HIV/AIDS Skepticism

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

Archive for February, 2008


Posted by Henry Bauer on 2008/02/13

In science, hypotheses get modified as data accumulates. In HIV/AIDS research, the basic dogmas are not modified as actual data falsify them. “HIV” continues to be pronounced a sexually transmitted virus even as a great deal of evidence from epidemiology and from clinical practice says that it isn’t (WHAT “HIV” IS NOT: IT’S NOT SEXUALLY TRANSMITTED, 6 January 2008). Condom use is urged in face of the evidence that they make no difference (or are even associated with a HIGHER rate of HIV-positive—see CONDOMS AND HIV: WHAT EVERYONE KNOWS IS ONCE AGAIN WRONG, 10 February 2008 ).

Breastfeeding is associated with less “transmission of HIV” than not breastfeeding (MORE HIV, LESS INFECTION: THE BREASTFEEDING CONUNDRUM, 21 November 2007). Nevirapine and AZT are known to produce irreversible, lifelong mitochondrial damage to babies exposed to them (FIRST: DO NO HARM!, 19 December 2007). And still there are further “studies” carried on to see whether those toxic drugs can prevent “HIV infection” supposedly incurred through breastfeeding:

“Longer drug regimen found to help babies avoid H.I.V.”, by Lawrence K. Altman, New York Times 5 February 2008

“Over recent years, giving an antiretroviral drug to a woman infected with the AIDS virus in labor and to her baby at birth has reduced the risk of transmitting the virus to the baby. Yet many babies born uninfected go on to acquire H.I.V. . . in the lengthy period of breast feeding because of contamination of the mother’s milk. Now researchers have found for the first time that the incidence of the virus among breast-fed infants can be significantly reduced by extending antiretroviral drugs for much longer periods, up to six months. . . . Breast feeding accounts for up to 48 percent of H.I.V. infections among infants in developing countries . . . . Centers for Disease Control and Prevention . . . paid for three of the five breast-feeding studies reported at the 15th Conference on Retroviruses and Opportunistic Infections . . . . Additional studies will be needed to determine the cost effectiveness of longer-term therapy. . . . ‘The next series of studies will need to determine the optimal time for treating mothers and infants,’ said Dr. Fauci, whose agency paid for the fifth breast-feeding study. The studies reported here evaluated regimens and the potential of drug resistance among mothers and babies in India and African countries. In a study in the Kisumu area of Kenya, along Lake Victoria, infected mothers took a combination of antiretrovirals from the 34th week of pregnancy and for the first six months of breast feeding their children. The newborns were given the standard single dose of nevirapine to prevent H.I.V. infection that might have occurred in delivery. Of 497 newborns, 12, or 2.4 percent, were infected by the end of the first week of life, from infection in the womb or at birth. An additional 15 infants, or 3 percent, became infected 8 days to 12 months from breast feeding. In a study in Blantyre, Malawi, more than 3,000 infants received one of three regimens of antiretrovirals for the first 14 weeks of life. After nine months of observation, the group that received nevirapine for 14 weeks had the lowest percent of infected infants, 3.1 percent. That compared with 10 percent among the control group, which received one dose of nevirapine and one week of another antiretroviral, AZT. Another part of the Kisumu study showed that most of the infants infected in the first six months of life showed laboratory evidence of genetic resistance to the antiretroviral drugs in the study. But the authors cautioned that the finding did not mean that the drugs would necessarily fail in treating the infants.”


All the earlier studies that showed breastfeeding in developing countries to be beneficial are simply ignored.

All the studies showing the harm to babies from nevirapine and AZT are ignored. The decrease in “infections” was reported, but how did the babies fare in terms of overall health?

Additional studies are always needed. The number of HIV/AIDS researchers is vast, and they need grants.

Such studies are carried out most readily in Africa. One reason is that ethical requirements for clinical trials include that all those who enroll must be offered no less than the usual standard of care. That requirement is most readily met in Africa, where the usual standard of care in many places is no care at all. That’s why it’s possible in Africa to study whether it’s worth feeding malnourished people (DRUGS OR FOOD?, 25 December 2007) and whether it’s worth de-worming children (ARE INTESTINAL WORMS GOOD FOR US? ARE THEY GOOD FOR AFRICANS? FOR AFRICAN CHILDREN?, 30 December 2007) by contrast to treating them with antiretroviral drugs whose costs exceed those of food and of de-worming medications by orders of magnitude.

Words fail me at this stage. The “drugs or food” issue had even been raised in a couple of editorials in the New York Times without bringing any warranted chorus of outrage.

Posted in antiretroviral drugs, clinical trials, HIV in children, HIV transmission | Tagged: | 4 Comments »


Posted by Henry Bauer on 2008/02/10

It’s a universally believed shibboleth that using condoms cuts the risk of becoming HIV-positive. For example, a recent exchange in the British Medical Journal (BMJ, 26 January 2008, 336: 184-5) was quoted to the effect that “Consistent condom use can reduce the spread of HIV” (ScienceDaily [Jan. 25, 2008]). That exchange, as well as an earlier editorial in the BMJ (24 July 2004, 329: 185-6), cite for this a workshop held by the National Institute of Allergy and Infectious Diseases in June 2000.

The actual findings are less than unambiguous. According to the Executive Summary in the workshop report: “The published data documenting effectiveness of the male condom were strongest for HIV. The Panel concluded that, based on a meta-analysis of published studies ‘always’ users of the male condom significantly reduced the risk of HIV infection in men and women. These data provided strong evidence for the effectiveness of condoms in preventing HIV transmission in both men and women who engage in vaginal intercourse.”

This is notably less than a definitive claim: “strong evidence” is not the same as “proof”. The report itself acknowledges that nothing new is being revealed: “HIV infection is the only STD for which formal meta-analyses have been published . . . . The most recent analysis by Davis and Weller . . . was evaluated.”

The latter, a meta-analysis (quantitative assessment) of a dozen studies had concluded, “Among those who reported never using condoms, the summary estimate of HIV/AIDS incidence from the seven studies was 6.7 seroconversions per 100 person years”. Now: if there are 67 acts of intercourse per year, that corresponds to a transmission rate of a mere 1 per 1000 unprotected acts; at more than 67 acts per year, it corresponds to an even lower rate of apparent transmission. As often pointed out, such rates are far too low to bring about an epidemic (see, for instance, James Chin, “The AIDS Pandemic”; or Chakraborty et al., AIDS 15 [2001] 621-6).

One can accept without qualms the results of studies that find apparent transmission of HIV not to exceed a few parts per thousand, for higher rates would be more readily observed. But one could well have qualms about how accurately one could specify such very low apparent rates. Consider how many people must be observed over how long a period of time in order to make such a measurement reliably. If you study 100 discordant couples (one HIV-positive, the other not) for a year, you might observe a few seroconversions on average, but owing to the usual chance variations, to get a quantitatively meaningful rate one would need to observe many hundreds of discordant couples. That this is far from easily done is illustrated by the most cited such study (Padian et al., American Journal of Epidemiology, 146 [1997] 350-7), which managed to enroll fewer than 450 such couples over a ten-year period.

For a good measurement of yet lower rates than a few per thousand, even larger numbers of discordant couples would have to be enrolled; which makes one wonder how meaningful could be the finding of the meta-analysis that always using condoms reduced the rate to 0.9 seroconversions per 100 person years, in other words a few per 10,000. Nevertheless, these numbers have been cited to claim that condom use can reduce transmission of HIV by 85%.

On the other hand, several studies have not supported the claim that condom use decreases apparent transmission of the “HIV-positive” condition at all (see pp. 44, 109, 115 in The Origins, Persistence and Failings of HIV/AIDS Theory).

To those earlier-cited data one can now add remarkably detailed official figures from Rwanda’s Demographic and Health Survey (2005 edition, published July 2006).


The suggested reason for this overwhelming contradiction of the conventional wisdom seems a little thin: “It is difficult to establish the exact relationship between condom use and HIV. Condoms could be used by those who are HIV negative to protect themselves from the disease, but they could also be used by those who are seropositive to protect their partners” (p. 236); in other words, it’s being suggested that those who are already HIV-positive might be more likely to use condoms.

One might also speculate that condom use could be more frequent among those who have sex often or with many partners, and whose greater consequent risk is not balanced by the protective effect of the condoms. But there seems to be no correlation between rate of testing HIV-positive and sexual behavior, for example, “Paradoxically, it is not only women who have engaged in higher-risk sex, but also those who had no intercourse in the past 12 months that prevalence rates are the highest (8.2 percent and 8.9 percent, respectively)” (p. 235). While HIV-positive rates are reported to rise somewhat with numbers of sexual partners, on the other hand for men who reported no sex in the past 12 months the HIV-positive rate was 2.9%; for those who had higher-risk sex in the last 12 months, it was a bit less, 2.7%; and for those who had had lower-risk sex, it was highest at 3.5%. In other words, the apparent relationship between sexual behavior and HIV-positive rate is so inconsistent or even itself paradoxical as to exclude this as a plausible explanation for the comparative figures in the tables shown above.

The facts seem quite clear. There is no indication that use of condoms decreases the risk of becoming HIV-positive. What’s more, there is no correlation between becoming HIV-positive and having sex, not having sex, or having high-risk sex.

Here is yet another piece of evidence, from official data, that HIV tests do not track a sexually transmitted condition.

(Nothing here suggests, of course, that one shouldn’t use condoms. They offer some protection—though far from certain—against a number of actual STDs like syphilis or gonorrhea; and they are a fairly effective—though by no means certain—means of contraception.)

Posted in HIV absurdities, HIV risk groups, HIV/AIDS numbers, sexual transmission | Tagged: , , , | 5 Comments »


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”.

Posted in antiretroviral drugs, clinical trials, experts, HIV absurdities, HIV and race, HIV risk groups, HIV transmission, HIV/AIDS numbers, sexual transmission, vaccines | Tagged: , | 2 Comments »


Posted by Henry Bauer on 2008/02/07

The COMMENT by G. listed as “Re COMMENTS” gives a link that is simply too delicious to leave in such obscurity. Here’s the story:

Pre-Chewed Food Gave HIV to Kids
ATLANTA (Feb. 6) – For the first time, health officials report that the AIDS virus can be spread by a mother pre-chewing her infant’s food, a practice mainly seen in poor, developing countries.

Three such cases were reported in the United States from 1993-2004 . . . .

It’s blood, not saliva, that carried the virus because in at least two of the cases the infected mothers had bleeding gums or mouth sores . . . .

CDC officials say more study is needed. But they are asking parents and caregivers with HIV not to pre-chew infants’ food, and are trying to educate doctors about this kind of transmission.

Health officials believe chewed-food transmission is rare in the United States, where such behavior is considered unusual. In some countries, mothers do it because they have no access to baby food or a means of pulverizing food for toothless infants.

“But even one case is too many,” . . . The first involved a 15-month-old African-American boy in Miami, diagnosed in 1993. His great-aunt was infected with HIV and pre-chewed food for the boy when he was between the ages of 9 months and 14 months.

Then a 3-year-old Caribbean-American boy was diagnosed in 1995, also in Miami. His HIV-infected mother pre-chewed food for her son.

Still uncertain they had definitively connected the practice to the spread of HIV, the doctors wanted more evidence. It was years later before they could confirm a third case, which occurred in 2004. A 9-month-old African-American girl was diagnosed with HIV in Memphis. The mother began pre-chewing the girl’s food when she was about four months old.

All three children were infected with HIV at a time they would have been teething and had inflamed gums. It may be that both a caregiver and a child must have wounds in their mouths for the virus to have a good chance of passing from one bloodstream to another, the investigators said.

Previous studies have linked pre-chewing to the spread of other infections including Helicobacter pylori, a bacteria that causes stomach ailments, and streptococcal pharyngitis, which triggers sore throat. That research, too, is preliminary and needs to be confirmed . . . .

In developing nations without other feeding options, any campaign against pre-chewing could be nutritionally harmful . . . . “This would really take a lot of thinking before you could say, ‘We’ve had three cases in 11 years, so you have to stop pre-chewing your child’s food,”‘ Hagen said.

Posted in HIV absurdities, HIV in children, HIV transmission | Tagged: , , , | Leave a Comment »


Posted by Henry Bauer on 2008/02/07

Statistics may seem to be plain information, but often they are issued in order to send messages. So the choice of numbers is naturally determined by what the desired message is.

Want to show that the HIV/AIDS epidemic is even worse than we thought?

“AIDS advocacy groups say the new figures [to be released by the Centers for Disease Control and Prevention] will put the number of Americans infected with the AIDS virus each year close to 50 percent higher than previous estimates, at 55,000 instead of 40,000”
[WASHINGTON (Reuters) “Under 1 percent of U.S. adults have HIV: report”, by Maggie Fox; 29 January 2008]

Want to show that the epidemic is not as bad as we thought?

“The CDC has estimated in the past that more than 1 million Americans in total are infected with the human immunodeficiency virus that causes AIDS.”
“In 1999 to 2006, the prevalence of HIV infection among adults aged 18-49 years in the civilian noninstitutionalized household population of the United States was 0.47 percent . . . . [which means] anywhere between 447,000 people and 841,000 people, with 618,000 the middle number. . . . . [according to] the National Center for Health Statistics . . . . The agency’s snapshot of HIV infection in the United States shows the rate continues to be stable. . . . The report covers adults aged 18 to 49 and only people living in households — not prisoners, the homeless or patients in institutions” [emphases added]

Want to show that there’s still ample cause for concern, even though the HIV/AIDS epidemic is not as bad as we thought?

Even if overall the numbers are stable—“We can say the prevalence is basically stable in this U.S., household-based population”—, it’s always possible to pick out sectors where there are grounds for grave concern:

“We do see the disparities by race/ethnicity . . . confirms other surveys that show black men are far more likely than other Americans to be infected. . . . Black men aged 40 to 49 had the highest rate of infection, at close to 4 percent” [emphasis added].
Also, “2% of non-Hispanic blacks were HIV-positive, compared with 0.23% of whites and 0.3% of Mexican-Americans” (Kaiser Health Disparities Report: A Weekly Look At Race, Ethnicity And Health, 31 January 2008).


Want to show that we must leave these important matters to the experts, because lay people can’t handle such complicated calculations?

Just try to put all the official numbers about HIV/AIDS together. The result will be great respect for the experts’ ability to remain unruffled in the face of blatant contradictions. For instance, the number of new infections is worse than we thought, more like 55,000 annually. Therefore the total number living with HIV/AIDS should have been rising at 55,000 per year. Yet we‘ve just had official assurance that the rate of HIV among Americans has been stable for something like a decade. What’s been happening to those 55,000 new cases annually?

A natural thought is that there have been 55,000 deaths from HIV disease per year. But if you look at the official statistics, you get the following (for 2004, from National Vital Statistics Report, 56 #5, 20 November 2007):

Deaths from HIV disease: 5608 white Americans, 7271 black, 84 Native American, 100 Asian Americans; the total of which is 13,063. (By the way: “HIV disease was also briefly among the top five killers for the black population during the 1990s” [emphasis added]).

Or by ethnicity: 1758 Hispanic deaths, 11,195 non-Hispanics: total is 12,953. (Again: “HIV disease was one of the top five causes of death for the Hispanic population in the mid-1990s but quickly dropped out of this group”.)

[13,063 minus 12,953 equals 110 people who are neither Hispanic nor non-Hispanic, apparently, but who died anyway.
The report does note, in very fine print, that reporting of ethnicity and race can be somewhat inconsistent, but annoying little inconsistencies like 110 apparently missing people could all be avoided if these reports didn’t claim more accuracy for the numbers than they deserve. Since uncertainties exist in the reporting of ethnicity and race, how about not giving numbers to 5 significant figures and just publishing “13,000”? That would be more honest as well as less annoying. Perhaps statisticians employed by federal agencies could take a short course in the use of “significant figures”—see MATHEMATICAL AND STATISTICAL LIES ABOUT HIV/AIDS, 2 December 2007.]

Anyway: About 13,000 a year die from HIV disease. About 55,000 newly contract it each year. Therefore the total number living with HIV/AIDS should be rising at the rate of about 42,000 per year. Yet the total number of Americans living with HIV/AIDS has remained stable since the mid-1980s, at about 1 million (references cited in the Preface, pp. 1-2, of The Origins, Persistence and Failings of HIV/AIDS Theory)—or maybe less, if you use numbers from the National Household Survey, above, rather than from the Centers for Disease Control and Prevention.

Perhaps, then, those 42,000 disappearing mysteriously each year represent people who eventually revert to HIV-negative after once having tested HIV-positive?
But of course the orthodox view is that seroreversion is exceedingly rare.
On the other hand, the evidence is that seroreversion is far from rare—see HIV “INFECTION” DISAPPEARS SPONTANEOUSLY, 22 January 2008).


With deaths from AIDS or “HIV disease”, you can also pick just about any number:

The Centers for Disease Control and Prevention likes to be on the safe side with its estimates. Where the National Vital Statistics Report (above) states 13,063 or 12,953 reported HIV/AIDS deaths for 2004, the Centers for Disease Control and Prevention estimates 18,099 for the same year (HIV/AIDS Surveillance Report, volume 17, revised June 2007).

Leave aside this discrepancy between 13,000 and 18,000 and consider only the methodology for a moment. It indicates that I should moderate my criticism, above, about reporting 13,063 and 12,953 when all that’s relatively reliably known is “about 13,000”. I had been tempted to repeat it concerning the estimate of 18,099 which should obviously have been given instead as “about 18,000”. But then it occurred to me that these estimates originate in computer programs, whose capabilities stretch to a much larger number of digits than a mere 5. Quite likely the computer spat out not 18,099 but something like 18,098.783. Instead of criticizing the resident experts, I should congratulate them for rounding up the estimate to the nearest person.

Posted in experts, HIV absurdities, HIV/AIDS numbers | Tagged: , , , | 1 Comment »