CDC MONGERS FEAR AND HAWKS DEADLY VACCINE

The Centers for Disease Control and Prevention (CDC):
— have confused correlation with causation, thus committing perhaps the most elementary error against which students of statistics are warned (p. 194 in The Origin, Persistence and Failings of HIV/AIDS Theory);
— invented an “hierarchical” classification scheme that set HIV/AIDS on a wrong course and made multivariate analysis impossible (ibid, p. 19);
— disseminated propaganda that everyone was at risk for AIDS while knowing that “for most heterosexuals, the risk from a single act of sex was smaller than the risk of ever getting hit by lightning” (Bennett and Sharpe, Wall Street Journal, 1 May, pp. A1, 6);
— use incompetent computer models (ibid, p. 223) and disseminate their flawed estimates rather than actual counts (pp. 221-2);
— reduced retroactively some actually reported numbers, thereby obfuscating a decline in “AIDS” deaths (ibid, p. 221);
— had the gall to say in 2005 that “HIV infections” in the United States had surpassed a million “for the first time” when they had been estimating about a million for the past two decades (ibid, pp. 1-2);
— increasingly commingle “HIV” and “AIDS” data so that the lack of correlation between them is obscured;
— and for reasons not difficult to infer, they have invented “HIV disease” (post of Friday, 28 December 2007).

Given all that (and more), I hardly imagined that I would ever be taken aback at anything said or done by the CDC. Still they managed to surprise me with the 11 March announcement that

“1 in 4 Teenage Girls Has a Sexually Transmitted Disease
– 3.2 Million Female Adolescents Estimated to Have at Least One of the Most Common STDs” (CDC Press Release, 2008 National STD Prevention Conference—Confronting Challenges, Applying Solutions)

1 of every 4 teenage females just seems awfully high. But how can one argue with scientific facts?

“Chicago [March 11, 2008] – A CDC study released today estimates that one in four (26 percent) young women between the ages of 14 and 19 in the United States – or 3.2 million teenage girls – is infected with at least one of the most common sexually transmitted diseases (human papillomavirus (HPV), chlamydia, herpes simplex virus, and trichomoniasis).… The two most common STDs overall were human papillomavirus, or HPV (18 percent), and chlamydia (4 percent). …CDC also recommends that girls and women between the ages of 11 and 26 who have not been vaccinated or who have not completed the full series of shots be fully vaccinated against HPV.”

The study was based on data from a survey done in 2003-4. Why did it take more than 3 years to release information of this importance? Perhaps there was no point in frightening people before an HPV vaccine was available?

“ ‘The statistics are certainly disheartening,’ said Dr. Dorothy Furgerson, medical director at Planned Parenthood Mar Monte” (Julie Sevrens Lyons, Mercury News).

Indeed. But disheartening perhaps for other reasons than Dr. Furgerson had in mind:
“The new study by CDC researcher Dr. Sara Forhan is an analysis of nationally representative records on girls and women ages 14 to 19 who participated in a 2003-04 government health survey. . . . [of] 838 teens”

One might wonder whether 838 could be truly representative nationally. But the main point here has to do with human papillomavirus and the touting of “full” vaccination against it. Here are some other facts from the CDC itself:

“Approximately 20 million Americans are currently infected with HPV, and another 6.2 million people become newly infected each year. At least 50% of sexually active men and women acquire genital HPV infection at some point in their lives
….
The American Cancer Society estimates that in 2008, 11,070 women will be diagnosed with cervical cancer in the U.S. . . . [and with other] HPV-related cancers . . .
3,460 women diagnosed with vulvar cancer;
2,210 women diagnosed with vaginal and other female genital cancers;
1,250 men diagnosed with penile and other male genital cancers; and
3,050 women and 2,020 men diagnosed with anal cancer.”

In other words, with 6.2 million newly infected with HPV annually, about 20,000 women annually will be diagnosed with a cancer “related” to HPV.

Keep in mind that it has never been proven that HPV causes the cancer; all the CDC has, once again, is a correlation.

Evidently the chance of contracting one of these “HPV-related” cancers if one is infected with HPV is 20,000 out of 6.2 million, about 1 in 300 or 3.3 per 1000. Can something that is “associated” with a cancer only three times in a thousand really be said to cause that cancer?

Even were that so, consider the relative risks of vaccination and of not vaccinating. Leave aside that the HPV vaccine, Gardasil, costs $120 for each of three required shots. Consider only that it was approved in June 2006 by the Food and Drug Administration, and that within less than a year there had come numerous reports of dangerous “side”-effects:

“Judicial Watch Uncovers Three Deaths Relating To HPV Vaccine” (24 May 2007)

“Judicial Watch . . . today released documents obtained from the U.S. Food and Drug Administration (FDA) under the provisions of the Freedom of Information Act, detailing 1,637 reports of adverse reactions to the vaccination for human papillomavirus (HPV), Gardasil. Three deaths were related to the vaccine. . . . As of May 11, 2007, the 1,637 adverse vaccination reactions reported to the FDA . . . included 371 serious reactions. Of the 42 women who received the vaccine while pregnant, 18 experienced side effects ranging from spontaneous abortion to fetal abnormities. Side effects published by Merck & Co. warn the public about potential pain, fever, nausea, dizziness and itching after receiving the vaccine. Indeed, 77% of the adverse reactions reported are typical side effects to vaccinations. But other more serious side effects reported include paralysis, Bells Palsy, Guillain-Barre Syndrome, and seizures. ‘The FDA adverse event reports on the HPV vaccine read like a catalog of horrors,’ stated Judicial Watch President Tom Fitton. ‘Any state or local government now beset by Merck’s lobbying campaigns to mandate this HPV vaccine for young girls ought to take a look at these adverse health reports. It looks as if an unproven vaccine with dangerous side effects is being pushed as a miracle drug.’”

Yet the CDC is urging this dangerous vaccine on all females aged between 11 and 26… Evidently, press releases from the CDC ought to carry a “black box warning”:

Not that it’s necessarily better elsewhere:

“Glaxo wins European Union approval to sell Cervarix” (byline Marthe Fourcade)
“Sept. 24 (Bloomberg) — GlaxoSmithKline Plc won European Union approval for its cervical cancer vaccine Cervarix, allowing the company to compete with Merck & Co.’s Gardasil in the world’s second-largest pharmaceutical market. The vaccine was cleared for sale in 27 countries . . . .”

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Sometimes toxic things (think antiretroviral drugs) have temporarily beneficial side-effects (the general phenomenon is known as “hormesis”). In this case, the toxic press-release from the CDC has the side-benefit of allowing me to recommend the book “Virus Mania” by Torsten Engelbrecht and Claus Köhnlein (www.trafford.com/06-3226 or orders@ trafford.com; 320 pp, softcover, US$24.00, C$27.60, EUR18.71, £12.40).

I had been in a quandary, what to write about this book, which I’d just been reading. It contains some important eye-opening material; but the translation from German leaves quite a bit to be desired, and the tone is strident at times in indicting institutions and companies for deliberate deception and putting profits ahead of everything else. But any such defects are dwarfed by those in CDC publications. Readers should of course reach their own opinion by checking the sources cited in “Virus Mania”—just as they should always check in CDC publications for inconsistency of data, for estimates masquerading as facts, and so on. But all quibbles aside,“Virus Mania” reveals palpable facts that bring into serious question the widespread official propaganda about hepatitis C, mad-cow disease, SARS, avian flu, and cervical cancer, as well as more generally about vaccination and virology—not to mention AIDS, of course.

HERPES AND HIV

“People infected with the herpes simplex type 2 virus, known as genital herpes, were 15 times more likely to also be infected with HIV” (WASHINGTON [Reuters] “Under 1 percent of U.S. adults have HIV: report”, by Maggie Fox; 29 January 2008).
The report itself gives the HIV-positive rate as 1.99% [Note the accuracy! Significantly different from 2%, apparently!] among those with herpes and 0.13% among the others, a ratio of 15.3, laudably rounded to 15 in the media report.

A friend helped me with this interesting exercise in understanding the relevant official statistics:

According to the National Institute for Allergy and Infectious Diseases, about 45 million Americans above age 12, about 1 in 5, have genital herpes. Therefore there are about 5 times 45 million Americans older than 12, namely, 225 million.

Now we’re told that 0.47% of adults (18-49 years old) are HIV-positive, or 618,000 (“anywhere between 447,000 people and 841,000 people, with 618,000 the middle number”). Therefore, American adults between 18 and 49 number 618,000 divided by 0.47%, which is about 130,000,000. How many of those have herpes? Since 45 out of 225 million have herpes, 45 times 130 divided by 225, in other words, 26 million . (Yes, you could also get that as 1 in 5 among 130 million equals 26 million. But I wanted to show that I could make things nearly as complicated as the experts can).

So we have 26 million who are 15 times more likely to be HIV-positive than the other 104 million; and the total number of HIV-positives is 618,000. Say “x” is the rate of being HIV-positive for those who don’t have herpes. Then “15x” is the rate of HIV-positive among those who do have herpes. Then (104x) millions plus (26 times 15x) millions must equal 618,000. The solution of that algebraic equation is that x (the rate of HIV-positive among American adults who are not infected by herpes, remember) is 0.125%. (That’s reassuringly comparable to the usual HIV-positive rate of a few per thousand in low-risk groups, Table 3, p. 25 in The Origins, Persistence and Failings of HIV/AIDS Theory.) For those who ARE herpes-infected, the HIV+ rate is 15 times greater than that, in other words, 1.875%. (Note here that I am following the Centers for Disease Control and Prevention and other federal agencies in giving numbers to as many “significant” figures as possible.)

Now: 26 million of the 18-49-year-old Americans have herpes. At a rate of 1.875%, that amounts to 487,500 who are HIV-positive. The other 104 million who don’t have herpes contribute another 104 times 0.125%, in other words, 130,000. Note that—unlike typical numbers from federal agencies (for instance, HIV/AIDS: NUMBERS THAT DON’T ADD UP, 29 November 2007; MATHEMATICAL AND STATISTICAL LIES ABOUT HIV/AIDS, 2 December 2007), these numbers DO add up: 487,500 plus 130,000 equals 617,500, which is close enough to 618,000.

But now think about what this means. Among all the HIV-positive adults in the United States, nearly 80% (487,500 out of 618,000) are supposed to have herpes?

That seems unlikely, to put it mildly; a polite Australian might say, “Not bloody likely”. Fortunately, other sources of data are available to check this conclusion, at least indirectly. For example, the experts know that treating herpes reduces the viral load of “HIV”:

“Treating herpes simplex virus type 2 appears to reduce HIV-1 plasma levels by more than 50% in men infected with both viruses” (HIV NONSENSE: TODAY AND EVERY DAY, 22 November 2007).

Now, if treating herpes gets rid of “HIV” and thereby reduces “HIV infection”, then anti-herpes drugs should also reduce the risk of becoming infected by “HIV” in the first place. But it doesn’t:

“A once-promising experiment to see whether treating genital herpes with a common drug could dramatically reduce susceptibility to HIV infection has found no protection whatsoever” (“Anticipated ’slam dunk’ AIDS treatment fails”, by Sabin Russell, 5 February 2008).

The experts are suitably puzzled and dismayed by this: “This was a huge setback for HIV prevention”; “Many people thought this was going to be a slam dunk”; “as was the case with circumcision, this carefully monitored trial was based on years of prior studies that strongly suggested the idea would work”; “This was the study everyone thought they had already had the answer to”.

[This is not unlike what has happened with vaccines intended to prevent “HIV infection”. Innumerable approaches that were fully expected to work have turned out to be ineffective, leaving the experts at a loss to understand why. The simple and obvious but unacceptable explanation is that HIV/AIDS theory is wrong and that “HIV” is not an infectious agent.]

But the failure of anti-herpes treatment in relation to “HIV” was not the only conundrum: “One puzzle facing scientists is that the acyclovir treatments reduced herpes lesions by different percentages in different groups: 32 percent among African women, 41 percent among gay men in Peru, and 50 percent among gay men in the United States. But prior studies had shown the drug was capable of 80 percent suppression”.

And then there are some more points of confusion:
“Nearly 20 years of various studies on herpes had shown that herpes infection nearly tripled the risk of contracting HIV”.
Pardon me! What about “People infected with the herpes simplex type 2 virus, known as genital herpes, were 15 times more likely to also be infected with HIV”? Which is it? Three times or fifteen times?

Well, in the Data Brief that gives those numbers of 1.99% and 0.13%, ratio 15.3, the document’s second paragraph states, “Herpes simplex-virus type 2 (HSV-2) infection is associated with HIV infection; some studies have shown that HSV-2 infection doubles the risk of HIV acquisition”.

So: Is it twice, thrice, or fifteen times? I’m reminded that as to HIV/AIDS, the dictum applies, “Pick a number; pick **any** number” (see post of 7 February 2008).

One of the references cited in the Data Brief sheds further light. It’s a review of 31 separate studies of the association between HIV and herpes. Overall, the chance of being HIV-positive is said to be 3.9 times greater if one has herpes. However, if one already has herpes, the chance of becoming HIV-positive is only doubled (factor of 2.1, to be precise). I suppose this means that HIV-positive people are at considerable risk of contracting herpes; that’s in keeping with what had seemed the surprising result of the earlier calculation, that 80% of HIV-positive Americans have herpes.

Clearly then, treating herpes will reduce the chance of becoming HIV-positive. Indeed, as noted above, treating herpes reduces amount of “HIV” by 50%. However, as also noted above, everyone was shocked to find that treating herpes doesn’t protect against “HIV”.

But let’s not give up. There’s always room for another clinical trial, “testing whether the anti-herpes drug might block certain HIV infections involving couples. This one will treat herpes in HIV-infected men or women whose sexual partner is HIV-negative, and may or may not have herpes. The experiment will attempt to show that by taking acyclovir, the HIV-infected person will be less infectious, and far less likely to transmit the AIDS virus to his or her partner”.

After all, the results could be “as exciting as the findings in 2005 and 2006 that adult male circumcision—the surgical removal of the foreskin— reduced by as much as 60 percent the risk that those men would contract HIV”. Who would play the part of spoil-sport by pointing out that circumcision does not lower the risk of becoming HIV-positive? See RWANDA: CIRCUMCISE ALL MEN—EVEN IF IT MEANS MORE HIV INFECTION, 3 February 2008.

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There is a common thread that connects the conundrums of herpes and “HIV”, circumcision and “HIV”, and vaccines against “HIV”: the results are not reproducible. When the outcome of one experiment is used as a basis for further work, the expected effect doesn’t eventuate. The orthodox view of “HIV” is ineffective in planning experiments, and it is unable to explain the unexpected results that are so often obtained. One way of putting this might be to say, “HIV/AIDS theory has been falsified”.

TO AVOID HIV LATER, DAMAGE YOUR KIDNEYS AND LIVER NOW

Clinical trials on human beings are under way to gauge how well tenofovir and emtricitabine protect against HIV infection, with the hope that a regular diet of them could be recommended as prophylaxis.

It’s already known, mind you, that these drugs can produce bone demineralization with chronic use, kidney damage, lactic acidosis (including fatalities), liver damage (including fatalities), and liver cancer. The danger of side effects is greatest when first starting the drugs but also when one stops taking them.

The brilliant idea that this may be useful prophylaxis is based on studies in “humanized” mice—FIVE mice, that is—engineered to have a “human-type” immune system. The media (http://cbs11tv.com/local/HIV.Transmission.Prevention.2.631367.html) help everyone understand how significant this is by pointing out that “Humanized mice . . . have the same immune systems and infection fighting cells as humans”; which could make one wonder why there’s even a need for trials in actual human beings.

The concept of prophylaxis using drugs that treat the actual illness is in itself a remarkable advance. Perhaps instead of exposing babies to the dangers of vaccination, we should simply place them on life-long diets of antibiotics? Come to think of it, we do already practice this sort of prophylaxis by feeding antiretroviral drugs to every available pregnant woman who happens to be HIV-positive—see FIRST: DO NO HARM! (19 December 2007).

As to humanizing mice, I’m sorely tempted to speculate about the possibility of engineering mice to have human-type intelligence—sufficient, at the very least, for carrying on HIV/AIDS research and clinical trials.

* * * * * *

Here is what the Official Treatment Guidelines, December 2007 version, say about the side effects of tenofovir and emtricitabine, which are described in the media story below as “fewer . . . than other HIV treatments”:

“Renal impairment, manifested by increases in serum creatinine, glycosuria, hypophosphatemia, and acute tubular necrosis, has been reported with tenofovir use [152, 153]. The extent of this toxicity is still undefined. . . .
. . . .
Discontinuation of emtricitabine, lamivudine, or tenofovir in patients with hepatitis B coinfection. Patients with hepatitis B coinfection (hepatitis B surface antigen or HBeAg positive) and receiving one or a combination of these NRTIs may experience an exacerbation of hepatitis upon drug discontinuation [164, 165]. If any of the above agents is discontinued, the patients should be closely monitored for exacerbation of hepatitis or for hepatic flare (AII).
. . . .
Need to discontinue emtricitabine, lamivudine, or tenofovir: Monitor clinical course with frequent liver function tests, and consider the use of interferon, adefovir dipivoxil, or telbivudine to prevent flares, especially in patients with marginal hepatic reserve.
. . . .
Pertinent Black Box Warning Information:
Emtricitabine (EMTRIVA); or in combination product with tenofovir DF (TRUVADA) or with tenofovir DF and efavirenz (ATRIPLA):
—Lactic acidosis and severe hepatomegaly with steatosis, including fatal cases, have been reported with the use of nucleoside analogues alone or in combination with other antiretrovirals.
—Emtricitabine is not indicated for the treatment of hepatitis B infection (HBV), the safety and efficacy have not been established in patients with HIV/HBV coinfection.
—Severe acute exacerbations of hepatitis B have been reported in patients who discontinued emtricitabine – hepatic function should be monitored closely with both clinical and laboratory follow-up for at least several months after discontinuation of tenofovir in HIV/HBV coinfected patients.
—If appropriate, initiation of anti-HBV therapy may be warranted after discontinuation of tenofovir.
. . . .
Tenofovir (VIREAD); or in combination product with emtricitabine (TRUVADA) or with efavirenz and emtricitabine (ATRIPLA)
—Lactic acidosis and severe hepatomegaly with steatosis, including fatal cases, have been reported with the use of nucleoside analogs alone or in combination with other antiretrovirals.
—Tenofovir is not indicated for the treatment of chronic hepatitis B (HBV) infection, safety and efficacy in patients with HIV/HBV coinfection have not been established.
—Severe acute exacerbations of hepatitis B have been reported in patients who discontinued tenofovir – hepatic function should be monitored closely with both clinical and laboratory follow-up for at least several months after discontinuation of tenofovir in HIV/HBV coinfected patients.
—If appropriate, initiation of anti-HBV therapy may be warranted after discontinuation of tenofovir.
. . . .
Studies in monkeys show decreased fetal growth and reduction in fetal bone porosity within two months of starting maternal therapy [371]. Clinical studies in humans (particularly children) show bone demineralization with chronic use; clinical significance unknown [252, 372]. Significant placental passage in humans (cord:maternal blood ratio ~1.0).”

Tenofovir also produces liver cancer in mice.

* * * * * *

Here’s the media report of this study:

“After 25 years of researchers around the globe being confounded by HIV, scientists in Dallas have shown that the virus’s transmission can be stopped with medications. The scientific first, though performed only in lab mice, bodes well for a future when people at high risk for HIV infection would have a convenient way to protect themselves from the virus. . . . experts who have long advocated safe-sex practices are worried that people will seek these drugs without waiting for scientific proof from human studies. . . . One of the drugs, tenofovir, is reportedly being sold at gay dance clubs on both coasts as a protection against HIV. . . .
Someday, people at high risk of HIV infection could be encouraged by doctors to take a daily pill . . . .
The experiment involved injecting five mice for seven days with two drugs that are commonly used to treat AIDS patients, tenofovir and emtricitabine. On the third day, the mice were inoculated vaginally with HIV, to mimic how most women and girls become infected. ‘Women have no way of protecting themselves from … [sexually transmitted diseases] and HIV,’ said Dr. Garcia, a professor of internal medicine. A preventive medication ‘would empower them to at least have a fighting chance.’ . . .
An important step toward the current UT Southwestern study was Dr. Garcia’s 2006 development of a mouse that had been made susceptible to HIV via transplantation of a ‘humanized’ immune system’. . . .
The two [drugs] . . . have fewer side effects than other HIV treatments. The two drugs are part of several studies in people, funded by the U.S. government, that are testing safety and effectiveness in preventing HIV infection among intravenous drug abusers, young men and women who are sexually active and men who have sex with men. Test sites include San Francisco, Atlanta, Botswana, Thailand, Peru and Ecuador” [emphases added].
(“Dallas scientists stop HIV from spreading in mice—Experts caution that Dallas team’s findings were only in mice”, by Sue Goetinck Ambrose & Sherry Jacobson , Dallas Morning News, 15 January 2008).
The source article is “Antiretroviral pre-exposure prophylaxis prevents vaginal transmission of HIV-1 in humanized BLT mice” by Denton et al., PLoS Medicine 5 #1, e16 doi:10.1371/journal.pmed.0050016 in PLoS Medicine

HISTORY OF AZT

In FIRST: DO NO HARM! (19 December), I wrote, “The toxicity of AZT was known long before its introduction as an antiretroviral drug: it had been found too toxic to be used in cancer chemotherapy”. A knowledgeable correspondent informed me that AZT failed to qualify for cancer chemotherapy not because it was too toxic but because it wasn’t effective.

As always, I’m grateful for the comment; I do wish to be as accurate as possible, and can’t check everything that I’ve absorbed from a lot of reading, not all of which I can recall in any detail. A very positive benefit of being set straight is that when I try to learn more in order to correct errors, it sometimes leads to unsuspected new grist for the dissident mill; for instance, Sharon Stone’s assertion about AIDS deaths among women (WORLD AIDS DAY, 22 December) caused me to look at the official statistics for AIDS deaths and to discover the category of death-causing “HIV DISEASE” (28 December). Those death statistics will be featured again in later posts, for the way they vary with age is yet another illustration of the vacuity of HIV/AIDS theory.

Back to AZT and toxicity and cancer. Looking further into it, there seems to be some doubt about the matter. AIDS WIKI says this:
“AZT was originally intended to treat cancer, but failed to show efficacy and had an unacceptably high toxicity profile. (Note: There is some dispute over whether a high toxicity profile contributed to the shelving of AZT. Horwitz himself appears to have given conflicting testimony in various interviews.)”

I came across a confirmation that AZT had been found useless against leukemia in mice by Horwitz in 1964, but had shown possible promise against breast cancer (Science News, 28 June 1997, 151 #26, p. 397, citing a June 15 article in Cancer Research).

At any rate, AZT was known to be highly toxic at the time it was tried against AIDS. For a very readable account of the intrigues and machinations that led to its approval, read Bruce Nussbaum’s “Good Intentions: How Big Business and the Medical Establishment Are Corrupting the Fight Against AIDS” (1990, Atlantic Monthly Press).

Nothing about that book’s title and sub-title has become obsolete in the nearly two decades since it was written. Nussbaum is hardly a radical, and he isn’t a dissident who questions whether HIV causes AIDS. He was an investigative reporter and is now a senior editor at Business Week. His book describes “the puppet master, the brilliant Dr. David Barry, Burroughs Wellcome’s chief strategist; Dr. Tony Fauci, who grabbed control of the government’s AIDS research program only to squander $1 billion without developing a single new drug. . . . An old-boy network of powerful medical researchers dominates in every disease field . . . . They control the major committees, they run the most important trials. They are accountable to no one. despite the billions of taxpayers’ dollars that go to them every year, there is no public oversight. Medical scientists have convinced society that only they can police themselves” (from the jacket blurb).

That’s a pretty good summary of what dissidents are still up against today.

It’s not just that there’s a powerful medical establishment, it’s also that HIV/AIDS theory has tentacles reaching not only into medical practice but also into several different fields of research—epidemiology, immunology, virology. The epidemiologists have recognized that the observed rates of apparent sexual transmission of HIV are far too low to cause epidemics; but they don’t dare stand up and tell the immunologists and virologists and physicians that they are wrong, because they imagine that those people know what they are doing within their own areas of expertise. So the epidemiologists leave their observations as anomalies to be cleared up at some future time and speculate about special circumstances that might somehow make transmission more efficient—when it’s not being observed, of course. The immunologists are happy to have as an excuse for getting nowhere with vaccines, the virologists’ assertions that HIV mutates in an unprecedented fashion. Physicians can only treat their patients with what they are told to try by those whom they must trust to have carried out proper studies. There’s nothing unusual about this general state of affairs: scientists in closely related fields tend not to question what their colleagues in those other fields tell them, and apparently unexplainable anomalies are shoved aside in the belief that later on they will become explicable. That’s what Thomas Kuhn described in his much cited and little understood “Structure of Scientific Revolutions”, and it fits the realities much better than Karl Popper’s suggestion that contradictory evidence at once falsifies a theory; as Imre Lakatos pointed out, the mainstream belief is continually propped up by subsidiary ad hoc hypotheses made up more or less on the spur of each bit of contradictory evidence. If science really is self-correcting, it often takes its own good time about it—like 4 decades over the laws of heredity.

At any rate, that so many different specialties are involved in HIV/AIDS underscores why I’m so grateful when others check what I write, because one can hardly say much about HIV/AIDS without touching on questions of immunology, epidemiology, virology, and more.

Just now, what I would very much like to understand is, what criteria are used in the trials of potential vaccines? I know there’s been controversy over whether “HIV antibodies” represent a successful or potentially successful reaction against a retrovirus. I’ve learned that there are several different sorts of antibodies. I’ve learned that vaccinology often makes use of “adjuvants”, which stimulate the immune system in a non-specific fashion. What I’m curious about is this: The standard way of detecting infection by HIV is via tests for antibodies; but aren’t vaccines designed to stimulate the generation of antibodies?

That’s a genuine plea for explanation, not a rhetorical question.