HIV/AIDS Skepticism

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

Posts Tagged ‘HIV disease’


Posted by Henry Bauer on 2008/03/19

This post is longer than I prefer, but I saw no good way to split it into parts. It explains that the way “HIV infections” and deaths from “HIV disease” vary with age and with race and over time constitutes a resounding disproof of HIV/AIDS theory.


A couple of years ago, I had come to the conclusion that the demographics of positive “HIV”-tests, data published largely by the Centers for Disease Control and Prevention (CDC), represent definitive proof that “HIV” is not an infection. Icing on that cake is the fact that “HIV” and “AIDS” are not correlated—again, in officially published statistics—, as became clear to me while writing The Origin, Persistence and Failings of HIV/AIDS Theory (see chapter 9). Now I’ve found that a more direct line of proof lies in comparing the data on deaths from “HIV disease”—as the CDC has come to call it—with data from “HIV” tests.

In earlier blogs, I had argued that “HIV disease” is not an illness, citing among other things Table A below (see WORLD AIDS DAY . . ., 22 December 2007; “HIV DISEASE”, 28 December 2007; HOW TO TEST THEORIES . . ., 7 January 2008).

TABLE A (click in table for full size)

There I had waffled about how the racial disparities and sex differences in “HIV” deaths parallel those found on “HIV” tests, and how strange it is that blacks and Hispanics are more susceptible to “catching” HIV and yet survive to later ages than do whites or Asians or Native Americans equally suffering from “HIV disease”, and how all this supports the hypothesis that testing “HIV”-positive is a non-specific indication of some sort of physiological stress. But I had failed to grasp the significance of the fact that the age distribution of deaths from “HIV disease” reaches a maximum in people in the prime years of life, mid-thirties to early forties. That is the very opposite of how people react to infectious diseases, where everyone is about equally at risk of infection, but the young and the old are most at risk of succumbing to the infection, from pneumonia, say, or influenza; so the variation with age of “HIV” deaths is the very opposite of how death rates from infectious diseases vary with age; and for the same reason, it’s the very opposite of how all-cause death rates vary with age (Table B).

TABLE B (click in table for full size)


Even death rates from chronic diseases—diabetes, say—or “diseases of old age”—heart and cardiovascular, say, or cancer—show the same trend, though the death rates at very young ages are much less prominent:

TABLE C (click in table for full size)


The all-cause death rates of people in their thirties or forties are comparatively low, between ¼ and ½ of the age-adjusted overall death-rate (Table B, 193.5 or 427 compared to 800.8). Nowhere have I found mention of an illness that is most life-threatening for people aged 35-44 or 45-54—except, of course, “HIV disease”.

One might quibble that the numbers in Table A are not rates for each of the given age-groups; but adjusting for the age distribution in the population makes little difference, as shown by the age distribution of reported death-rates from “HIV disease” (Table D, which is Table 42, p. 236, in “National Center for Health Statistics: Health, United States, 2007 with Chartbook on Trends in the Health of Americans”, Hyattsville, MD, 2007) : for males as for females and in every calendar year, the highest rate of death from “HIV disease” comes at ages 35-44 with the single exception of females in 1987 when it came at 25-34.

TABLE D (click in table for full size)


 * in table D means rates based on fewer than 20 deaths, considered unreliable

The failure of HIV/AIDS theory is demonstrated not only by this incongruous age-dependence of death rates. Note how constant over the years is the shape of this age distribution. While the magnitudes of the rates go up from 1987 to 1995 and then down, they do so in similar fashion in each age group. By contrast, HIV/AIDS theory would have predicted high death-rates at relatively early ages in 1987 and before, when there were no treatments for AIDS and victims were dying within months, or at most a year or two, after diagnosis; then—HIV/AIDS theory would have it—the highest death-rates would have moved steadily to older ages as treatments were introduced, and particularly after the supposedly revolutionary introduction of “life-saving” HAART in the mid-1990s and the development of continually better individual drugs. But there is no such trend; the actual data show no change at all, over the years, in the age range within which people are most at risk of dying of “HIV disease”. For two decades, the greatest risk of dying from “HIV disease” has been experienced by people between 35 and 44years of age.

Also to be noted is that from 1987 into the mid-1990s, every age-group saw a great increase in death rates. That was the era of AZT monotherapy, initially deploying doses so high that even the mainstream acknowledged their toxicity by cutting them back drastically. Discontinuation of monotherapy in favor of “cocktails” then allowed the death rates to fall back again; but, as mentioned above, there is no indication at all that years of survival were increased by introduction of HAART as monotherapy was phased out.

(After writing this I was struck by a sinking feeling that, like increasing arrays of HIV/AIDS numbers issued by the CDC, Table D might have been drawn from computer models, which would explain their astonishing regularity. Then I noticed the phrase in fine print just below the Table’s header, “Data are based on death certificates”, and I was reassured —at least provisionally.)


That “HIV”-positive” is not an illness is, of course, the reason that African Americans survive “HIV disease” to later ages than do white, Asian, and Native Americans (Table A), one of the points to which I had drawn attention earlier (7 January). Black people test “HIV”-positive more often than others under all circumstances and in both sexes and at all ages (The Origin, Persistence and Failings of HIV/AIDS Theory, Figures 13-17, pp. 53-6), so when they die they still test positive more often at every age, even to an appreciable extent at ages where others test positive so rarely as not to show up in the statistics (above 55 for men and above 45 for women, Table A).

These variations with age of death rates from “HIV disease” run exactly as would be expected on the hypothesis that testing “HIV”-positive is a non-specific response by the immune system to some sort of physiological stress and that, for a given challenge to health, the strength of that immune response varies according to the capacity of the individual’s immune system (The Origin, Persistence and Failings of HIV/AIDS Theory).

From the teens into the “golden years”, external health challenges do not (on average, overall) vary systematically with age, so on average the variation with age of the tendency to test “HIV”-positive reflects the capabilities of the immune system, which tend to be at their best in the middle years of life:



Health challenges are considerably higher, though, at very early ages, because newborns experience the stress of birth and because young children meet many health challenges for the first time as their immune systems are just learning to cope with them. So the graph rises to the left not because the immune system is fully capable, as in the middle years, but because the stresses and health challenges encountered in those years are exceptionally great.

But why should deaths from “HIV disease” parallel the tendency to test “HIV”-positive in the middle years if that tendency represents a capable immune-system response?

Because of the manner in which the CDC defines “HIV disease”.

After “HIV” had become accepted as the cause of “AIDS”, an increasing number of diseases were included by the CDC as “AIDS-defining” just because a significant number of people with those diseases were reported as testing “HIV”-positive. As Rebecca Culshaw noted, this led to the extraordinary situation that the death from any cause of a person known to be “HIV”-positive would be reported as a death from “HIV disease”—even when the immediate cause of death was heart attack, liver failure, CMV infection, or even suicide, a car accident, or drowning (“Science Sold Out”, 2007, p. 30, citing Massachusetts Department of Health, 2002). (There may be a financial incentive to do this: federal funds to “fight HIV/AIDS” are apportioned to states and cities according to the perceived relative impacts of HIV/AIDS.)

Now: illness and death are in and of themselves often associated with positive “HIV”-tests (after all, they represent extreme challenges to health). Hospital patients (admitted for reasons not connected with HIV/AIDS) test “HIV”-positive at between 0.1 and 7.6% (The Origin, Persistence and Failings of HIV/AIDS Theory, Table 3 p. 25; Table 23 p. 81); and moreover the tests vary with age as in the diagram above (ibid., Table 26 p. 98); emergency-room patients tested at 5-6% (ibid., pp. 48, 85); “HIV”-positive rates in autopsies were reported in one instance as between 1.9 and 3.7% and increasing in proportion to the degree of death-causing trauma, and in another instance at 18% with no indications of AIDS (ibid., p. 85). Since even accident and trauma victims tend to test “HIV”-positive, as well as people ill for a wide variety of other reasons, there is then a definite probability that anyone who is seriously ill will test “HIV”-positive, and so anyone who dies for any reason may well have tested “HIV”-positive while in hospital, or may well do so in autopsy, with a probability of a few percent or more; that’s much higher than the “normal” rate in the US population as a whole, which is an order of magnitude lower at a few per thousand or less.

The maximum death-rates from “HIV disease” in 2004 (Table D) were 10.9 (per 100,000) at ages 35-44 and 10.6 at ages 45-54. The all-cause death-rates for those age groups were (Table B) 194 and 427 respectively. Thus deaths from “HIV disease” represented respectively 5.5% (10.9/194) and 2.5% (10.6/427) of all deaths in those age groups, quite comparable to the frequency of positive “HIV”-tests among non-AIDS hospital patients and emergency-room patients and in autopsies. Thus deaths from “HIV disease” are merely that fraction of all deaths in which the non-specific “HIV”-positive reaction happened to turn up in response to the health challenge that had caused the death.

So death rates from “HIV disease” parallel the age variation of “HIV” tests simply because all deaths of “HIV”-positives are called deaths from “HIV disease”, and because “HIV” tests are so highly non-specific as to react to many life-threatening conditions. And that is also why the age variation of death rates ascribed to “HIV disease” is (for chronic diseases) unlike or (for infectious diseases) opposite to the variation with age of death rates from every other malady.

Figure 1 is schematic, not quantitative. I had mentioned in connection with its first appearance (ibid., p. 26) that the actual “middle” age of the peak appears to vary somewhat with sex and with race. To compare the actual years of that peak on “HIV” tests with the peak years of “HIV” deaths, I wanted “HIV”-test data for the population as a whole, since the death-data in Table A are also for the population as a whole. The most appropriate data-sets are those, totaling nearly 10,000,000 tests, published in 1995-8 by CDC for all public testing-sites (clinics for TB, HIV, STD, drugs, family planning, prenatal care, and more, as well as prisons and colleges and some reports from private medical practices). Pooling the actual numbers for each of those four years and making the appropriate calculations delivers the following results:

TABLE E (click in table for full size)


The highlighted cells and the “XXX” overlap or straddle in 12 of 13 cases; there is a good quantitative correspondence between the ages of maximum probability of testing “HIV”-positive and the ages of maximum rate of dying from “HIV disease”. But under HIV/AIDS theory, infection by HIV is supposed to be followed by a “latent period” of about 10 years: the peak ages for deaths from “HIV disease” should be a decade or more later than the peak ages for “HIV” infection, rather than overlapping in the same age-ranges. Furthermore, the difference between age of “infection” and age of death should have increased during the years—from the mid-1990s on—when “life-saving” antiretroviral treatments supposedly extended the life spans of “HIV”-positive people by a significant amount. Yet in 2002-4 (Tables A and D), the peak ages for “HIV” infection and for deaths from “HIV disease” are virtually the same as the ages where infections were most common in 1995-8, even though most people “infected” in 1995-98 should have survived well beyond 2005-8!

All this is inexplicable under HIV/AIDS theory, whereas it comports perfectly with the alternative theory that testing “HIV”-positive denotes physiological stress.

HIV/AIDS theory lacks substantive legs to stand on. “HIV” is not any cause of illness. Testing “HIV”-positive signals the presence of some sort of challenge to health. The tendency to test “HIV”-positive depends on what the health challenge is, and on how strongly an individual tends to respond.

Posted in HIV absurdities, HIV and race, HIV as stress, HIV does not cause AIDS, HIV tests, HIV varies with age, HIV/AIDS numbers | Tagged: , , , , , , | 5 Comments »


Posted by Henry Bauer on 2008/01/07

Here’s another puzzler for HIV/AIDS theory:

Why do blacks and Hispanics suffering from “HIV disease” live longer than Asians, Native Americans, or whites suffering from “HIV disease”?
— Among American women, between 2002 and 2004, all deaths from “HIV disease” among Asians, Native Americans, and whites occurred before age 45; but one third of black and Hispanic women with “HIV disease” lived past 45.
— Among American men, between 2002 and 2004, all deaths from “HIV disease” among Asians, Native Americans, and whites occurred before age 55; but more than 10% of black and Hispanic men with “HIV disease” lived past 55.

It’s generally believed that black and Hispanic Americans do not enjoy as high a level of medical care as do white Americans. So why do they stave off this disease better?

Could it be because they are not being treated with “life-saving” or “life-prolonging” antiretroviral drugs?

* * * * * *

A good theory can make predictions that turn out to be accurate, and it can explain new results as they come in.

HIV/AIDS theory fails on both counts.
— The first prediction was made already as the theory was being announced in 1984: a vaccine against the virus would likely be available within two or three years.
Not only is there no vaccine: scores of attempts have all failed, and we have yet to discover what physiological properties of a vaccine would protect against “HIV infection”.
— A second prediction was that AIDS would spread into the general population since its cause was a sexually transmitted agent.
There has been no spread into the general population. There has been no breaking out geographically either—Sub-Saharan Africa remains the only region with an HIV-positive rate ≥5%; the Caribbean remains the only other region with an HIV-positive rate ≥1%.

— New results, far from being explained by HIV/AIDS theory, have brought conundrum after conundrum: the epidemiology of “HIV” is unlike that of any other sexually transmitted agent, indeed of any infectious agent (The Origins, Persistence and Failings of HIV/AIDS Theory); married women are a high-risk group (TO AVOID HIV INFECTION, DON’T GET MARRIED, 18 November); more exposure results in less infection (MORE HIV, LESS INFECTION…, 21 November); “infection” rates from this incurable illness have declined dramatically without the inevitably required increase in deaths (NOTEWORTHY SUCCESSES AGAINST AIDS IN AFRICA, 4 December 2007); and more.

By contrast, an alternative theory—I’ll call it the “stress theory”—successfully predicts demographic characteristics of “HIV infection” and has remained able to explain new results as they come in.

The stress theory holds that testing HIV-positive is analogous to running a fever. The Perth Group has written copiously about the evidence that positive HIV-tests signify oxidative stress. My book shows that the epidemiology of “HIV” supports the similar, possibly identical view that testing HIV-positive is a rather non-specific physiological response to some sort of challenge or stress.

This evidence-based stress theory predicts that whenever HIV tests are carried out on some group of people matched for other variables, the rate of testing positive will increase from the teen years into middle age before declining again at higher ages. Below the teens, the rate of testing positive will increase with decreasing age, reaching a high among newborns. Males will always test positive more often than females, except in the lower teen years when the reverse is often observed.

The stress theory further predicts that among any group of people matched for other variables, the rate of testing positive will go in the sequence
Asian ≤ White ≤ Native American ≤ Hispanic ≤ Black

This theory has sufficed to explain every significant new result since the book was published.

Take the variation with age. That females test positive more often than males in the early teen years seems difficult to explain if testing positive means infection by a venereal disease whose chief carriers are gay and bisexual men: one would expect teenaged boys to be at greater risk than girls. On the other hand, this phenomenon fits the notion of physiological stress, since menarche (the onset of menstruation) is more physiologically stressful than what boys experience at puberty. At any rate, that female teens test positive more often than male teens was noted already in the mid-1980s among applicants for military service, in the Job Corps, and in a two-decade survey of military cohorts, all in the United States.

I was recently led to look at data from various African countries in quite another connection, and—lo and behold—came across the statement that in Zambia, “The HIV prevalence among girls 14-19 years old is six times that of boys in the same age group” (Summary Country Profile for HIV/AIDS Treatment Scale-Up, World Health Organization, 2005).

* * * * * *

Earlier, a ludicrously mistaken assertion by Sharon Stone (WORLD AIDS DAY…, 22 December 2007) had caused me to look up data about deaths from “HIV disease” in the United States. The following tables show some of the numbers I found. (The trends were the same for each individual year—2002, 2003, 2004—so I aggregated them to lessen the effect of stochastic (chance, random) variations in the smaller numbers. The reports are available at


For both males and females, the numbers vary with age as predicted by the stress theory, reaching a peak in middle age. The numbers for males are significantly higher than for females—except for that teenage phenomenon of females affected more than males: among the only groups where there were significant numbers of deaths among young teens—African Americans and Hispanics—the numbers for females are greater than those for males in the years 10-14 and 15-19.

And, too, the relative mortality rates vary with race precisely as predicted by the stress theory,
Asian ≤ White ≤ Native American ≤ Hispanic ≤ Black

Further: I mentioned in the book (especially p. 246 ff.) that black women seem particularly prone to test HIV-positive. The black-to-white ratio for “HIV” deaths among women, 24, is more than 3 times that for men, 7.4.

* * * * * *

The very fact that these numbers reflect deaths is in itself consonant with the stress theory. Hospital patients and trauma victims test positive at relatively high rates, higher the more critically ill they are (pp. 84-5 in The Origins, Persistence and Failings of HIV/AIDS Theory) . Therefore, among people who die from any one of a number of possible causes, one expects a certain proportion to test HIV-positive. The Centers for Disease Control and Prevention ascribes deaths to “HIV disease” whenever the person was HIV-positive, no matter what the real cause of death was, the manifest cause: cervical cancer, tuberculosis, unexplained weight loss, or just about anything else. So one would expect deaths from “HIV disease” to show the same demographic characteristics as “HIV infection” among living people, and the mortality statistics bear that out.

* * * * * *

It would be interesting to hear from defenders of HIV/AIDS theory their explanation for the age and racial distribution of these deaths on the basis of a supposedly sexually transmitted disease which, untreated, is supposed to bring death within a dozen or so years after infection: How is it that black and Hispanic females manage to survive to age 45-54 before succumbing to this disease whereas Asians, Native Americans, and whites don’t get beyond 44? How is it that black and Hispanic males manage to survive to age 55-64 before succumbing to this disease whereas Asians, Native Americans, and whites don’t get beyond 54?

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Posted by Henry Bauer on 2007/12/28

Sharon Stone’s assertion that AIDS is “the fourth leading killer of women in America” (WORLD AIDS DAY…, 22 December) led me to discover that official death statistics now contain the category “HIV disease”.

Perhaps this is a natural progression from the belief that HIV causes AIDS; but it muddies the waters even further by declaring “HIV” to be something that causes harm without specifying what that harm is.

The trouble is that testing HIV-positive can result from a large number of conditions; and the Centers for Disease Control and Prevention has kept expanding the list of “AIDS-defining” diseases, to include just about any medical condition if an appreciable number of people suffering from it have tested HIV-positive. Thus cervical cancer became an AIDS-defining illness in 1993, even though that is said to be caused by human papillomavirus, not by HIV, and even though the incidence of cervical cancer has been decreasing throughout the AIDS era; and tuberculosis now comes in two forms, identical in clinical diagnosis and symptoms and differing solely in “HIV” status—one is tuberculosis, the other is “HIV disease” or “AIDS”.

AIDS, as described and named in the early 1980s, bears little if any relationship to what the Centers for Disease Control and Prevention (CDC) now call “HIV disease”. Historians and sociologists of medical science will find it fascinating as well as onerous to untangle how the former was transformed into the latter.

In the 1980s, all people suffering from AIDS were manifestly and seriously ill, expected to die within a matter of months after being diagnosed. By 1997 (the latest year in which the CDC reports detailed this information), more than half of the people “living with AIDS” (PWAs) were not even ill. Out of a cumulative total of 315,000 PWAs, 180,000 had been diagnosed as having AIDS purely on the basis of laboratory tests, amounts of CD4+ cells, even if they evidenced no symptoms of illness; they were “persons reported with immunosuppression as their only AIDS-indicator condition” (CDC Surveillance Report for 1997, p. 18).

“These persons may also have other AIDS-indicator conditions that are unreported”, the document continues. That may of course be so, but in absence of reporting one has to assume that there was nothing to report. Beyond that, the remark illustrates the lack of relevant information that is a major hindrance to understanding what is really going on in “HIV/AIDS”.

For example (WORLD AIDS DAY…, 22 December), official death statistics have it that about 2% of deaths in 2004 among black females aged between 10 and 14 were from “HIV disease”–which means they were HIV-positive when they died, but they might also have had flu, pneumonia, malaria, tuberculosis, or any of the host of other conditions known to be capable of causing a positive HIV-test. Without knowing from what immediate, manifest sickness those young black female teenagers died, it is hardly possible to judge the validity of labeling those deaths as “HIV disease”.

When were these unfortunate teens first found to be HIV-positive? If it was only at death, perhaps it was death that caused the positive HIV-test, for fatal trauma seems to be associated with a high probability of testing HIV-positive (see references cited at p. 85 in The Origins, Persistence and Failings of HIV/AIDS Theory).

If it was at birth, were the children treated with antiretroviral drugs, whose “side” effects could well have resulted in death a decade or so later?

If the children had not been born HIV-positive, how and when did they become “infected”?

These questions are pressing if only because it is only black and Hispanic teenagers who are reported to be so at risk in those early teen years: not Native American, Asian, or white teens (from CDC National Vital Statistics Reports, 56 #5, 20 November 2007):


Under HIV/AIDS and “HIV disease” theory, one has to accept that these young teens were HIV-positive because of sexual intercourse or needle-sharing, or had been infected by their mothers. Must we accept that African-American and Hispanic communities have so much higher an incidence of child molestation or children using dirty needles to inject drugs than do Native American, Asian or white American communities? Or that African-American and Hispanic men infect their female partners with HIV so much more often than do Native American, Asian, or white men?

Rhetorical as those last questions may be, the earlier ones illustrate the genuine need for specific information that is presently hidden under the umbrella of “HIV disease”.

* * * * * *

Up to 1987, the Centers for Disease Control and Prevention had reported 29,000 cases of AIDS and 16,300 deaths: for both cases and deaths, 65% from Pneumocystis carinii pneumonia (PCP), 20-25% from other opportunistic infections, and 10-15% from Kaposi’s sarcoma (KS). In 1997, 61% of the 60,000 people with “AIDS-indicator conditions” may not have been ill at all, they had no reported symptoms of opportunistic infections, having been diagnosed on the basis of lab tests. PCP accounted for only 15% of “AIDS” cases in 1997 instead of 65% a decade earlier, and KS accounted for only 2.5% instead of 10-15%.

By what sleight of evidence did “AIDS” of the early 1980s become “HIV disease” of the late 1990s?

In 1987, the Centers for Disease Control and Prevention expanded the criteria for an AIDS diagnosis to include “HIV wasting syndrome” and “HIV encephalopathy”. Those terms imply that HIV had been found to cause a particular type of wasting and a particular type of brain disease, but that’s not the case; the terms simply mean that some people with those two conditions had tested HIV-positive. But as already noted above, dozens of conditions are known to be associated with testing HIV-positive—autoimmune diseases, herpes, pregnancy, malaria, flu and vaccination against it or against hepatitis or against tetanus. The Centers for Disease Control and Prevention, supposedly the nation’s prime resource for epidemiology, persistently makes the elementary mistake of taking correlations as indicating causation (see, for instance, p. 194 in The Origins, Persistence and Failings of HIV/AIDS Theory). Instead of recognizing that any number of circumstances that disturb the immune system can simulate a positive HIV-test, CDC kept expanding what it called “AIDS-defining” conditions without proof that HIV is the cause of those conditions.

“HIV wasting syndrome” is not even clearly defined. For example, “Involuntary weight loss of greater than 10 percent associated with intermittent or constant fever and chronic diarrhoea or fatigue for more than 30 days in the absence of a defined cause other than HIV infection. A constant feature is major muscle wasting with scattered myofibre degeneration. A variety of aetiologies, which vary among patients, contributes to this syndrome.” That last sentence reveals that the actual causes—note the plural “aetiologies”—vary among those who suffer from the wasting, in other words, the common factor of “HIV” is not the cause, even though the term “HIV wasting syndrome” implies that it is.

Or consider the “fact sheet” at “AIDS wasting is not well understood”, and several factors can contribute, such as “low food intake”, “poor nutrient absorption”, “altered metabolism”. Perhaps all those can indeed be caused by a retrovirus, but there are any number of other possible causes as well, which would be invoked readily enough in people who are not HIV-positive.

Or look at what Gay Health News has to say: “symptoms of wasting include weight loss, loss of fat and muscle mass (particularly on the sides of your head), diarrhea, fever, malnutrition, depression, poor appetite and weakness”. Surely no one would suggest that those can be directly caused by a retrovirus!

But the National Institute of Allergy and Infectious Diseases asserts that it can: “HIV wasting syndrome [is] . . . defined as unintended and progressive weight loss often accompanied by weakness, fever, nutritional deficiencies and diarrhea. . . . Wasting can occur as a result of HIV infection itself [emphasis added] but also is commonly associated with HIV-related opportunistic infections and cancers”. What this really means is that when HIV-positive people in high-risk groups lose weight, “HIV” is taken to be the reason for the weight loss. How that might come about is no better understood, however, than how “HIV” is supposed to kill immune-system cells.

* * * * * *

Assertions about HIV/AIDS and “HIV disease” are based on a variety of assumptions grounded in the belief that HIV is the sexually transmitted cause of AIDS. That belief has survived the facts that “HIV” has never been isolated from an “infected” person; that a significant number of HIV-positive people never become ill; that a significant number of AIDS patients are HIV-negative; that “HIV” and AIDS are not correlated chronologically, geographically, or in their relative impact on different groups of people; that laboratory tests for viral load and CD4 cells do not correlate with one another and that neither correlates with the patient’s health; and more.

Belief in HIV/AIDS theory also entails acceptance of a variety of implausible things, such as that married women are at the highest risk of infection for a venereal disease (TO AVOID HIV INFECTION, DON’T GET MARRIED, 18 November); that babies are less likely to become infected, the more infected mothers’ milk they imbibe (MORE HIV, LESS INFECTION: THE BREASTFEEDING CONUNDRUM, 21 November); that a venereal disease has remained voluntarily quarantined in the same geographic and social boundaries for more than two decades; that this venereal disease displays demographic regularities not shown by any other venereal disease; that this “virus” mutates more rapidly than any other, yet all mutants remain equally cunning and equally deadly—though some portions of the virus remain sufficiently not-mutated as to allow its ancestry to be traced decades into the past.

Not to mention that this virus kills by means of a quite novel mechanism, a so-called “bystander” mechanism (Rowland-Jones & Dong, Nature Medicine, 13: 1413-5): it is supposed to incite certain unknown others to do the killing via certain unknown signals.

“Bystander”, perhaps. But a better term might be “Abracadabra!” or “Open sesame!” mechanism, since the phenomenon reeks of magic; or perhaps it is a psychic phenomenon akin to extrasensory perception or psychokinesis, where a physical effect is brought about by non-physical means.

Posted in HIV and race, HIV does not cause AIDS, HIV in children, HIV risk groups, HIV tests, HIV transmission, HIV/AIDS numbers, sexual transmission | Tagged: , , , , , , , | 1 Comment »