HIV/AIDS Skepticism

Pointing to evidence that HIV is not the necessary and sufficient cause of AIDS


Posted by Henry Bauer on 2008/02/08

“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.


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”.

2 Responses to “HERPES AND HIV”

  1. MacDonald said

    I am going to resist the temptation to go for HSV-2 this time – suffice to say, among the risk groups, one of the surest indications of imminent HIV infection is active Herpes (Herpes virus shedding). When one takes into consideration that HSV-2 can be AIDS-defining, and also frequently accounts for over 50% – more than HIV combined with all other co-factors – of the viral load, it does not seem far fetched to hypothesize that HSV-2 under certain, as yet undefined, circumstances quite reliably produces a false-positive HIV test.

    [The association between infection with HSV-2 (the virus that causes genital herpes) and the risk of HIV acquisition has been well-studied. A recent meta-analysis found that individuals with HSV-2 infection had a three-fold increase in their risk of HIV acquisition, and it has been estimated that approximately half of all HIV infections can be attributed to HSV-2– ]

    Anyway I was going to resist the temptation to go for the virus that, even on a conservative estimate, on its own, ACCOUNTS FOR MORE THAN HALF OF ALL HIV INFECTIONS, AND MORE THAN HALF OF THE VIRAL LOAD ONCE INFECTED!!!, and point to this peculiarity:

    “Prof Churchyard, who heads the Aurum Institute for Health Research, said that research presented at the 15th Conference on Retroviruses and Opportunistic Infections in Boston this week indicated circumcising HIV-positive men might increase the chance of harm to women. There were ‘incredibly high’ rates of HIV transmission in the first six months after circumcision, probably because the men were having sex before their wounds had healed, he said.”

    First: How can it take a small wound 6 months to heal while leaving the man quite capable of sexual intercourse?

    Second: In a country where HIV prevalence is higher among young women than men, how can wounded men transmit HIV at a higher rate than they acquire it?

    Third: How can they even contemplate citing a professor named Churchyard?

    Well perhaps this is why:

    [says Churchyard] “Circumcision reduces the risks for uninfected men, so it would have an overall effect on the population, and women could still benefit indirectly.”

    In other words, continue with circumcision because when comparing men’s lowered risk with women’s elevated risk there might be a net gain once we’re past the first 6 months. It would be interesting to see how the “indirect benefit” to women is calculated on that model.

  2. hhbauer said

    I too would be interested in the logic applied to calculate that “indirect benefit”, as well as the underlying assumptions. For instance, I might postulate that uninfected men are uninfected because they have demonstrated that they behave in such a way as to avoid infection; and therefore reducing their risk of infection would be entirely irrelevant to the population as a whole.

    I would also like Churchyard’s comment on the reports and data in RWANDA: CIRCUMCISE ALL MEN—EVEN IF IT MEANS MORE HIV INFECTION (3 February 2008), which throw considerable doubt on any benefit from circumcision.

    [[MacDonald had also sent me the link to the story that contains the Churchyard silliness (“Minister Breaks Bad News About Aids Prevention”, Business Day [Johannesburg], 8 February 2008; with the numbers on which Churchyard was commenting: “the annual HIV rate in the wives of the men who had been circumcised was 14,4% over two years, compared to 9,1% among the women whose husbands had not been circumcised”.]]

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