How Effective Is the HPV Vaccine at Preventing Cancer? A Closer Look…

By Jeanne Lenzer | November 23, 2011 12:51 pm

Some people have taken issue with the conclusion and analysis in my previous post, “Should Boys Be Given the HPV Vaccine? The Science Is Weaker Than the Marketing,” including epidemiologist Tara Smith in her blog, Aetiology, at ScienceBlogs. Here’s a clarification of some of the points in my post, and a response to some of hers.

First I’ll reiterate the key point of my post: There are many, many instances in which researchers have promised cures and interventions that were expected to work based on eminently reasonable logic, but did not pan out. Take one recent recent example: bypass a clogged artery and you will prevent strokes (see Sharon Begley’s excellent blog post on “When Biology Refuses to Listen to Medical Logic”). And now comes one more eminently logical assumption: prevent cervical lesions from some strains of HPV in some people for some period of time, and you will save lives from cervical cancer overall. Unfortunately, while the two HPV vaccines on the market may decrease the serious illness and death from cervical cancer, no study has proved that at this point, since no study has been conducted long enough to observe the development of cervical cancer or cervical cancer deaths.

Conclusive studies with the most important, clinically relevant end points should precede wide uptake of any intervention. The data currently rely on surrogate end points (markers of possible cancer) and are simply not conclusive. So we can’t truly say how effective the vaccine is.

Wake Forest medical researcher Curt Furberg, a former FDA advisor and co-author of the textbook Fundamentals of Clinical Trials, told me, “Getting data from markers is a first step. But we have burned our fingers too many times with surrogate markers. You should try to determine the real health benefit. Everything will be up in the air until we have the answer to the question: Will it prevent cancer? And until we have that answer, we should limit its use to girls enrolled in studies of the vaccine.”

Here are some other reasons why the HPV vaccines may not be as effective as advertised:

Duration of Protection:

An important issue raised by Diane Harper, an HPV researcher, is how long the vaccine will remain effective. She says the antibody titers in women who receive the vaccine fall off over time—i.e., the vaccine loses effectiveness. “One third of women lose antibody titers and hence protection from HPV by 5 years,” and “at 8.5 years, 15 percent have lost all detectable antibody titers to HPV-16, which leaves them completely unprotected from HPV-16 and -18, the only two cancer-causing strains that Gardasil was supposed to protect against.”

Harper says because of the vaccine’s limited duration, it likely won’t decrease the cervical cancer rate significantly below where it is with the routine Pap screening currently in use, although it may postpone cancer until later in life. Booster shots could presumably extend the effectiveness of the vaccine, she says, but we don’t yet have data on that. (Harper has received funding from Merck and GlaxoSmithKline for research on their HPV vaccines.)

HPV Rates in Pre-Sexual-Activity Girls:

Smith dismisses my concern that many girls and women were excluded from the FUTURE I and II analyses, which I said prevented a real-world analysis and inflated the value of the vaccine. She said those test subjects should be excluded from the analysis because, as she and a number of readers have suggested, the subjects in the trials were older than the 9- and 11- year old girls the vaccine targets. And because they were older (15 to 26 years of age), many were sexually active and already had HPV. Smith says excluding these girls is reasonable since they did not represent the ideal vaccine candidate. What makes an ideal candidate? Nine- to 11-year-old girls are allegedly ideal since they presumably won’t be sexually active and won’t have HPV—i.e., they will be “susceptible” to the virus and vaccine.

The problem with that logic is that while sexual contact is taken to be the primary transmission mechanism for HPV, some studies have found that the HPV infection rate is far from negligible among girls who are not yet sexually active. One small study found that 15 percent of all newborns had genital HPV at birth, rising to 18 percent at six months. Another set of researchers detected HPV in nearly one in five girls (18 percent) ages 4 to 15 years (median age 9.5 years) who were virgins (girls who were victims of verified or suspected abuse, and girls that became sexually active during the trial, were excluded from the study). That percentage could be higher in the real-world cohort of vaccine recipients, since abused girls would not be excluded from vaccination. Another, much larger study found that among females aged 14-19 who said they’d never had sex (vaginal, anal, or oral), 9.8 percent were HPV positive. (Among all 14-19-year-olds, the rate of high-risk HPV was 25 percent, which is relevant for the teenagers who are vaccinated along with the pre-teens.)

Furberg says that before deciding that 9- and 11-year-old girls are good candidates for the vaccine, manufacturers need to answer the question: “Can you extrapolate benefit from a subgroup of tested subjects [those who were not HPV infected] to the girls you want to vaccinate? You should at least find out first whether the proportion [of HPV-infected girls] is high. I don’t think you need to do another study—but you need to answer the question.”

Although the HPV rates are probably higher in the study’s population (who were mostly sexual active) than in the pre-teens the vaccine is aimed at, we don’t have data on what the HPV infection rate is among the target population—though we have good evidence it’s not negligible—so we can’t truly say what the vaccine effectiveness will be.

Effects on Pap Screening Rates:

Doctors and researchers are clear about the fact that the HPV vaccine will not reduce the need for Pap smears, as the vaccine only works against some cancer-causing strains of HPV. It’s less clear that all the women who receive the shot will know that as well. If Pap screening rates go down because some women assume they’re immune to all HPV strains for life, “there is a real risk that cervical cancer will increase in the U.S.” says Harper. Only time will tell how HPV vaccinations will affect screening rates—an experiment that’s now being run on a pool of many millions of women.

Overall Vaccine Effectiveness in FUTURES Studies:

While Smith is right that 44 percent I mentioned in my post (effectiveness in preventing high-grade lesions due to the vaccine strains, in the intent-to-treat population) isn’t a perfect measure, she doesn’t get any closer to showing how the vaccine fares on its most important test: how much it decreases cervical cancer in the real world. A later study after the end of the FUTURES trials found that the vaccine was 30 percent effective in preventing cervical lesions for all carcinogenic strains of HPV—43 percent against high-grade lesions—among females who tested negative for all of those strains at the beginning of the study. That rate probably overestimates effectiveness because some of the vaccinated girls are most likely HPV positive. Indeed, in the final tally, the vaccine was 19 percent effective at preventing high-grade lesions in the intent-to-treat population.

And again, there are also questions about the duration of the vaccine’s potency, and the possibility that Pap screening rates may go down, plus the fundamental problem that the trials measure lesions rather than cases of cancer. We can’t say with certainty how HPV vaccination will affect cancer rates, but we can certainly say the effectiveness won’t come near the 98 percent cited as the primary end point in the FUTURES II study.

Testing for Actual Efficacy vs. Cancer:

In the FUTURES II report, the authors say there’s no feasible alternative to using cervical lesions as an end point to stand in for actual invasive cancer:

Although prevention of invasive cervical cancer is the main goal of prophylactic HPV vaccination, it is ethically unacceptable to use invasive cancer as the end point in efficacy trials. Cervical intraepithelial neoplasia grade 3 and adenocarcinoma in situ, which the International Federation of Obstetrics and Gynecology classifies as stage 0 noninvasive cervical cancers, are clinically important outcomes because they are likely to persist and may become invasive without treatment.

But Otis Brawley, chief medical and scientific officer of the American Cancer Society, says it is indeed possible, though costly and lengthy, to do such a test.

I would love to see a public health initiative to see this out [several decades]. You need to follow girls who get the vaccine at age 10 and then look at them and compare them at ages 40 and 50 to a cohort of girls who didn’t get the vaccine, and you should assess not just cervical cancer outcomes but the amount of testing and treatment that is necessary for both groups.

Of course, women in the study would be encouraged to get Pap smears and have any dangerous cervical lesions treated. But just as some women in the general female population get cervical cancer even under the current Pap screening regime, so too will some women in a long-term study. Comparing the placebo and vaccine groups will show the true long-term effectiveness of the vaccine. And a trial that looked at women vaccinated as adults, like the older subjects in the FUTURES studies, could provide some real-world results faster than Brawley’s example.

Gardasil for Prevention of Head and Neck Cancer:

Smith correctly points out that HPV-caused head and neck cancers are much more common in men than anal cancer (and seem to be on the rise), and she says Gardasil would be a good way to prevent those cancers. But on what evidence? Researchers at the National Cancer Institute and the CDC told the Wall Street Journal that there’s no clinical-trial data showing the vaccine prevents cancer in males, and Merck said it “has no plans to study the potential of Gardasil to prevent these cancers.” Again, it’s biologically plausible that the vaccine will prevent oral cancers, but there’s no clinical evidence of that. What’s more, the evidence we do have suggests antibody titers may decrease faster in men than in women; Harper says the vaccine loses effectiveness against HPV-18 in 40 percent of men after two years, as opposed to five years in women.

Other Researchers’ Questions About Vaccine Effectiveness:

Many other experts have voiced concerns about the effectiveness, costliness, or potential side effects of the HPV vaccines, in public and in private. Here are a couple more examples:

A huge publicity & PR campaign (not counterbalanced by independent experts, scholars and the medical profession) has obscured the fact that millions of healthy teenage girls are being vaccinated under a promise: that vaccination programs will prevent cervical cancer—just a reasonable hypothesis, untested, which could easily be refuted. It is a huge mistake to vaccinate healthy persons under a promise. As a physician, I believe systematic, universal vaccination programs have a crucial role in our societies. And, hence, I deplore that the credibility of such programs is jeopardized by unbalanced commercial influences.

—Cancer epidemiologist and physician Miquel Porta, in email interview

Despite great expectations and promising results of clinical trials, we still lack sufficient evidence of an effective vaccine against cervical cancer. Several strains of human papillomavirus (HPV) can cause cervical cancer, and two vaccines directed against the currently most important oncogenic strains (i.e., the HPV-16 and HPV-18 serotypes) have been developed. That is the good news. The bad news is that the overall effect of the vaccines on cervical cancer remains unknown. As Kim and Goldie point out in this issue of the Journal, the real impact of HPV vaccination on cervical cancer will not be observable for decades….

With so many essential questions still unanswered, there is good reason to be cautious about introducing large-scale vaccination programs. Instead, we should concentrate on finding more solid answers through research rather than base consequential and costly decisions on yet unproven assumptions.

—Charlotte J. Haug, editor-in-chief of the The Journal of the Norwegian Medical Association, in the New England Journal of Medicine


The burden of proof regarding any new intervention should be on “them that sells their wares.” Right now, the data from the manufacturer-sponsored studies are far from conclusive, which brings us back to the problem neatly summed up by Steven Nissen, a Cleveland Clinic researcher and FDA advisor who’s seen many logical interventions that failed: “The road to hell is paved with biological plausibility.”

Let’s see the evidence first.

Jeanne Lenzer

(A side note on terminology: Smith says I called high-grade lesions “innocent cellular abnormalities,” which is incorrect. I used “innocent cellular abnormalities” to refer to low-grade lesions: grade 1 cervical intraepithelial neoplasia, or CIN1. The issue is that in the 2007 NEJM papers on the FUTURES trials, the vaccine seemed to disproportionately prevent those low-grade lesions and had a smaller effect on the high-grade lesions (CIN2 and CIN3 and adenocarcinoma in situ), as pointed out in a New England Journal of Medicine editorial that accompanied the study. (“No efficacy was demonstrable for higher-grade disease, but the trial may have lacked adequate power to detect a difference [in FUTURES I]…the efficacy appears to be significant only for grade 2 cervical intraepithelial neoplasia; no efficacy was demonstrable for grade 3 cervical intraepithelial neoplasia or adenocarcinoma in situ [in FUTURES II].” But this disproportionate effect seemed to disappear in the later paper that included the end-of-study FUTURES data, so it’s not as big a concern as the points previously mentioned. [Ed note: Due to a production error, the original post linked to the wrong skeptical editorial in the NEJM. These quotes are from the right one.])
Jeanne Lenzer is a medical investigative journalist and frequent contributor to the British medical journal BMJ. Her work has been published in The AtlanticThe New York Times MagazineNewsweek Japan, and many other outlets.


CATEGORIZED UNDER: Health & Medicine, Top Posts
  • Evan

    I’m a molecular biologist and I’m sympathetic to all of the points you raise; these vaccines have indeed not been shown to prevent cancer, despite the plausibility of that hypothesis.
    However, I wonder if there is a lacuna in your analysis. You are very firm with requiring empirical evidence to back up any and all assertions, except the last one you make: that those who market an intervention must do rigorous, fifty year trials, and prove effectiveness conclusively before treatment of the population can even start. Why on earth should this be so? This assertion seems to be based on a cost benefit analysis, and it is indeed *plausible* that the costs and benefits work out so that this strict version of the precautionary principle is indeed always the best strategy. But I can think of many cases where such a strict precautionary principle (don’t act until you’re certain) is plausibly too extreme.
    An commitment to an strict precautionary principles in medicine may very well be justified (I think it might be, especially in this case). But whether it is or not is an empirical question! I don’t know whether there are studies of this; I suspect that really good ones would take centuries to complete. But your failure to even broach this consideration leaves your discussion completely one sided and seems like an attempt to smuggle in your own preferred level of skepticism under the guise of scientific rigor.

  • Jeanne Lenzer

    Author responds:
    Evan, I think you are right that the precautionary principle is not something that must prevail in every instance since, as you point out, the harm-benefit ratio could tilt so far in an obvious direction as to not warrant waiting. Such is the case for the use of penicillin against deadly bacterial pneumonias – there are no RCTs for the initial use of penicillin, nor does there need to be.

    However, it is precisely because there is a proven way to prevent deaths from cervical cancer – Pap tests – that we should abide by the precautionary principle when it comes to this new vaccine. One study showed that of the 4,800 women in the U.S. who died of cervical cancer, half had never had a Pap test and the other half hadn’t had one within 10 years of diagnosis, according to Otis Brawley, chief medical and scientific officer at the American Cancer Society. If we are really concerned about deaths from cervical cancer, we would ensure that all women have free access to medical care and Pap tests – especially since they are still necessary even for women who have had the HPV vaccine.

    If you want to make the argument based on other, rarer cancers, then an entirely different set of analyses need to be brought up and I don’t intend to argue those here or in future posts. As other experts have said, there is reason for caution.

    Jeanne Lenzer

  • William Jamison

    I wonder if you’ve had the opportunity to review recent articles published in Lancet Oncology concerning HPV vaccine efficacy?

    Here are the details:

    1 Lehtinen M, Paavonen J, Wheeler CM, et al. Overall effi cacy of HPV-16/18
    AS04-adjuvanted vaccine against grade 3 or greater cervical intraepithelial
    neoplasia: 4-year end-of-study analysis of the randomised, double-blind
    PATRICIA trial. Lancet Oncol 2011; published online Nov 9. DOI:10.1016/

    2 Wheeler CM, Castellsagué X, Garland SM, et al. Cross-protective effi cacy of
    HPV-16/18 AS04-adjuvanted vaccine against cervical infection and
    precancer caused by non-vaccine oncogenic HPV types: 4-year end-ofstudy
    analysis of the randomised, double-blind PATRICIA trial. Lancet Oncol
    2011; published online Nov 9. DOI:10.1016/S1470-2045(11)70287-X.

    In these studies, authors demonstrate high efficacy in preventing CIN2/3 lesions, which of course are precursor lesions of invasive carcinoma. Such lesions typically can be detected on pap examination, and if they are, they must be removed surgically. Of course such surgery carries risk for the patient, i.e., pain/discomfort and the possibility of interference with later efforts to become pregnant.

    With that said, would you agree with the statement that prevention of CIN2/3 alone is a valuable medical benefit to be had from these vaccines?

  • dyson

    Just one quick response Jeanne – I’ll no doubt have other comments later – You cite Curt Furburg as saying “Will it prevent cancer? And until we have that answer, we should limit its use to girls enrolled in studies of the vaccine.”

    Now this research strategy will not work. If HPV is limited to prospective studies, it will NEVER be able to demonstrate its full effectiveness. Why not? Well if you are monitoring a study group of women to see how many develop invasive cancer, I think you will find NONE of the study population will, because as soon as any develop precancerous CIN 2/3 changes, they will be treated with invasive surgery to prevent progression. They will not get cancer. The trial your will “show” unvaccinated women do not develop cancer. It would only show unvaccinated women get CIN2/3 and vaccinated women do not (which we already know)

    This is a marked contrast to what the “real world” experience would be (you know, the one you wanted in your last blog post on the topic). If there is widespread vaccination, 2 different opulations of women will emerge – vaxed versus unvaxed, and since in the real world lots of women don’t get smears, or get them late, you WILL see cases of cancer developing. So epidemiological studies should clearly demonstrate vaccine effectiveness or not at this point.

    But then you might have to wait 10 years for some really definitive answer to emerge that would satisfy you and the antivax crowd, and by then it will be too late for the 120 thousand women who will develop invasive cancer and 40,000 who will die. Is that what you want, just to avert the extremely rare (and as yet causally uncorroborated) death following the vaccine?

    These vaccines clearly prevent CIN2/3 precancerous lesions, and only a fool would think that none of these would go on to cause invasive cancer, so the vaccine will do exactly what it says on the tin.

  • dyson

    Jeanne, Your citation of research that points to HPV infection in the under 10s is a straw man. If the vaccine is effective in HPV naive population, the benefits will accrue in thes polulation.

    And if you think the HPV infection rates in girls under 10 is such a problem than I fully expect your next blog item to be one calling for all little girls to get pap smears. After all, that is the rational and appropriate thing to do if you believe your own propaganda.

  • Miquel Porta

    Thank you for raising & debating very important points in a very rational way.

    My views are explained in detail in:
    Porta M. The improbable plunge. What facts refute reasons to expect that the effectiveness of HPV vaccination programs to prevent cervical cancer could be low? Preventive Medicine 2009; 48: 407-410.
    you may try to access the paper through the following link:

  • dyson


    I’ll take your commentary one section at a time. First, your attempt to compare the abortive attempts to do carotid artery bypasses to the HPV vaccine trials is comparing chalk and cheese. Scientists came up with a biologically plausible concept of arterial bypass they hypothesized might help prevent stroke – trials showed it didn’t, so the concept was binned. With HPV, scientists know that cancer of the cervix develops in stages, starting with dysplastic lesions and moving through progressively more invasive phases until fully invasive cancer results. They know that treatment of the early invasive stages will prevent invasive cancer, and they know from trials that merely monitoring the early stages rather than treating them does not stop a high proportion of them progressing to invasive cancer. So when scientists demonstrate that by vaccination they can dramatically reduce the risks of the earlier stages of cancer, this is not a failure, but a resounding success.

    Duration of protection.
    As you say, antibody levels decline gradually following vaccination, and are “only” 85% after 8.5 years. Two points – first, as an infection clinician I am very wary of assessing vaccine-induced protection based solely on antibody levels – we have discovered that even when humoral antibody levels decline, there still remain sufficient alternative pathways of prompting a protective vaccine-induced immune response, so most authorities regard antibody levels as being notoriously difficult to correlate with clinical protection. We know this happens with other vaccines. In Hepatitis B for example, vaccine-induced antibody levels decline within 10 years, but vaccine-induced protection on exposure to wild Hepatitis B remains intact. Secondly, because antibody levels decline sooner than hoped, that doesn’t mean the vaccine is “ineffective”. The worst case scenario would be that you might need to recommend boosters at around 10 years after the first course. That’s hardly a reason to label the vaccine a failure.

    HPVrates in girls who are not sexually active.
    You tell us that some studies indicate HPV can infect babies or small girls. You don’t indicate if there is any significant involvement of the oncogenic strains though, do you? If these (unusual) infections merely represent one of the other scores of wart virus strains, then that is of zero relevance to the adolescent HPV vaccine program. The point being made by many of us, including Tara, is that this vaccine will work in those who are HPV 16/18 naïve. That applies whether they are 4 years old or 14. If you genuinely think that HPV infection in childhood is an issue, you logically should be calling for either (a) HPV vaccination to be part of the routine childhood schedule, with boosters at 10-12 years of age, or (b) Pap smears or HPV screening to be done on little girls to detect any early changes. However I hope the fact that cervical cancer (which takes 5-20 years to develop) doesn’t occur in children or young adolescents should tell you that HPV subtypes that might infect kids are rare, benign and not oncogenic. So this entire issue of HPV in children is irrelevant and quite specious to the subject of later adolescent HPV vaccination. I call straw man.

    Effects on Pap screening rates.
    I take your point that some women who get vaccinated may completely forego future screening (how many we don’t know, but this is one speculation you seem to accept as gospel truth, while at the same time you pretend to come over all rational and anti-speculation in other areas). This argument is another straw man – it has nothing to do with vaccine efficacy, but is something that health educators need to get over to the vaccinated population, and keep on hammering the message home.

    Overall vaccine efficacy in the FUTURES studies.
    You like to look at “the real world”. I understand why, since at least 2 different major studies that look at the HPV naïve subpopulation indicate the HPV vaccine is 100% effective at preventing the pre-invasive CIN2/3 changes. Yet even the “real world” studies that include significant numbers of HPV infected women at baseline show the benefits of the vaccine. The Munoz study you cite reads quite differently to me than it seems to read to you. To me it shows that if one started immunizing women blindly, accepting that the majority may already be infected with HPV, you will still reduce the rate of pre-invasive cervical changes by 19% and genital warts by 62% within as little as 3 years. Can you imagine how successfully this vaccine will eliminate these problems when it is given to the primarily HPV-naïve adolescent population, and think how good the figures may be after 5 or 10 years, not just three? The Munoz paper which you have cherry-picked says the vaccine is highly effective, but you don’t mention that do you? It concludes: “In the longer term, substantial reductions in the rates of cervical, vulvar, and vaginal cancers may follow.” Forgive me if I value their own interpretation of their results to yours.

    Testing for efficacy vs cancer.
    Here we come back to the issue of using surrogates (such as CIN) for cancer as an end point. I agree, the use of surrogate end points is tricky. But not when they are clinically-relevant endpoint and they exist on a continuum between early changes and pathologically invasive disease. In this instance these surrogates are entirely appropriate, firstly because they do genuinely represent pre-invasive malignant lesions, and secondly because as I have already mentioned, any prospective trial looking at cancer as an end point will find hardly any cases (since the abnormal CIN cases picked up through trial surveillance will all be treated before they can progress). How is it you want “real world” experience rather than trial data for some things, but for this end point you seek the opposite – a plea for limited long term prospective studies without using wider epidemiological evidence? The only way to demonstrate “real world” efficacy is to let the vaccination program get on with it, and the results will be clear soon enough.

    Prevention of other cancers.
    This is quite plausible. There admittedly is scanty evidence yet, but an effect here would be a bonus. Nothing about this “speculation” detracts from the current proven efficacy of the vaccine against oncogenic HPV with respect to cervical cancer though, so this is another straw man fallacy raised by you to try and dilute the evidence base for the vaccine.

    Other Researchers’ questions about the vaccine effectiveness.
    You start this section by quoting someone who queries the vaccination policy and the commercial influences behind the program. Any evidence to refute the effectiveness? No. Another straw man. You then quote someone who agrees the true impact against cervical cancer will take years to demonstrate. I refer you to what I said above – it is clear that we can look at the effectiveness now against earlier grades of cervical cancer rather than invasive carcinoma; I agree that will take a while to emerge.

    My conclusion:
    You seem to have taken an ideological stance against this vaccine rather than a science-based one. Perhaps this is based on understandable concerns about its marketing and various contentious decisions about the vaccine program implementation and mandates in a couple of States. You tried to package this concern into a scientific-based commentary against vaccine efficacy in your previous blog post. You failed to do this effectively.

    You now have produced a second commentary which has failed to look at any newer evidence, but merely cherry-picks quotations and bits of articles you think support your stance. That attempt has also failed.

  • Dan

    I’ll second dyson’s comments.

    Getting back to your original question of whether boys should be vaccinated. The strongest arguments against vaccination is a potential lack of cost effectiveness (see papers by Kim et al) and the lack of evidence of the vaccine protecting against HPV-related oral cancers which is the most common HPV-related cancer in heterosexual men.

    If you’d like to continue to advocate for further research in the HPV area, I would concentrate on these areas and would suggesting abandoning many of your other arguments for the reasons stated above. I agree with dyson that many of your arguments are cherry picked and ideological. Vaccinating boys is a real question that I think should be discussed and researched further. I’d recommend a more balanced evidence based approach in the future.

  • William Jamison

    Bravo Dyson, and Dan, and thank you both for attempting to dispel the specious propaganda now being used in an effort to undermine wide-spread use of this life-saving vaccine.

  • William Jamison

    To the author:

    I still await your response to my query posed in #3 above. Please respond. Thank you.

  • Chris

    Why does the next blog post need a password?

  • Amos Zeeberg (Discover Web Editor)

    Still seeing that problem, Chris? Hopefully not…

  • David Jordan

    The author of this piece asks the wrong questions. The real question should be if the vaccine is effective at preventing HPV infection in girls, regardless of HPV – Cancer link. If it is then the next question is it also effective in the male population. While I believe that the evidence for the HPV – Cancer link is very strong, eliminating an STD should also be part of the discussion.

  • akili

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  • honestobserver123

    No that’s not the real question. Most cases of HPV do not cause cervical cancer, hpv is one factor there are other co-factors which need to be present for cervical cancer to develop. So the assumption cannot be made that temporarily reducing some strains of hpv will prevent cases of cervical cancer.

  • Venus65

    Because cervical cancer takes up to 30 years to develop from HPV.


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