Virologists first began the study of cervical cancer (CC) in the early 1900’s when an Italian doctor conducted a survey and discovered that CC was more often found among married women than among nuns.
Eager to make a scientific connection between the results of the survey and the disease they quickly postulated that sexual activity was the primary risk factor. Although many sexually transmitted bacteria and protozoans were proposed as causative factors in the disease, it wasn’t until 1966, when virologists, following the isolation of the Epstein-Barr virus
(a strain of the ubiquitous herpes virus), suggested, based on a laboratory study, that a higher percentage of CC patients had previously been infected by the herpes virus than had women without the tumor.
This revelation was quickly followed by the elucidation of both the herpes simplex type 1 virus which causes sores around the mouth; and type 2 which causes sores in the genital area - including the cervix. Virologists quickly proposed that type 2 was the cause of CC,... a supposition that was eventually proven wrong.
Yet this conjecture led to the concept of a “latent” virus which eventually became the key support for the theory that HPV caused CC.
In order to explain how a cervical tumor would appear years after exposure to the herpes simplex type 2 virus, scientists constructed a “new” hypothesis: that is to say that during the primary infection when millions of cells were killed an occasional virus would mistakenly mix with a cell’s DNA (thereby becoming
impotent in the process) mutating the genetic code of a few surviving cells which would eventually grow into a tumor years later.
Unfortunately, for the proponents of this theory, further research demonstrated that approximately 85 % of all American adults have been infected by the herpes virus, many without any outward symptoms,
including millions of women without any hint of CC. Additionally, many women with CC were found to mhave never been infected by the herpes virus.
Even in those women with CC and a history of herpes, the viral fragments left over in the tumor cells were different and inactive indicating that NO particular part of the herpes virus was or could be responsible.
Virologists, however, never allowed these facts to discourage them. In 1983 they proposed a NEW hypothesis; that is to say that the herpes virus was a “hit-and-run” virus which briefly infected the cervix, then mysteriously
vanished never to be seen again. The hypothesis, although ridiculous, actually lasted into the early 1990’s when they quietly retreated from the herpes virus hypothesis altogether.
In 1977, a German herpes virologist, Harald zur Hausen, proposed another virus as the causative factor in the development of CC, the human papilloma virus. He based this on the observation that cervical warts
could occasionally turn into full-fledged cancers.
Utilizing new laboratory techniques in the early 1980’s
zur Hausen was able to isolate small broken left-over pieces of the papilloma virus in the tumor cells of some patients.
However, zur Hausen and his virology colleagues soon discovered that more than one-half of the American adult population (therefore, half of the adult women) had been infected by the virus, but only a very few ever
developed CC. zur Hausen’s theory appeared to violate Koch’s first postulate (Koch’s Laws of Infectious Disease) since at least one-third of all
women with cervical cancer never developed CC. The remaining two-thirds are infected with over a dozen different strains of HPV.
The human papilloma virus tends to infect younger, more sexually active women with an average age of approximately 20 years. CC on the other hand is a disease afflicting older women usually detected between
the ages of 40-70 years. Based on these observations zur Hausen calculated a highly improbable “latency” period of between 20 to 50 years. Additionally, the HPV virus does not reactivate when a tumor appears.
zur Hausen postulated that HPV caused a genetic mutation which eventually produced the tumor. But each leftover piece of the virus caused different irrelevant mutations. In addition, cervical cancer grows from one
single cell which begs the question of why millions of other infected cervical cells never develop into tumors.
HPV causes papillomas (genital warts) on young, sexually active adults. The warts are not malignant and may appear or disappear almost overnight. They typically disappear spontaneously as a result of antiviral immunity.
But cancers, especially solid tumors, usually develop more slowly over time. CC begins as a benign hyperplasia. Most hyperplasias regress and disappear, but occasionally one may develop into a dysplasia, or a larger growth of
abnormal cells. In certain instances a dysplasia may develop into a neoplasia, or cancer. A small percentage of these neoplasias will become malignant and develop into cervical cancer.
It has been proposed that dysplasias may actually encourage the growth of HPV. It is interesting to note that equal numbers of men and women have genital warts, yet penile cancer in men is exceedingly rare.
A cancer virus that infects both men and women equally should produce equal numbers of tumors.
It is thought that the rampant use of oral hormonal contraceptives by females, as well as the documented increase in female smokers, may be factors influencing the development of CC. Oral contraceptives contain
powerful sex steroids that have direct effects upon the function of cervical cells, and may explain the superficial “correlation between CC and the number of sexual contacts a woman has had. Since men do NOT use oral contraceptives it may explain the rarity of penile cancer. Finally, CC is
not contagious.
The study by Merck & Co., Inc., evaluated women between the ages of 9-26 years. Although it is not unheard of that a young woman is diagnosed with CC, it is rare. One would not expect to find women in this age
population developing CC. I am not aware of any valid study which proves conclusively that HPV causes CC.
So, as a parent, if you are worried about your daughter developing genital warts, by all means get the shots. I would not, however, make the assumption at this time that the vaccine will prevent her from eventually developing CC.
If our Gov was really concerned about preventing disease, theywould close the friggin borders and discontinue shipment of products from China, Mexico and India (to start with.)
“Why would anyone not want their daughters and mothers and sisters to be protected as best they can from cancer?”
Go swathe them all in bubble wrap and keep them imprisoned at home.
Meanwhile, feed them every drug that comes down the pike to “protect” them.
By all means, keep the pharmaceutical industry healthy and happy.
You and your NOW buddies are a bunch of kooks!
Because telling the truth about it would have meant threatened the "...just have sex whenever and however you want...it's perfectly fine as long as you use a condom..." campaign.