidemiologic Studies of Brain Tumors.
Cancer Causes and Control, 6(3), 240-256.
Bookchin, D., & Schumaker, J. (1997). Tainted Polio Vaccine Still Carries
Its Threat 40 Years Later.
The Boston Globe, January 26.
Carbone, M., et al. (1996). SV-40 Like Sequences in Human Bone Tumors.
Oncogene, 13(3), 527-535.
Elswood, B. F., & Stricker, R. B. (1995). Polio Vaccines and the Origin
of AIDS.
Medical Hypotheses, 42(6), 347-354.
Fisher, B. L. (1997). Workshop on Simian Virus 40: A Possible Human Polyomavirus.
National Vaccine Information Center, January 27, On-line at http://www.909shot.com/polio197.htm http://www.909shot.com/polio197.htm.
Krieg, P., Amtmann E, Jonas, D., Fischer, H., Zang, K., & Sauer G. (1981).
Episomal Simian Virus 40 Genomes in Human Brain Tumors.
Proceedings of the National Academy of Sciences of the United States of America,
78(10), 6446-6450.
Lednicky, J. A., Garcea, R. L., Bergsagel, D. J., & Butel, J. S. (1995).
Natural Simian Virus 40 Strains are Present in Human choroid Plexus and Ependymoma
tumors.
Virology, 212(2), 710-717.
Martini, F., et al. (1995). Human Brain Tumors and Simian Virus 40.
Journal of the National Cancer Institute, 87(17), 1331.
Martini, F., et al. (1996). SV-40 Early Region and Large T Antigen in Human
Brain Tumors, Peripheral Blood Cells, and Sperm Fluids From Healthy Individuals.
Cancer Research, 56(20), 4820-4825.
Pass, H. I., Kennedy, R. C., & Carbone, M. (1996). Evidence for and Implications
of SV-40 Like Sequences in Human Mesotheliomas.
Important Advances in Oncology, 89-108.
Rock, A. (1996). The Lethal Dangers of the Billion Dollar Vaccine Business.
Money, December, pages 148-163.
Tognon, M., et al. (1996). Large T Antigen Coding Sequences of Two DNA Tumor
Viruses, BK and SV-40, and Nonrandom Chromosome Changes in Two Glioblastoma
Cell Lines.
Cancer Genetics and Cytogenics, 90(1), 17-23.
A Physicist's View
of Dr. Rife's Non-Drug
Treatment and Cure of
Microbial Associated Diseases
By Gary Wade [This is a revised issue, which takes into account some new information
received on Rife's frequency instrument. Figures 2 and 3 have been revised and
the old text commented on.]
During the 1920's and 30's, Dr. Royal Raymond Rife produced some rather astounding
accomplishments in medicine and biology.
First, he invented a new kind of optical microscope. This microscope could
be used to observe viruses in live cells and tissue culture.1,2 Rife built five
of these microscopes. Rife never published the plans to his microscope and to
this day those in the scientific establishment not familiar with Rife's work
wrongly claim that it is generally impossible to see or identify a virus with
any optical microscope.
Rife's second great accomplishment was to invent a variable frequency flashing
light source which could kill bacteria, rickettsias, protozoa, fungi, and viruses.
By 1939, Dr. Rife had both identified the microbes and the light flashing rates
(frequency) required to kill these microbes, which were associated with fifty-two
major diseases, including carcinoma and sarcoma cancers.2,3
In this article we will describe what Rife's frequency instrument was and how
it could destroy a microbe without harming the host/patient.
Figure 1 shows
a schematic view of the Rife frequency instrument in operation treating a patient.
The frequency instrument consisted of an old style X-ray tube, which had been
back filled with helium gas at very low pressure and had a current flow through
the tube driven by a sine wave voltage oscillator. When the voltage polarity
across the X-ray tube was such that the hot tungsten cathode was at a negative
voltage as compared to the metal plate anode, an electron current would flow
from the cathode to the anode. This electron current would collide with the
helium atoms exciting them and thereby generating light. Since the polarity
conditions for current flow through the X-ray tube were only met on one half
the sine wave voltage cycle there was one pulse of light produced for each complete
sine wave voltage oscillation cycle (see Figures 2
and 3). Another way to say this
is, that if a million cycles per second of sine wave voltage is applied across
the X-ray tube, the X-ray tube will produce one million pulses of light per
second. As a practical example, Rife found that the common carcinoma breast
cancer, (which is now reaching epidemic proportions among women), was killed
by a light pulse of 11,780,000 light pulses per second.4,5
[Note:Probably should be 23,560,000 pulses per second. It now seems that the
helium gas pressure (probably .003 milli torr) and voltage (Vrms=928 volts)
difference between the cathode and plate were such that electric current flows
in both directions in the X-ray tube. This would give twice the light pulses
per second than previously believed.gw]
For the currently trained biologist and medical researcher, all of the above
statements about Rife's work and accomplishments are suspect at best. The reason
for this is that they have a very limited knowledge of physics and no knowledge
of Rife's research results. For example, they do not know that Rife isolated
a viral sized, spore like, motile form of the E-coli bacteria that when exposed
to prolonged ultraviolet light became a virulent carcinogen, which invariably
caused carcinoma cancer when injected into lab animals. The key to getting Rife's
work and accomplishments into general medical and biological use is [to] end
to this ignorance about how and why Rife's frequency instrument worked to kill
microbes.
To that end I will now describe and illustrate how the Rife frequency instrument
can destroy a virus. I will illustrate how a specific virus can be destroyed
by a specific frequency of ultra sound. This ultra sound is generated by the
Rife frequency instrument. Note that light carries linear momentum and that
when the pulse of light from the Rife frequency instrument is absorbed by the
patient's skin layer that skin layer must recoil in the direction of light flow
to conserve linear momentum. When the light pulse has ended, the skin relaxes
back toward its non light pulse exposure position. In other words, periodic
light pulses generate periodic pressure pulses in the patient's skin layer which
travel into the patient's body. The Rife frequency instrument converts the patient's
entire exposed skin surface into an ultra sound transducer for the generation
of ultra sound. Even though the efficiency of ultra sound production is exceedingly
low by this method, it is still adequate to kill microbes. As a practical example,
Rife would treat his cancer patients using his frequency instrument for three
minutes of exposure once every three days. Usually his "terminally"
ill cancer patients would be cancer free in about thirty such treatments or
less, as was verified in the 1934, 1935, and 1937 test clinical trials carried
out by the U.S.C. Medical School Special Medical Research Committee.3 That same
committee then suppressed the research results.
The reason for the short three minute treatment is to kill off only a thin
outer layer of cancer tumor at one time. This allows the body's immune system
to remove this layer before the next treatment. The entire cancer tumor could
have been killed/destroyed in a single Rife frequency instrument treatment of
perhaps one to one and a half hours. However, then the cancer patient would
have a large mass or masses of dead cancer tissue in them, which would become
a feast for a massive bacterial infection. This bacterial infection could lead
to liver and kidney damage and general toxemia.
The Rife frequency instrument kills the "normal" carcinoma cancer
cell by rupturing the thousands of BX cancer viruses they contain and thereby
dumping the BX cancer virus contents into the cancer cell cytoplasm. This BX
cancer virus as Rife named it in 1931 is not a virus by the normal standard
usage of the term today. Rife based his definition on the fact that the BX cancer
virus could pass through the finest Berkefeld porcelain filter of the time (000
filter). The BX cancer virus is ovoid in shape, .066 microns along the major
axis and .05 microns along the minor axis. It is motile, driven by a proton
transport flagella the same as its bacterial parent, the E-coli bacteria. When
the BX cancer virus is ruptured it spills out its genome, ribosomes, RNA, enzymes,
and various proteins. When thousands of these ruptures occur all at once in
a carcinoma cancer cell the results are fatal to the cancer cell. A similar
situation occurs in the sarcoma cancer cell when the BY cancer viruses are all
disintegrated at once. The BY cancer virus is another form of the BX cancer
virus which Rife found caused sarcoma cancer after it had been exposed to prolonged
ultraviolet light exposure.
To see how the ultra sound generated by the Rife frequency instrument can destroy
a virus we will examine the outer protein coat (capsid) structure of a virus.
Most viruses of interest which cause diseases in plants and animals have an
icosahedral capsid structure as illustrated in Figure 4A and B. A specific example of this icosahedral capsid structure is illustrated in Figure
5. Each dark circle represents a
spherical protein molecule clump. When the virus capsid of Figure 5 is folded
together as indicated in Figure 4A and B, a simple virus capsid model has been
formed. Examination of this capsid model shows a large number of intersecting
and overlapping closed rings of protein molecule clumps. These closed rings
of periodically spaced protein clumps are illustrated in Figure 6A and B.
In classical physics when studying standing wave phenomenon the periodically
spaced protein clumps, as illustrated in Figure 6A and B, are known as the mass
beads on a string problem with circular boundary conditions. Figures 7A, B and
C, illustrate this classical physics
problem. Figures 8A and B illustrate one of the standing wave motion modes which
the closed periodically spaced protein clump rings of Figures 6A and B can sustain.
Figure 8A shows a ten member protein clump ring linearized for ease of graphing
wave motion displacement of the center of the protein clumps from their equilibrium
position. Figure 8B shows the most
stressful oscillation mode for the ten member protein clump ring. In this oscillation
mode, adjacent protein molecule clumps are always going in opposite directions
and therefore putting maximum stress on where they are bonded together. If this
oscillation mode is raised to a high enough displacement amplitude the ring
will rupture. If enough rings are ruptured, the virus capsid disintegrates.
The Rife frequency instrument when set to the frequency which corresponds to
the most stressful oscillation mode for the virus of interest, as illustrated
in Figure 8B, will destroy that virus capsid coat and therefore destroy the
virus.
The common virus capsid coat was chosen to show how the Rife frequency instrument
can destroy a microbe which have closed on themselves periodically spaced protein
clump structures. Bacteria, protozoa, rickettsias, and fungi all have these
closed on themselves periodically spaced protein clump structures in their outer
structure, which makes them susceptible to destruction by the Rife frequency
instrument.
Advancements in electron technology have made a much more efficient and vastly
more powerful replacement for the Rife frequency instrument. Namely, the piezo-electric
transducer, driven by an appropriate signal function generator as can be purchased
in any electronic test equipment store. In our present circumstances where antibiotic
resistant bacteria are about to become rampant, anti-viral drugs are largely
still just a bio-tech dream, and the war on cancer has been a dismal failure
for the cancer patient, but not for the so-called cancer researcher. It is long
since time for Rife's 1930's work to be implemented.
References
The New Microscopes, by R.E. Seidel, M.D. and M.Elizabeth Winter, Journal of
the Franklin Institute, Vol.237, Feb. 1944.
What has become of the Rife Microscope?, by Christopher Bird, New Age Journal,
March 1976.
The Cancer Cure that Worked! by Barry Lynes. Published in Canada by Marcus Books.P.O.Box
327, Queensville, Ontario, Canada L0G 1R0.
The Royal Rife Report, compiled by Allison Davidson, (see page 83). Published
by Borderland Sciences Research Foundation,PO Box 220,Bayside, CA 95524,Phone:(707)825-7733,
FAX (707) 825-7779,email: bsrf@asis.com,Web page: http://www.asis.com/bsrf/main.html
Dr. Rife and the Death of the Cancer Industry by Gary Wade, for info, write:
P.O.Box 3813, Alhambra, CA 91803.
Chronic Fatigue Alternative Treatment
SCIENCE NEWS, March 30 1991, pg 207
Shocking Treatment Proposed For AIDS
Zapping the AIDS virus with low voltage electric current can nearly eliminate
its ability to infect human white blood cells cultured in the laboratory, reports
a research team at the Albert Einstein College of Medicine in New York City.
William D Lyman and his colleagues found that exposure to 50 to 100 microamperes
of electricity - comparable to that produced by a cardiac pacemaker - reduced
the infectivity of the AIDS virus (HIV) by 50 to 95 percent. Their experiments,
described March 14 in Washington D.C., at the First International Symposium
on Combination Therapies, showed that the shocked viruses lost the ability to
make an enzyme crucial to their reproduction, and could no longer cause the
white cells to clump together - two key signs of virus infection. The finding
could lead to tests of implantable electrical devices or dialysis-like blood
treatments in HIV-infected patients Lyman says. In addition, he suggests that
blood banks might use electricity to zap HIV, and vaccine developers might use
electrically incapacitated viruses as the basis for an AIDS vaccine.
LONGEVITY, Dec 1992, pg 14
"Electrocuting" The AIDS Virus, A Safer-Yet Blood Supply
Despite official reassurances about the safety of the nation's blood supply,
concern lingers that small amounts of HIV-infected blood may be sneaking through,
especially since current screening detects only antibodies to the virus, which
can take months to form. But now a new electrical process for cleaning blood
of viruses may solve the problem. At the Albert Einstein College of Medicine
in New York City, Steven Kaali, M.D., has found that most of the AIDS viruses
in a blood sample will lose their infectious capability after being zapped by
a very low-level current. Repeated exposure appears to leave blood virtually
free of HIV, as well as Hepatitis- without harming blood cells. Kaali cautions
that it will take years of testing before a virus-electrocuting device is ready
for use. But, ultimately, he predicts, it could be used not just to purify blood,
but to treat people with AIDS, by channeling their blood out of the body, exposing
it to virus-killing current and then returning it. - Sharon McAuliffe
THE HOUSTON POST, March 20, 1991, section A-10 Your Health/Medicine
Scientists say Electric Current may help fight AIDS
Reuters News Service New York - Doctors at a prestigious New York medical center
are testing a new way to fight AIDS - using electrical energy to weaken the
killer virus - and say their first results are encouraging. Researchers William
Lyman and Steven Kaali of the Albert Einstein College of Medicine said Tuesday
that initial laboratory tests have shown electrical current can weaken the virus
believed to cause acquired immune deficiency syndrome. The two men said they
plan to move to the next phase of the experiment in April using blood samples
from people with AIDS. If their tests are successful, the researchers hope it
could lead to a new way to treat AIDS patients, possibly involving a dialysis-type
machine in which an AIDS patient's blood would be treated with electrical current
outside the body. "What we have done is expose the AIDS virus in laboratory
circumstances to electrical current and then incubated the virus with white
blood cells susceptible to the virus. We found that the virus became much more
ineffective," Kaali, a specialist in the medical use of electrical current,
said. He added that the use of electrical energy has no toxic side effects and
that a similar technique has been used as a treatment for reducing Herpes.
Marilyn D. Resh, Ph.D.
Head, Biochemical Virology Laboratory
Dr. Resh, an accomplished cell biologist, is exploring how RNA tumor viruses
cause normal cells to become cancerous. She is focusing on fatty acylated oncoproteins,
which bind to the cell membrane. Her work on membrane-bound viral proteins has
expanded to include the Gag proteins of HIV, and she is now studying how these
proteins bind to the cell membrane and form a virus particle.
LONDON, Feb 20 (Reuters) - Viruses that cause the common cold could hold important
clues to ways of tackling cancer, Scottish scientists said Tuesday.
About one-sixth of the 200 different types of cancer, including cervical cancer
and some kinds of leukemia, are triggered by viruses but how they do it is still
a mystery.
http://implants.clic.net/tony/Corner9/21.html
S e x u a l l y T r a n s m i t t e d V i r u s e s a n d C a n c e r s
Studies have long shown a link between certain strains of the human papillomavirus
and cervical cancer. The sexually transmitted human papillomaviruses (HPV) include
those that cause genital warts and viruses that elicit no symptoms at all. Cervical
cancer appears more common in women with AIDS. AIDS patients also have a higher
rate of precancerous growth on the cervix, called dysplasia.
http://www.usc.edu/hsc/info/pr/ccr/w98/first.html
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