In 1972, Stefania Jablonska of Poland, determined the human papilloma virus (herein

after called HPV) was found to be associated with skin cancer in epidermodysplasia
verruciformis. In 1978 Jablonska and Gerard Orth, of the Pasteur Institute, discovered HPV-5 in
skin cancer.i In 1976 Harald zur Hausen published the idea that HPV plays an important role in
the cause of cervical cancer. In 1983 and 1984 zur Hansen, et al, successful identified HPV 16
and HPV 18 in cervical cancer.ii
HPV is known as a sexually transmitted disease, classified as a type 1, non- enveloped
DNA class virus, belonging to the papillomaviridae family of viruses. There are currently around
two hundred types of known HPV, in which cause no symptoms whatsoever in humans. In some
instances this virus may cause warts, while in very rare cases, HPV may lead to cancer of the
cervix, vulva, vagina, anus, and penis in men.iii
HPV is found only in the basal cells of stratified epithelium as it attaches to epithelial
tissue via tissue trauma, which exposes basement membrane. iv The epithelial barrier is disrupted
primarily through sexual intercourse or light skin abrasions. The process of infection is very slow
as it takes 12-24 hours for transcription to initiate.
HPV has the ability to survive many months at low temperatures without a host. Because
of this, a method of spreading HPV infection is by an individual walking barefoot with a plantar
wart.v
E6 and E7 are the HPV proteins associated with cancer. The HPV genome is composed
of six early (E1, E2, E3, E4, E6 and E7) and two late (L1 and L2) proteins. After the host cell is
infected E1 and E2 are expressed first. High E2 levels repress expression of the E6 and E7
proteins. When the host and HPV genomes integrate, E2 function is disrupted, preventing
repression of E6/E7vi
The E6/E7 proteins deactivate tumor suppressor proteins, p53 and pRb. The viral
oncogenes E6 and E7 are hypothesized to modify the cell cycle so as to retain the differentiating
host keratinocyte in a state that is favorable to amplify viral genome replication and late gene
expression.vii E6 and host E6 associated protein (which has ubiquitin ligase activity) act to
ubiquitinate p53, leading to its proteosomal degradation. E7 acts as the primary transforming
protein. E7 competes for pRb, freeing the transcription factor E2F to trans-activate its targets and
pushing the cell cycle forwards. While all HPV can induce proliferation, only strains 16 and 18
can immortalize cell lines in vitro.
In the upper layers of the host epithelium, the late genes L1 and L2 are
transcribed/translated and serve as structural proteins which encapsidate the amplified viral
genomes. Once the genome is encapsidated, the capsid appears to undergo a redox-dependent
assembly/maturation event, which is tied to a natural redox gradient that spans both suprabasal
and cornified epithelial tissue layers. This assembly/maturation event stabilizes virions and
increases their specific infectivity. viii Virions can then be sloughed off in the dead squamous of the
host epithelium and the viral lifecycle continues. ix
A 2010 study has found that E6 and E7 are involved in beta-catenin nuclear accumulation
and activation of Wnt signaling in HPV-induced cancers.x
It is currently believed that HPV is the most common sexually transmitted disease in America
today.xi The American Social Health Association reported estimates that about 75-80% of
sexually active Americans will be infected with HPV at some point in their lifetime. By the age
of 50 more than 80% of American women will have contracted at least one strain of genital
HPV.xii
It had been estimated that in the year 2000, there were approximately 6.2 million new
HPV infections among Americans aged 15–44. According to this year 2000 estimated study, it is
believed that around 74% of HPV infections occurred in individuals between the ages 15–24. Of
the STD’s studied, genital HPV was the most common.xiii
One study found that, during 2003–2004, 26.8% of women aged 14 to 59 were infected
with at least one type of HPV. This was higher than previous estimates. 15.2% were infected with
one or more of the high-risk types that can cause cancer. xiv
The primary screening test for HPV was approved by the FDA in March of 2003 as an
adjunct to Pap testing and may be performed during a routine Pap smear. The test is
manufactured by Qiagen,xv which is considered a “hybrid capture” test.xvi This test can detect the
DNA of 18 of the most commonly infecting viruses, which appear in the cervix. While this test
can distinguish between low and high risk HPV types, it cannot determine the specific HPV
types.xvii
The only visual sign of low risk genital HPV is genital warts. This can be identified with
a visual scan.
Currently there is no specific HPV treatment. xviii However, in most instances, HPV clears
up on its own.xix The CDC has stated that the body’s immune system removes HPV on its own
within the first two years of infection.i
While the cure for HPV appears to be from within, doctors and scientists have been
attempting to determine an appropriate method of prevention. As with STD’s, condoms are often
the first mode of defense. Typically they offer protection against infection. However, any exposed
skin can lead to the transmission of HPV. Therefore condoms are not 100% effective in the
prevention of HPV.xx
 Much research has gone into studying topical microbials in an effort to prevent the spread
of HPV. One such substance is called carrageenan, which can be found in sexual lubricants. This
has been found successful in the prevention of the spread of HPV in animal studies. xxi
Another form of prevention, and possibly the most controversial comes from vaccines.
Gardasil, a drug developed by Merck & Co. was approved June 8, 2006 by the FDA for use in the
prevention of certain types of HPV. xxii These types are types 16, 18, 6, and 11. HPV types 16 and
18 cause an estimated 70% of cervical cancersxxiii and are also responsible for analxxiv, vulvar,
vaginalxxv, and penile cancer cases. HPV types 6 and 11 cause an estimated 90% of genital warts
cases.
Garsasil does not treat existing infection. Therefore, to be effective it must be given
before HPV infection occurs. The HPV strains that Gardasil protects against are sexually
transmitted, and HPV-16 has a 60% per-couple transmission rate. xxvi
The HPV major capsid protein, L1, can spontaneously self-assemble into virus-like
particles (VLPs) that resemble authentic HPV virions. Gardasil contains recombinant VLPs
assembled from the L1 proteins of HPV types 16, 18, 6 and 11. Since VLPs lack the viral DNA,
they cannot induce cancer. They do, however, trigger an antibody response that protects vaccine
recipients from becoming infected with the HPV types represented in the vaccine. The L1
proteins are produced by separate fermentations in recombinant Saccharomyces cerevisiae and
self-assembled into VLPs.xxvii
Side effects of Gardasil include: pain at injection site, headache, fever, nausea, dizziness,
vomiting, fainting, difficulty breathing, bronchospasm, hives, rashes, swollen glands, joint pain,
tiredness, weakness, leg pain, shortness of breath, chest pain, aching muscles, muscle weakness,
seizure, stomach pains, excess bruising, blood clots, and death.
While HPV does appear to affect most of the population of the United States, it appears a
healthy immune system treats it alone. HPV is not a virus, which appears will cause widespread
death.
The cause of cancer derived from HPV has admittedly not been studied by Merck and the
exact period of effectiveness of Gardasil is not known. xxviii The chance of side effects from
Gardasil, in my mind, is too great to chance to vaccinate my own child with. Each parent and
child should make their own educated determination on how to treat their own body.
i
Human papillomaviruses World Health Organization, International Agency for Research on Cancer 2007
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ii
HPV, The Shy Virus. Soundprint.org radio program. 6 December 2008. Retrieved 6 December 2008.
iii
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2008. Retrieved 13 November 2009.
iv
Schiller, J. T.; Day, P. M.; Kines, R. C. (2010). "Current understanding of the mechanism of HPV infection".
Gynecologic Oncology 118 (1 Suppl): S12
v
Human Papillomavirus at eMedicine
vi
Ganguly, N; Parihar, SP (2009). "Human papillomavirus E6 and E7 oncoproteins as risk factors for
tumorigenesis". Journal of biosciences 34 (1): 113–23
vii
Münger; Howley, PM (2002). "Human papillomavirus immortalization and transformation functions". Virus
research 89 (2): 213–28
viii
Conway MJ, Alam S, Ryndock EJ, et al. (October 2009). "Tissue-spanning redox gradient-dependent
assembly of native human papillomavirus type 16 virions". Journal of Virology 83 (20): 10515–26
ix
Bryan JT, Brown DR (March 2001). "Transmission of human papillomavirus type 11 infection by
desquamated cornified cells". Virology 281 (1): 35–42.
x
Rampias, T.; Boutati, E.; Pectasides, E.; Sasaki, C.; Kountourakis, P.; Weinberger, P.; Psyrri, A. (2010).
"Activation of Wnt signaling pathway by human papillomavirus E6 and E7 oncogenes in HPV16-positive
oropharyngeal squamous carcinoma cells". Molecular cancer research : MCR 8 (3): 433–443
xi
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United States". JAMA 297 (8): 813–9.
xii
American Social Health Association — HPV Resource Center". Retrieved 17 August 2007
xiii
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Diseases Among American Youth: Incidence and Prevalence Estimates, 2000". Perspectives on Sexual and
Reproductive Health 36 (1): 6
xiv
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United States". JAMA 297 (8): 813–9.
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xvi
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xvii
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2008. Retrieved 13 November 2009
xviii
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19 February 2008. Retrieved 21 February 2008.
xix
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xx
Manhart LE, Koutsky LA. (2002). "Do condoms prevent genital HPV infection, external genital warts, or
cervical neoplasia? A meta-analysis". Sex Transm Dis 29 (11): 725–35
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Buck, C.; Thompson, C.; Roberts, J.; Müller, M.; Lowy, D.; Schiller, J. (2006). "Carrageenan is a potent
inhibitor of papillomavirus infection". PLoS pathogens 2 (7): e69
xxii
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Retrieved 2009-11-12
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1167–73
xxiv
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Lesions in Men (Update2)". Bloomberg News. Retrieved 2009-11-12
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Include Preventing Certain Vulvar and Vaginal Cancers". Press release. Retrieved 2009-11-11
xxvi
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