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

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.

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.

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:
http://www.sciencedirect.com/science/article/pii/S0091743509002023

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.