I am new here and study for doctor specializing in venereal diseases, now I read all about
HPV and cancer.
I am convinced that only
HPV in the throat does not cause cancer, it requires additional impact as many tests indicate there is an investigation which can be bought here;
http://www.amjoto.com/article/PIIS0196070911000287/abstractI copy a snippet below.
In the case of transfer between a man and woman and woman who is performing oral sex;
I disagree that the risk is greater when a man performs oral sex on a woman than vice versa, there are also other things that makes this not true, among gay men is oral cancer increases most and why there is no increase of lesbians,
HPV is almost as common among them.
That transmission is easier for a man?
HPV requires friction to get into the skin, usually through small wounds, friction occurs during intercourse and when a woman gives you oral sex, when a man gives, it is usually only lightly touched, the virus is present in all skin, someone wrote
"(Squamous cell) They line every opening To The Human Body" this is not true squamous cell exist on all skin and to the entire penis.
Men infecting women very easily through sexual intercourse when the penis enters a hot and humid area, compared to the mouth.
One reason may be that women's infection in the vagina persists longer than a man's penis and that therefore the man who gives oral sex to the same woman several times subjected to virus for several years, which seems to be a prerequisite for cancer, repeated exposures.
In the U.S., approximately 7000 cases of oral cancer caused by
HPV, 2 / 3 is a smoker and 2 / 3 is men, there is absolutely a connection, the other a few thousand people who do not smoke and get cancer ... amazingly few people and we know nothing about their status, HIV, oral health, etc.
They are very quick to link oral sex to increase with HIV sweep under the rug, we must not forget that oral cancer is most common in HIV infected and this infection following the development of oral cancer late 70's and 80's
4. Discussion
Overall, the putative evidence from the above review
points to smoking posing an additional risk of development
of HNSCC in the presence of
HPV infection. Where
counterexamples of such an association exist, the studies
are limited by small sample sizes [16,24], weak statistical
evidence [16,17,24-26], and inconsistent definitions of
smoking status [25]. Criteria of light and heavy smoking, as
well as the definition of current, never, and former smokers,
are not uniform. The dose and duration of tobacco exposure
in most of the studies are self-reported. The strength of the
reported conclusions would have been greater if the exposure
had been confirmed with cotinine or other bioassays. On the
other hand, the studies showing an additive or synergistic
interaction between smoking and
HPV have larger sample
sizes and adequate controls [20�23], which support greater
generalizability of these results to other populations.
4.1. Is it biologically plausible that smoking can promote
development of
HPV-related HNSCC?
A positive association between smoking and
HPV toward
causation of HNSCC appears to be biologically plausible
based on our review of clinical studies and supporting
evidence of pathologic interactions between the 2 risk
factors. Human papillomavirus may have evolved mechanisms
to escape immunosurveillance, but the transient nature
of infection lends little credence to its ability to cause
neoplastic changes in the absence of any contributory factors
[11,14,22,34]. In
HPV infection of head and neck particularly,
the viral copy number has not been found to be
substantially increased, suggesting that alternate pathways
mediated by cocarcinogens such as tobacco may be involved
in HNSCC related to
HPV [35].
Tobacco has been potentially linked with all major phases of
HPV-related carcinogenesis: initiation, promotion, and progression.
Histopathologically, smoking causes cellular and
structural alterations in tonsils, leading to an increased oral
acquisition of
HPV [36]. This has been corroborated clinically,
as researchers have observed a high prevalence of
HPVinfection in smokers, particularly current smokers [37].
Smoking is also known to suppress the mediators of immune
function, thus facilitating persistence of
HPV infection�a step
crucial to development of
HPV-related cancer [8,11]. Inactivation
of the tumor-suppressor gene p53 by the
HPV E6
oncoprotein is an important step in causation of
HPV-related
malignancy at the molecular level [19,20,26,38]. The DNA
damage caused by smoking may further impair the cell's ability
to recuperate from the mutagenic insults along with an increase
in frequency of p53 mutations [39,40]. It has also been
suggested that the carcinogenetic potential of
HPV increases
with viral integration with host DNA, an effect resulting in
overexpression of
HPV oncogenes. The process of integration
occurs at fragile sites or �hot spots� ofDNA breakage, and there
is evidence that tobacco smoking induces DNA breaks in
human cells [41-43]. Thus, an increased frequency of
HPVintegration in smokers may increase the risk of carcinogenesis in
the presence of
HPV infection. Moreover, laboratory research
has found current smokers to have statistically significantly
greater viral loads than never smokers, thus implying that
cessation may result in attenuation of the viral load [44].
Tobacco-associated genetic or epigenetic alterations have
also been postulated to result in acceleration of the disease
progression in
HPV-infected individuals [31,32,45]. This is
supported by clinical and pathologic evidence of a poorer
survival of
HPV-positive HNSCC patients who are smokers
as compared with
HPV-positive patients who are nonsmokers
[31-33,45,46].
4.2. Can individual susceptibilities influence measures of
association between
HPV and tobacco exposure
for development of HNSCC in different studies?
As the current paradigm is shifting toward understanding
the molecular progression of
HPV-related head and neck
tumors, it is becoming recognized that individual susceptibilities
may explain the variation in relationship between
smoking and
HPV. Variants of highly polymorphic but
critical tumor-suppressor genes such as p53 and p73 interact
with the
HPV oncoproteins E6 and E7 and result in a much
higher risk of
HPV-16�associated oral cancer in nonsmokers
than never smokers [47-49]. The frequency of the high-risk
polymorphisms among cases in one of the studies was 40%
to 44% [48]. Although a detailed discussion of these
individual variations is beyond the scope of our review, it
would be a relevant factor for future studies on the
interaction between
HPV and smoking.
5. Conclusion
Our review of the existing literature on the association
between smoking and
HPV in causation of HNSCC identifies
smoking to have the potential to promote infection,
persistence, and the carcinogenetic effect of
HPV. Although
prospective studies on the natural history would better
unravel the possible interactions, on the basis of the current
laboratory and clinical studies, we conclude that the HPVrelated
tumors should not be considered as an occurrence
exclusive to nonsmokers. Thus, along with close surveillance
for early detection of HNSCC, early cessation of smoking
should be considered imperative in smokers, particularly
heavy smokers with
HPV infection. Current evidence
indicates that stop-smoking efforts can lead to a reduction
in the viral loads and slow the progression to
HPV-related
malignancy. Cessation is also important in view of evidence
of a poorer survival status in smokers with
HPV-positive
HNSCC as compared with nonsmokers.
