Thanks, Brian. I can completely understand the FDA's age parameters given the percentage of women identified by their gynecologist as being infected. The only way a vaccine would not work on me is if I had been exposed to HPV-16 because I would already have antibodies for it. According to my doctor, I have never been exposed to HPV-16. I do not have antibodies for it.

I also spoke with a gynecologic oncologist about HPV and about general immunology as well. This is the information I received: Once someone contracts any virus, the body either dies from it or recovers from it. But, the virus antibody remains identifiable in the host. Rarely, a virus is active in a host without symptoms causing a carrier situation. It is never really "cleared" by the body. This is why vaccination is unnecessary when immunity has been conferred by a virus such as chicken pox, etc. With vaccination or illness, there are antibodies present--the proteins from the dead virus present, either way. However, regarding the more insidious viruses such as HPV and HIV, exposure causes changes to take place within the cells that eventually cause immune system damage in the case of HIV and, often times, cancer in the case of HPV-16. Regarding HPV, there are no symptoms of the active virus. It is only when tissue cells begin to show signs of abnormal structure does it usually become detected and an HPV-16 or other cancer causing strain is identified. At this point, the host is more than likely no longer contagious but the permanent damage has already been inflicted. The cells are acting on the programming caused by the initial virus not actually the virus itself.

With the chicken pox virus, it can cause shingles long after the host has recovered from the virus. However, a host can only get chicken pox once and immunity is conferred. In the herpes virus, it can flare up because of some trigger experienced by the host or the host can be outbreak-free. However, in both cases, antibodies are still present. Transmission and systemic exposure depends on the virus and to what body system(s) it prefers to attack and what type of contagion is present when it manifests. It is presumed that HPV is not contagious after the host has recovered from the initial exposure. However, with other viruses, such as herpes, the host is contagious whenever there is an outbreak present.

Whether someone has been infected once or multiple times with HPV or any combination of it's strains, it will have produced antibodies. Does multiple exposures cause more of a risk for cellular damage? Probably. But, once someone has gotten it, they have it for the rest of their life. Like the old saying goes, "love may come and love may go...but HPV (like herpes) is forever."

One thing that is happening with HPV is a mutation process that is producing new strains of HPV. There are over 100 strains of HPV and more to come. Some are benign and some are not. If you think about the influenza virus, that is why no one becomes immune from the flu and why there isn't an effective vaccine. It mutates from year to year. When a virus mutates, there is no built in immunity to the new virus strain. If someone does not retain a life-long immunity to HPV, the mutation process may be to blame. However, antibodies would still be present. Therefore, if no antibody to a particular strain exists in an individual, then a vaccine would be effective at preventing that individual from becoming infected with that particular strain. Medicine will be forever playing catch-up with HPV. The HPV vaccination program is a step in the right direction, without a doubt.

So, that's the information I have received from a general gyn and an oncologic gyn who deals with cervical cancer detection and treatment on an every day basis.

Immunology and and HPV are both tricky subjects. There is still so much to be learned about HPV. Considering I have had one partner in 27 years and am testing negative, I don't think it is unreasonable to assume I have not been exposed to an active HPV-16 virus. Certainly, I can contract it at some point forward. But, who's to say I'm not one of the 20% who won't have it by the time I'm 60?

I will be more than happy to pay the $150-$180 per dose x 3 if my doctor would be allowed to administer it. After all, there are many other therapies, Erbitux for one, that don't work on everyone. And, there is no way of knowing on whom it will work. Erbitux costs tens of thousands of dollars by the time someone has received 8 infusions at $4,600 a dose. Considering what oral cancer does to a person and the havoc treatment wreaks on him or her, I think I'd rather take my chances with the vaccine.

As for the few married couples who have developed HPV+ oral cancer, perhaps one of them had the active virus and exposed the other. They just both happened to be unlucky or their lifestyle contributed to developing oral cancer. Since the odds allow for that to happen...it had to happen to someone.

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/abstract
I 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 HPV
infection 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 HPV
integration 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.

I forgot to write ... there is research to suggest that when infection of the membrane of the mouth occurs, and it is not "massaged" through friction when the virus can infect only the upper layer of the membrane, also induces an immune response and virsuet fought normal, but the reaction is not as strong as if the virus infects through wounds, etc., because the body does not get immune to the infected HPV variant without infection can occur again and again with the same virus.

That would explain a lot of differences between man o woman, the woman create a lasting immunrespins by the virus penetrates further down, perhaps in the mouth but mostly in the vagina and then the woman is immune.

Conclusion better to get a big infection than many small ... just as in the case of the common cold

I think we should award college credit for anyone keeping up with this thread.

Good stuff.

Overall, our review points to smoking tobacco posing an additional risk for development of head and neck cancer in the presence of HPV infection. This is consistent with available laboratory data that show evidence of biological plausibility for interaction between smoking and progression of HPV infection to carcinogenesis. It is therefore important that cessation of smoking is promoted in smokers with HPV infection. In the end this is kind of a no shit statement� when you have two strong risk factors instead of one, the world is going to be worse for you. Please note they use of the word plausibility, In spite of many articles not in their bibliography which clearly show that HPV is a unique pathway, they say that it is plausible that there is some synergy between the two.

Rightfully the article piece you have posted states that they have poorer outcomes. That is not the same as saying that it requires the two things to have happened (smoking and HPV infection) simultaneously to develop a malignancy. This is just observations on a subset of patients that smoke and have HPV, which is not the largest group of HPV+ oral cancer patents. Most oral cancer patients in the US that are HPV etiology are non smokers.

This paper is part of a meta analysis of many other papers. It is just indicating that there is indeed a sub set of individuals that are both smokers and HPV+, but it is very clear at the end where they say that we do not know the life history of the virus, and that would give definite answers to things which they are only speculating on. This is not a study, it is a review of many studies.

Meta analysis is highly useful. But there is always the potential for bias in them as they select the articles that they wish to look at, and that introduces bias of its own. The most recent example was one done by the ADA that was listed over 100 articles in its bibliography, but when I questioned a friend that had been part of the process he acknowledged that they omitted 60 of them as not worthy of being included in their analysis. Those 60 were peer reviewed published articles!! The ADA's conclusion was that screening in oral cancer does not work�. The Cochran Group is notorious for doing this kind of thing as well.

The penis is covered with normal epithelium, not squamous cells. There is more but I don't agree with most of your conclusions.

I can understand that we all can not have the same opinions, and HPV is a difficult virus to understand, there are so many different research findings, I am not suggesting that there is no cancer in which only the HPV is involved, I know that this does happend , but oral cancer is on the whole a multifactorial disease and the number who get cancer of the only HPV is incredibly small number, so small that it is difficult to statement as statistics or draw conclusions, there are many adoption from all sides




http://www.merckmanuals.com/home/sec18/ch216/ch216c.html

http://www.springerlink.com/content/870485v71w88nw67


Tobacco, alcohol, and human papillomavirus (HPV) are major risk factors for head and neck cancer (HNC), but it is unclear whether there are two distinct HNC risk groups, one associated with HPV and the other with tobacco/alcohol. Because HPV-positive HNC are clinically distinct from HPV-negative cases in treatment response and with more favorable prognoses, determining whether these differences result from infection alone or in association with other HNC risk factors is important for developing future therapeutic strategies. Incident cases of HNC (n = 201) and age-gender frequency-matched controls (n = 324) were recruited to assess anti-HPV VLP (virus like particles) antibodies 16, 18, 31, and 33. Multivariate logistic regression and stratified analyses were used to calculate adjusted odds ratios (OR). HPV-seronegative and seropositive/heavy tobacco users had similar increased adjusted risks of HNC (HPV-seronegative OR = 2.6, 1.4�5.0; HPV-seropositive OR = 2.3, 1.1�4.8), as did HPV-seronegative (OR = 4.3, 2.1�9.1) versus HPV-seropositive/heavy alcohol users (OR = 3.9, 1.6�9.4). Similar HPV/tobacco/alcohol risk profiles also were seen in oropharyngeal and oral cavity tumor sites. Our finding that tobacco/alcohol use increased the risk of HNC in both HPV-seropositive and HPV-seronegative individuals is consistent with the observation that HPV infection is not a sufficient cause of HNC but requires the accumulation of additional cellular changes.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2917346/

CONCLUSIONS:
HPV16 E6 and E7 alone are not sufficient for invasive growth. However, the synergistic activity of H-Ras and E6 was sufficient to result in invasive growth.
Our findings also suggest that HPV related carcinogenesis is a multi-step process. We have found that expression of HPV viral oncogenes alone is not sufficient to permit metastatic growth. This result supports the clinical finding that not all patients with persistent HPV infection develop cancer. It is likely that at least one additional cellular mutation in the presence of HPV oncogenes is required for metastatic growth. E6 transgenic mouse data also support these findings. In one study, only 14% of mice that overexpressed E6 developed malignant tumors, suggesting that E6 is not sufficient to induce tumor growth by itself. Chromosomal analysis of the tumors that developed in these mice indicated that they exhibited other genetic alterations compared to the surrounding tissue10. The fact that H-Ras synergizes with E6 to result in invasive growth may shed light into what other cellular pathways need to be altered to result in invasive tumorigenic growth. H-Ras activation is a downstream event of growth factor signaling34. Growth factor receptor overexpression is common in HNSCCA35. Although H-Ras mutations have not been reported in HPV related HSCCA, it is possible that alterations like growth factor overexpression or other components of the growth factor signaling cascade could synergize with HPV oncogenes to allow invasive growth.

With all due respect to Brian and as the founder of the association,but what is your goal?
Is it that it should be in the headlines "Oral sex cause cancer, everyone should immediately stop oral sex"? in my country we have about 100 cases per year of tonsilcancer are caused by HPV, and no overestimation was probably 3 million people is in oral sex, maybe 40-50 times a year, there are 150 million exposures, the number of cases HPV exist, we can only speculate
Blaming the oral sex is enough to make it all too easy

The rules of the forum is that you do not "sell something" or representing economic interests, I do not think DR. Gillison would clear the entrance exam:)

Dr. Gillison worked for 3 years with Merck & Co., the maker of the HPV vaccine Gardasil

Forum monitors comment: This post is staying on the boards only to demonstrate this individuals prejudice and lack of information, particularly about someone that is clearly recognized as an authority on the subject matter by her peers. This is the kind of attack and nonsense that unregulated boards allow everyday.

forgetting, of these 100 cases, nearly 70 people smoking and haveinfection with HPV.
10% have HIV, 80% are over 65 years, 20% are immigrants from countries with a history of chewing tobacco

How many cancer cases do you have in us? is there a national register of the number of cases and Whether the man had another cofactor to HPV infection, you say that there are more non smokers, would be interesting to see statistics on paper

Sorry it was not my intention, but I understand that you may have a different culture in the U.S. than I am used to, that one must be careful to question.

I am convinced that he is right in substance, but that one must be careful to exploit people's fears in this case the link oral cancer, some cup was placed there by the weak with regard to the selection and the result, no other activity would be linked to cancer if so few results of the activity was cancer, but to do it with oral sex just because so many are frightened. I lead a group of students in the subject and it has gone so far that it begins to look each other in the throat, I try to calm reflection and understanding.

Certainly one must be cautious in their sexual relationships, but fear not to take unreasonable proportions, to be aware of any. changes in the neck is as important and natural as to draw attention to other bodily changes that may indicate cancer, I hope that's the direction you have and not so scared to give oral sex cancer, that's where I think it's that simple not.