The fact that you don't understand what I'm trying to explain is exactly why they can get away with bending the truth in their statements. This is not an "inactive form", and it will not "become active" once injected. It isn't the virus. It is a protein that will self-assemble into the same structure as the HPV capsid protein. This will also lead to a response from the immune system, but it is actually misleading to say that it is an "inactive form". It's just something that most people will take at face value because they don't have a better understanding of how it works, which is why they are able to put it on their flier.
H.P.V. Shots for young girls.
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The fact that you don't understand what I'm trying to explain is exactly why they can get away with bending the truth in their statements. This is not an "inactive form", and it will not "become active" once injected. It isn't the virus. It is a protein that will self-assemble into the same structure as the HPV capsid protein. This will also lead to a response from the immune system, but it is actually misleading to say that it is an "inactive form". It's just something that most people will take at face value because they don't have a better understanding of how it works, which is why they are able to put it on their flier.
jillio
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I understand exactly what you are trying to say. I am saying that that it is quite truthful to say that it is an inactive form of the virus. Are you trying to say that the proteins used to create the vaccine do not replicate and alter to produce the same protein as that found in the live viral infection, and thus create an immune response that allows for antibody production, leading to immunity to infection?
I refer you back to post #194.
Yes, I am saying that. It does not form the same protein as in a live viral infection. Again, it is a virus-like protein. In this case, it assembles into a similar structure as the HPV capsid, triggering a similar antibody response. It isn't HPV. I don't know how much more clearly I can say it. There are different ways to make vaccines, and one of them (and the one that most people think of) is to deactive the virus, or "kill" it somehow. This is not one of those vaccines.
jillio
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It does not trigger a "similar" anibody. It triggers the antibody specific to 4 different forms of the virus. Therefore, the protein is specific to the strains of HPV being vaccinated against.
And no, it isn't HPV. HPV is the manifest form of the disease. The vaccination protects against the manifest form of the disease, thus preventing contraction and transmission.
Yes, it triggers the same antibodies. The similar was supposed to be carrying over from the "similar structure". Same structure, same antibodies. But it isn't HPV, which you're finally admitting now. And what does this even mean, "HPV is the manifest form of the disease. "?
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jillio
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What part exactly of the sentence don't you understand?
Same structure, same antibodies. The vaccine does not contain virus, it contains proteins, which, when introduced to the host, change and alter, producing the same immune system response as the original virus would promote. Just in a safer and less tragic way than waiting to become infected and then having your immune system kick in to fight the infection. That is the whole point.
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Human Papillomavirus Vaccination — Reasons for Caution
Charlotte J. Haug, M.D., Ph.D.
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 Goldie1 point out in this issue of the Journal, the real impact of HPV vaccination on cervical cancer will not be observable for decades.
Although it was licensed for use in the United States in June 2006, the first phase 3 trials of the HPV vaccine with clinically relevant end points — cervical intraepithelial neoplasia grades 2 and 3 (CIN 2/3) — were not reported until May 2007, first in the Journal2 and 1 month later in the Lancet.3,4 The vaccine was highly successful in reducing the incidence of precancerous cervical lesions caused by HPV-16 and HPV-18, but a number of critical questions remained unanswered.5,6 For instance, will the vaccine ultimately prevent not only cervical lesions, but also cervical cancer and death? How long will protection conferred by the vaccine last? Since most HPV infections are easily cleared by the immune system, how will vaccination affect natural immunity against HPV, and with what implications? How will the vaccine affect preadolescent girls, given that the only trials conducted in this cohort have been on the immune response? The studies with clinical end points (i.e., CIN 2/3) involved 16- to 24-year-old women. How will vaccination affect screening practices? Since the vaccines protect against only two of the oncogenic strains of HPV, women must continue to be screened for cervical lesions. Vaccinated women may feel protected from cervical cancer and may be less likely than unvaccinated women to pursue screening. How will the vaccine affect other oncogenic strains of HPV? If HPV-16 and HPV-18 are effectively suppressed, will there be selective pressure on the remaining strains of HPV? Other strains may emerge as significant oncogenic serotypes.
Resolving the first essential questions will require decades of observation of large numbers of women. The last question may be answered sooner. Published reports of trials show an increasing trend of precancerous cervical lesions caused by HPV serotypes other than HPV-16 and HPV-18.2,4,6 The results were not statistically significant, however, possibly because there were too few clinically relevant end points in the observation periods reported. If randomized, controlled trials involving vaccinated and unvaccinated women continue for a few more years, we will most likely be able to tell whether this is a true trend. If so, there is reason for serious concern.
By the summer of 2007, there were definitely promising results with regard to the effectiveness of the HPV vaccine in the prevention of precancerous lesions (i.e., CIN 2/3) caused by the HPV-16 and HPV-18 serotypes. However, serious questions regarding the overall effectiveness of the vaccine in the protection against cervical cancer remained to be answered, and more long-term studies were called for before large-scale vaccination programs could be recommended.5,6 Unfortunately, no longer-term results from such studies have been published since then.
In the meantime, there has been pressure on policymakers worldwide to introduce the HPV vaccine in national or statewide vaccination programs. How can policymakers make rational choices about the introduction of medical interventions that might do good in the future, but for which evidence is insufficient, especially since we will not know for many years whether the intervention will work or — in the worst case — do harm? One way to provide decision support is to develop mathematical models of the natural history of the disease in question, introduce various intervention strategies, and use cost-effectiveness analysis to estimate the costs and health benefits associated with each clinical intervention. The results are typically expressed in terms of the amount we will have to pay for the extra health benefit of the treatment — that is, in dollars per life-year or quality-adjusted life-year (QALY) saved. Cost-effectiveness analyses are tools for decision making under conditions of uncertainty. These analyses do not in themselves provide evidence that medical interventions are effective. In this issue of the Journal, Kim and Goldie present a model of HPV vaccination, and they use a cost-effectiveness analysis to make projections of the possible health and economic implications of the use of the vaccine.1
To evaluate the quality of a cost-effectiveness analysis, it is essential to appraise the model's input variables, the uncertainties, and the choices the researchers have made. To set up such an analysis of a preventive medical intervention — in this case, a vaccine given to healthy 12-year-old girls — that might have an effect on the incidence of cervical cancer decades from now is extremely complex. The analysis has to model the natural history of HPV infection in this cohort of girls over their lifetime, the effect of the vaccine over all those years (whether it is the same effect or one that is waning), the effect on other HPV strains, the effect of the vaccine on the natural immunity against HPV infections, the sexual behavior of the girls and women and their partners, and finally, women's cervical-cancer screening practices.
The model presented by Kim and Goldie is well done and ambitious, and it includes most of these factors. They conclude that under certain assumptions, vaccinating 12-year-old girls is associated with an incremental cost-effectiveness ratio of $43,600 per QALY gained, whereas adding a catch-up program for older girls and women is not cost-effective. However, their base-case assumptions are quite optimistic. They presume lifelong protection of the vaccine (i.e., no need for a booster dose), that the vaccine has the same effect on preadolescent girls as on older women, that no replacement with other oncogenic strains of HPV takes place, that vaccinated women continue to attend screening programs, and that natural immunity against HPV is unaffected. Whether these assumptions are reasonable is exactly what needs to be tested in trials and follow-up studies. If the authors' baseline assumptions are not correct, vaccination becomes less favorable and even less effective than screening alone. For example, as shown in the article, if the protection of the vaccine wanes after 10 years, vaccination is much less cost-effective and screening is more effective than catch-up programs.
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.
No potential conflict of interest relevant to this article was reported.
NEJM -- Human Papillomavirus Vaccination -- Reasons for Caution
And, another one, it's 24 long pages :
A Judicial Watch Special Report
Examining the FDA's HPV Vaccine Records
http://www.judicialwatch.org/documents/2008/JWReportFDAhpvVaccineRecords.pdf
Charlotte J. Haug, M.D., Ph.D.
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 Goldie1 point out in this issue of the Journal, the real impact of HPV vaccination on cervical cancer will not be observable for decades.
Although it was licensed for use in the United States in June 2006, the first phase 3 trials of the HPV vaccine with clinically relevant end points — cervical intraepithelial neoplasia grades 2 and 3 (CIN 2/3) — were not reported until May 2007, first in the Journal2 and 1 month later in the Lancet.3,4 The vaccine was highly successful in reducing the incidence of precancerous cervical lesions caused by HPV-16 and HPV-18, but a number of critical questions remained unanswered.5,6 For instance, will the vaccine ultimately prevent not only cervical lesions, but also cervical cancer and death? How long will protection conferred by the vaccine last? Since most HPV infections are easily cleared by the immune system, how will vaccination affect natural immunity against HPV, and with what implications? How will the vaccine affect preadolescent girls, given that the only trials conducted in this cohort have been on the immune response? The studies with clinical end points (i.e., CIN 2/3) involved 16- to 24-year-old women. How will vaccination affect screening practices? Since the vaccines protect against only two of the oncogenic strains of HPV, women must continue to be screened for cervical lesions. Vaccinated women may feel protected from cervical cancer and may be less likely than unvaccinated women to pursue screening. How will the vaccine affect other oncogenic strains of HPV? If HPV-16 and HPV-18 are effectively suppressed, will there be selective pressure on the remaining strains of HPV? Other strains may emerge as significant oncogenic serotypes.
Resolving the first essential questions will require decades of observation of large numbers of women. The last question may be answered sooner. Published reports of trials show an increasing trend of precancerous cervical lesions caused by HPV serotypes other than HPV-16 and HPV-18.2,4,6 The results were not statistically significant, however, possibly because there were too few clinically relevant end points in the observation periods reported. If randomized, controlled trials involving vaccinated and unvaccinated women continue for a few more years, we will most likely be able to tell whether this is a true trend. If so, there is reason for serious concern.
By the summer of 2007, there were definitely promising results with regard to the effectiveness of the HPV vaccine in the prevention of precancerous lesions (i.e., CIN 2/3) caused by the HPV-16 and HPV-18 serotypes. However, serious questions regarding the overall effectiveness of the vaccine in the protection against cervical cancer remained to be answered, and more long-term studies were called for before large-scale vaccination programs could be recommended.5,6 Unfortunately, no longer-term results from such studies have been published since then.
In the meantime, there has been pressure on policymakers worldwide to introduce the HPV vaccine in national or statewide vaccination programs. How can policymakers make rational choices about the introduction of medical interventions that might do good in the future, but for which evidence is insufficient, especially since we will not know for many years whether the intervention will work or — in the worst case — do harm? One way to provide decision support is to develop mathematical models of the natural history of the disease in question, introduce various intervention strategies, and use cost-effectiveness analysis to estimate the costs and health benefits associated with each clinical intervention. The results are typically expressed in terms of the amount we will have to pay for the extra health benefit of the treatment — that is, in dollars per life-year or quality-adjusted life-year (QALY) saved. Cost-effectiveness analyses are tools for decision making under conditions of uncertainty. These analyses do not in themselves provide evidence that medical interventions are effective. In this issue of the Journal, Kim and Goldie present a model of HPV vaccination, and they use a cost-effectiveness analysis to make projections of the possible health and economic implications of the use of the vaccine.1
To evaluate the quality of a cost-effectiveness analysis, it is essential to appraise the model's input variables, the uncertainties, and the choices the researchers have made. To set up such an analysis of a preventive medical intervention — in this case, a vaccine given to healthy 12-year-old girls — that might have an effect on the incidence of cervical cancer decades from now is extremely complex. The analysis has to model the natural history of HPV infection in this cohort of girls over their lifetime, the effect of the vaccine over all those years (whether it is the same effect or one that is waning), the effect on other HPV strains, the effect of the vaccine on the natural immunity against HPV infections, the sexual behavior of the girls and women and their partners, and finally, women's cervical-cancer screening practices.
The model presented by Kim and Goldie is well done and ambitious, and it includes most of these factors. They conclude that under certain assumptions, vaccinating 12-year-old girls is associated with an incremental cost-effectiveness ratio of $43,600 per QALY gained, whereas adding a catch-up program for older girls and women is not cost-effective. However, their base-case assumptions are quite optimistic. They presume lifelong protection of the vaccine (i.e., no need for a booster dose), that the vaccine has the same effect on preadolescent girls as on older women, that no replacement with other oncogenic strains of HPV takes place, that vaccinated women continue to attend screening programs, and that natural immunity against HPV is unaffected. Whether these assumptions are reasonable is exactly what needs to be tested in trials and follow-up studies. If the authors' baseline assumptions are not correct, vaccination becomes less favorable and even less effective than screening alone. For example, as shown in the article, if the protection of the vaccine wanes after 10 years, vaccination is much less cost-effective and screening is more effective than catch-up programs.
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.
No potential conflict of interest relevant to this article was reported.
NEJM -- Human Papillomavirus Vaccination -- Reasons for Caution
And, another one, it's 24 long pages :
A Judicial Watch Special Report
Examining the FDA's HPV Vaccine Records
http://www.judicialwatch.org/documents/2008/JWReportFDAhpvVaccineRecords.pdf
Again, I know how vaccines work. You still don't seem to get the point. It isn't HPV. It is misleading for them to say so, but they are able to do it anyways.
I never said otherwise. I think people should educate themselves first, but that isn't even my biggest worry. The thing that I worry about the most is that they are creating a false sense of security, and that will pull attention away from further research and testing which could help us better understand not only HPV, but cervical cancer in general.
I do also worry though that they don't seem to be testing for HPV before giving people the vaccine, even though it will be ineffective, and - for all they know - could even be more harmful in someone who already has the virus.
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Just let her to find out for herself. It's no use to debate with her. She's not readin' some ADers' posts right.
Oceanbreeze
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I have done my homework. Here's a link. The link says it's made from an inactive virus. That's just semantics in my mind. Inactive and dead mean the same thing to me.
Gardasil HPV Vaccine (recombinant human papillomavirus quadrivalent vaccine) Information on MedicineNet.com
Which is exactly why they get away with this. Inactive and dead are much more similar. This is neither of those. A lot of the things that they say are "just semantics", but the fact is that they can and do mislead people.
And I'm not sure what you consider doing your homework, but here's the third sentence on that page. "The proteins in Gardasil are structural, virus-like proteins (VLP) that resemble the HPV virus." Sounds an awful lot like what I've said this whole page....
Oceanbreeze
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Exactly. You take the virus and you manipulate it. So? They've done that with all the other vaccines, too.
A vaccine is used to trick the immune system into creating antiboties. You do that by introducing an anactive virus into the body, so it can create an immune response to the Human Pap. Virus and the person is then protected.
Oceanbreeze
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Yes she is. You're just not understanding what she and others are saying.
They didn't manipulate it. But it's close enough that they get away with saying it. This is exactly my point. I really don't get why people keep thinking I don't understand how vaccines work.
All I'm trying to say is that there are ways for them to bend the truth. A lot of ways. And they do.