Virus Type of Cancer
SV-40, a pro-cancer virus invaccines
In 1955, Jonas Salkperformed a medical miracle when he discovered how to mass producepolio vaccine by growing it on the kidneys of rhesus monkeys. Whilethere is no question that thousands were saved from the ravages ofpolio 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 onmonkey tissues was extracted for vaccine production this SV-40 viruswas 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 ordiscredit the public health service, because instead of recalling thetainted vaccines, it quietly ordered the manufacturers to find a monkeyfree of SV-40 and continue production. As of 1963, the rhesus monkeyhad been replaced with the African green monkey for production of asafer polio vaccine, but between the years of 1955 and 1963 as many as98 million Americans had received doses of live polio virus vaccinestainted with SV-40.
Nowadays SV-40 has appeared in 61% of all new cancer patients --patients too young to have received the contaminated vaccine beingadministered forty years ago who are now believed to have been infectedby human to human transmission. Being a blood born organism, it is alsosuspected that SV-40 is transmissible from mother to child duringpregnancy. The more this matter is researched the more startling theevidence. Senior epidemiologist at the National Institutes of Health,Dr. Howard Strickler, has plotted a geographic pattern to the cancersassociated with SV-40 helping to confirm its link to the taintedvaccine. People who lived in Massachusetts and Illinois who receivedidentified lot numbers of the contaminated vaccine administered in the1950s are now demonstrating ten times the rate of the osteosarcoma bonetumors as those who received vaccine free of the SV-40 contaminate inother parts of the country.
DNA Polyoma Viruses
In 1964, studies were conducted on a polyoma virus (a tumor-producingDNA virus). It was discovered that the persistent genetic DNA materialin the polyoma virus brought about malignant transformations in hamsterembryo cell cultures. This was reported in the November 23, 1964 issueof the Journal of the American Medical Association.
SV-40 is one example of a DNA polyoma virus. Polyoma (manytumor-causing) viruses cause prolonged infection where tissue isdestroyed, integrate into the hosts genetic material, are capable ofmutating 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 virusescarry in proportion to the damage they can cause.
The 'D' in DNA and the 'R' in RNA have characteristics which aredependent on the kind of sugar molecule associated with it. DNA existspredominantly in the nucleus, but is also represented in the cytoplasmand in the mitochondria. RNA is also present in the cytoplasm. Whenviral RNA or DNA combines with the genetic material in the cell itself,the viral genetic material can become part of the host cell geneticcode, altering the genetic structure of the cell. When the altered cellduplicates, the encoded viral genetic material may affect cellularprocesses in such a way as to produce abnormal cells, which sometimesbecome malignant or cancerous.
Cancer-Causing RNA Viruses and DNA proviruses
The discovery in 1975 that viruses causing cancer in animals had aspecial enzyme called reverse transcriptase makes the problem even moreinteresting. These kind of viruses are called RNA viruses. When an RNAvirus has the reverse transcriptase enzyme within its structure, itallows the virus to actually form strands of DNA which easily integratewith the DNA of the host cell which it infects. Studies by Dr. RobertSimpson of Rutgers University indicate that RNA viruses which do notcause cancer can also form DNA, even without the presence of reversetranscriptase. DNA formed in this way from an RNA virus is called aprovirus. It is known that some non-cancerous viruses have a tendencyto exist as proviruses for long periods of time in cells withoutcausing any apparent disease. In other words, they remain latent. Someexamples of common RNA viruses that do not cause cancer, per se, buthave the capacity to form proviruses are influenza, measles, mumps andpolio 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 interactingwith cancer-causing chemicals; this has been indicated by experimentswhich show that cancer-causing substances that are present in too smalla quantity by itself will become active and create tumors when combinedwith single doses of virus. Malignant tumors appeared in five type ofinjected mice.' The viruses mentioned were ECHO9, B-4, Coxsackie, andPolio virus 2. The article further indicated that 'viruses may alsoactivate other cancer causing substances besides chemicals in theenvironment, such as DMBA, AF, and DBA.'
Even common non-tumor viruses, including those in smallpox vaccine andpolio virus 2, can act as carcinogens. It was reported in Science onDecember 15, 1961 that these common viruses acted as catalysts inproducing cancer when given to mice in combination with known organiccarcinogens in amounts too small to induce tumors themselves. Thismeans that some vaccinations will induce cancer, when combined with thegrowing problem of environmental pollution from toxic by-products ofagriculture (pesticides on and in food) and industry.
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Inherited virus may play role in breast cancerNEW YORK, Aug 12 (Reuters Health) -- An inherited virusmay be one of the factors that triggers breast cancer in humans,researchers report. Scientists say that a primitive retrovirus, humanmammary tumor virus (HMTV), has been identified in human breast cancertissues.
'If a definitive link to this retrovirus is established, HMTV maybecome a target for a vaccine to prevent breast cancer and a target fornew 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 malignantbreast tumors in mice. Speaking to attendees at the 11th InternationalCongress of Virology in Sydney, Australia, Garry explained thatvertebrate species other than mice -- including some humans -- carrysimilar viruses.
He said that his team had identified the virus, dubbed HMTV, in breastcancer tissue and other organ issue from breast cancer patients, andalso in tissues from individuals who did not have breast cancer.
The virus, he said, is likely to be 'a cofactor' for triggering breastcancer, along with other factors such as an individual's geneticmakeup. Dr. Orli Etingin, an oncologist and assistant professor ofmedicine 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 shebelieves that 'a lot more research really has to be done in order toconfirm the finding and also to establish what the relationship of thevirus is to the development of tumors in humans.'
JCvirus in the pathogenesis of colorectal cancer, an etiological agent oranother component in a multistep process?
Tatiana R. Coelho, Luis Almeida and Pedro A. Lazo
Virology Journal 2010, 7:42doi:10.1186/1743-422X-7-42
Published: 18 February 2010
JCV infection occurs early in childhood and last throughout life. JCVhas been associated to colorectal cancer and might contribute to thecancer phenotype by several mechanisms. Among JCV proteins,particularly two of them, large T-antigen and agnoprotein, caninterfere with cell cycle control and genomic instability mechanisms,but other viral proteins might also contribute to the process. Part ofviral DNA sequences are detected in carcinoma lesions, but lessfrequently in adenomas, and not in the normal surrounding tissue,suggesting they are integrated in the host cell genome and theseintegrations have been selected; in addition viral integration cancause a gene , or chromosomal damage. The inflammatory infiltrationcaused by a local chronic viral infection in the intestine cancontribute to the selection and expansion of a tumor prone cell in acytokine rich microenvironment. JCV may not be the cause of colorectalcancer, but it can be a relevant risk factor and able to facilitateprogression at one or several stages in tumor progression. JCVtransient effects might lead to selective expansion of tumor cells.