HIV/AIDS Skepticism

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

Archive for the ‘HIV as stress’ Category

HAART makes things worse: Elsevier journal publishes HIV/AIDS heresies

Posted by Henry Bauer on 2010/11/03

Tony Lance alerted me to a discussion on Questioning AIDS started by trueverax with links to some fascinating recent articles about “HIV” and oxidative stress, for example, Gil et al., “Altered oxidative stress indexes related to disease progression marker in human immunodeficiency virus infected patients with antiretroviral therapy”, Biomedicine & Pharmacotherapy (2010), doi:10.1016/j.biopha.2010.09.009; the journal is published by Elsevier Masson France.
This in-press article in an Elsevier journal seems no less heretical than those Elsevier withdrew a year ago from Medical Hypotheses after protests from HIV/AIDS vigilantes. As Tony had remarked, “The opening line probably caused the Perth Group to chuckle — or sob”. Indeed:

“It is generally accepted that oxidative stress (OS) is implicated
in immunological and metabolic abnormalities during HIV infection”

Beginning in the 1980s, the Perth Group has argued:
“That AIDS and all the phenomena inferred as ‘HIV’ are induced by changes in cellular redox brought about by the oxidative nature of substances and exposures common to all the AIDS risk groups and to the cells used in the ‘culture’ and ‘isolation’ of ‘HIV’”.
For example,
“There is no compelling reason for preferring the viral hypothesis of AIDS to one based on the activity of oxidising agents” — Eleni Papadopulos-Eleopulos, “Reappraisal of AIDS: Is the oxidation induced by the risk factors the primary cause?”, Medical Hypotheses 25 (1988)151-162.

The remarkable statement in the Abstract of Gil et al’s article, that the presence of oxidative stress in “HIV/AIDS” is “generally accepted”, is repeated in the text in this way:
“The redox balance is also severely disturbed in HIV infected individuals without HAART [7–13].” Those references are:
[7] Israel et al., Cellular and Molecular Life Sciences, 53 (1997) 864-70.
[8] Romero-Avila et al., Medical Hypotheses, 51 (1998) 169-73.
[9] Sönnerborg et al., Scandinavian Journal of Infectious Diseases, 20 (1988) 287-90.
[10] Favier et al., Chemico-biological Interactions, 91 (1994) 165-80.
[11] Allard et al., American Journal of Clinical Nutrition, 67 (1998) 143-7.
[12] Gil et al., Pharmacological Research, 47 (2003) 217-24.
[13] Pasupathi et al., Journal of Scientific Research, 1 (2009) 370-80.

I noticed that these seven articles, as well as the one in Biomedicine & Pharmacotherapy, are all in journals that do not specialize in HIV/AIDS. Yet the substance of these articles concerns HIV/AIDS more directly than it does anything else. Here’s a little research project for someone who has some time: Ask the authors of these articles whether they had tried to publish in a journal like JAIDS; and if not, why not?

Here’s another interesting fact about these articles: All the work was done outside the United States. Gil et al. worked in Cuba; Israel et al. in France; Romero-Alvira in Spain; Sönnerborg et al. in Sweden; Favier et al. in France; Allard et al. in Canada; Gil et al., 2003, in Cuba but with a co-worker in Italy; Pasupathi et al. in India.
It may not seem surprising, therefore, that none of these articles acknowledge research support from an American source. That is, it may not seem surprising to people not familiar with the fact that the National Institutes of Health (as well as a number of American foundations) do support considerable amounts of research outside the United States. Perhaps especially about HIV/AIDS; much research on HIV/AIDS in Africa, for example, is supported by American money.
But then again, it’s certainly no surprise that the National Institutes of Health would not support research on the role of oxidative stress in the conditions that are labeled “HIV-positive” or “AIDS”.

The discussion on Questioning AIDS also cites another study, from Africa, that reports correlation of “HIV-positive” status with lowered antioxidant activity: Bilbis et al., Annals of African Medicine, 9(#4) (2010) 235-9; not an AIDS-specialist journal, no research support acknowledged.

Now Gil et al. do not state outright that oxidative stress might be the cause of “HIV-positive” or of “AIDS”, they only point out that oxidative stress is present in those conditions. However, given that “HIV” virions have never been isolated from “HIV-positive” individuals, it is no great step from these findings to the stance taken by the Perth Group for more than two decades.
None of these articles cite the Perth work, of course. Even Romero-Alvira, who published in Medical Hypotheses in 1998, does not cite the 1988 Papadopulos-Eleopulos article in Medical Hypotheses.

*                    *                    *                    *                    *                    *                    *                    *

But the greatest heresy of Gil et al. (2010) lies not in pointing out the role of oxidative stress in HIV/AIDS: It is the finding, in a placebo-controlled trial, that HAART makes things worse.
A variety of measures of oxidative stress were used. Three groups of “HIV-positive” individuals were studied: One not subjected to antiretroviral drugs; one treated with AZT/3TC/ IND (zidovudine or Retrovir, a NRTI; lamivudine, a NRTI; indinavir, a protease inhibitor); one treated with D4T/3TC/ NEV (stavudine, Zerit, a NRTI; lamivudine, a NRTI; nevirapine or Viramune, a NNRTI):
“both combination . . . produced an increase in OS [oxidative stress] indexes paralleled to HIV progression marker change”; in the second (D4T) group to the extent that there was “a poor prognostic” under this treatment.
References are cited for the toxicity of HAART, including typical damage to mitochondrial function. The mitochondria are the energy-producing sites of all animal cells and play a significant role in the redox systems within all cells.
Perhaps most significant, it is pointed out that the surrogate markers typically used to assess the success of HAART, CD4 counts and viral load, did show “improvement” under HAART in these studies at the same time as oxidative stress increased:

increasing OS . . . occurs . . .
during apparently successful  HAART.
This  . . .  underline[s] HAART associated toxicity

[emphasis added].

This work serves to explain quite a few things about “HIV/AIDS” and HAART, for example that neither CD4 counts nor viral load is a good predictor of clinical outcomes (Rodriguez et al., JAMA, 296 (2006) 1498-1506).

Another reference cited in this thread on Questioning AIDS confirms the finding of increased oxidative stress as a result of HAART:

“HAART may affect oxidative stress in HIV-1-infected patients
. . . antiretroviral therapy plays an important role
in the synergy of HIV infection and oxidative stress”

(PMID: 19884983, Mandas et al., Journal of Biomedicine & Biotechnology, 2009;2009:749575. Epub 2009 Oct 26 — again, not an AIDS-specialist journal; work done in Italy).

Posted in antiretroviral drugs, clinical trials, experts, HIV as stress, HIV does not cause AIDS, HIV skepticism | Tagged: | 4 Comments »

Human Endogenous Retroviruses can resolve HIV/AIDS puzzles

Posted by Henry Bauer on 2010/09/02

Not much if anything was known about human endogenous retroviruses (HERVs) at the beginning of the AIDS era. By now, a great deal has been found out, and some of it is directly relevant to various conundrums and controversies about HIV. In my opinion, a recognition of the existence and characteristics of HERVs offers the possibility of resolving differing views among AIDS Rethinkers, as to whether HIV exists or whether it exists but is harmless.
Etienne de Harven has been drawing attention for some time to the importance of HERVs in relation to HIV/AIDS, and his views are now readily available in convenient form in a recently published review, described today in this press release:

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Association of American Physicians and Surgeons
1601 N. Tucson Blvd. Suite 9
Tucson, AZ 85716
(800) 635-1196
http://www.aapsonline.org

September 2, 2010
For Immediate Release

Are HERVs an Answer to AIDS Mysteries?

Contact: Etienne de Harven, M.D., by email: pitou.deharven@orange.fr, or Jane M. Orient, M.D.: (520) 323-3110.

Tucson, Ariz. Why is it so hard to isolate and purify human immunodeficiency virus (HIV)? Why has no one been able to see, by electron microscopy, a single HIV particle in the blood of AIDS patients, even those who have a “high viral load”? Why does HIV seem to mutate with startling rapidity? AIDS researchers have not been able to come up with answers to these questions.

HERVs—human endogenous retroviruses—might provide explanations that have been overlooked for 20 years, writes Professor Etienne de Harven, M.D., in the fall 2010 issue of the Journal of American Physicians and Surgeons,. HERVs are present in all of us, and fragments of their DNA may be confused with HIV in the polymerase chain reaction (PCR) tests used to estimate viral load.

The beautiful photographs of HIV published in both lay and scientific journals are embellished with special effects from computerized image reconstruction. Since they come from cell cultures, which are likely to be contaminated, the particles may be “elegant artifacts” rather than the exogenous virus—a virus of external origin—believed to cause AIDS, de Harven states.

About 8 percent of the human genome consists of sequences incorporated from retroviruses. When cells break down, DNA fragments are released into the circulation—including these viral sequences. Patients with clinical AIDS carry a large spectrum of infectious diseases, so a high level of circulating DNA is expected.

While “AIDS Rethinkers” may challenge the role of HIV in AIDS, or even its existence, they are obligated to explain the observations of clinicians and researchers. HERVs are, at a minimum, a confounding variable that needs to be investigated, de Harven notes.

Puzzles involving the interpretation of diagnostic tests for HIV, the epidemiology and transmission patterns of AIDS, and strategies for prevention and treatment cannot be solved without broadening AIDs research beyond the narrow confines accepted by the “Orthodoxers,” de Harven believes. Alternate hypotheses need to be objectively assessed, and conclusions must be based on scientific evidence rather than consensus.

The article can be downloaded free of charge from http://www.jpands.org/vol15no3/deharven.pdf.

Posted in HIV as stress, HIV does not cause AIDS, HIV skepticism, HIV tests, HIV transmission | Tagged: , , | 23 Comments »

Elsevier publishes another HIV-denialist article

Posted by Henry Bauer on 2010/01/13

“[T]here is extensive evidence that certain micronutrient deficiencies are associated with faster disease progression or increased mortality risk, and that dietary supplements . . . can prolong survival in HIV/AIDS. . . .
one aspect stands out in importance: the potential relationship to oxidative stress. . . . the antioxidant role of selenium in glutathione peroxidases . . . .
a daily supplement of 200 μg of selenium alone stopped progression of HIV-1 viral load increases, and lead [sic] to  improved  CD4  counts. . . . selenium status was reported to be 10 times  more  significant  than  CD4  cell  count  as  a  predictor  of   mortality. . . .
HIV infection is typically characterized by a dramatic decline in glutathione levels . . . [which] suggests an abnormal degree of biological oxidation, manifesting as elimination of cysteine sulfur as sulfate. A key feature of HIV disease is an apparent ‘antioxidant defect’ . . . [which] can be aggravated by co-factors such as malnutrition, co-infection with other microorganisms, and the use of various oxidant   drugs, such as nitrites. . . .
Intermediates of oxidative tryptophan metabolism have also been implicated in neurotoxicity, potentially contributing to AIDS dementia. . . .
oxidative   stress   can   induce niacin/NAD+ depletion. . . .
The oxidative stress-induced niacin sink (OSINS) model for HIV pathogenesis. . . . links oxidative stress and selenium to the observed tryptophan abnormalities and immunosuppression in HIV/AIDS. . . . [and] provides a mechanism whereby oxidative stress associated with HIV infection can contribute to immunosuppression via tryptophan deletion, as well as neurotoxicity via toxic tryptophan metabolites and ATP depletion. . . .
But whatever the source of oxidative stress, there would be a net effect towards niacin depletion and compensatory tryptophan oxidation. . . .
the need for certain nutrients in HIV infection may be largely secondary to an underlying defect that could be largely rectified by another nutrient, with antioxidants being the most fundamental to an effective regimen. . . .
whatever underlies or contributes to the antioxidant defect and increased oxidative stress . . . leads also to intracellular niacin depletion, and thereby to tryptophan depletion, with an end result of immunosuppression . . . and also T-cell loss” [emphases added].

It might seem natural to infer that this was written by the Perth Group, who have argued for upwards of two decades that “AIDS” results from oxidative stress, possibly with co-authorship by Rebecca Culshaw, who described the crucial role of glutathione, and by Harold Foster, who has long argued the central role of selenium, not to mention Matthias Rath, who has long spoken up for the value of micronutrients in treating AIDS patients.
But no. What’s more, none of those earlier publications are mentioned in this article by Ethan Will Taylor, “The oxidative stress-induced niacin sink (OSINS) model for HIV pathogenesis”, published on-line in Toxicology (Received 1 July 2009 — Received in revised form 10 October 2009 — Accepted 15 October 2009 — On-line at PubMed 24 October  [Epub ahead of print, PMID: 19857540, ).

(The review is described as “Hypothesis”, suggesting it might equally have been accepted by another Elsevier journal, Medical Hypotheses, were it not that the latter seems nowadays to bar anything that questions HIV/AIDS orthodoxy.)

At any rate, this article talks about “HIV-associated” oxidative stress and the benefits of nutritional supplements in “HIV-infected” people without demonstrating that “HIV” is actually involved. Essentially the same network of reactions and feedback applies in any situation of oxidative stress, as noted in the article: “whatever the source of oxidative stress . . . whatever underlies or contributes to the antioxidant defect and increased oxidative stress”. The only suggested involvement of HIV in the network of reactions is via a postulated stimulation of IDO (indoleamine-2,3-dioxygenase) by tat and nef proteins and an increased level of interferon γ ascribed to viral infection and immune activation.

If it could be shown that under generalized oxidative stress, substances are released that are capable of yielding an “HIV-positive” response, that would combine with this comprehensive review of the literature to make oxidative stress an entirely plausible cause of AIDS, a worthy alternative to the HIV/AIDS hypothesis.

In point of fact, it is already well and long known that “HIV-positive” is a condition that can be brought on by a large range of conditions and infections: hypergammaglobulinemia, tuberculosis, or vaccination against flu, and dozens more documented by Christine Johnson (“Whose antibodies are they anyway? Factors known to cause  false positive HIV antibody test results”, Continuum, #3, Sept./Oct. 1996, p.4, anti-tetanus shots (Saag et al., Nature Med 1996;2:625-9 and Gonnelli et al., Lancet 1991;337:731), and even pregnancy (Taha et al., AIDS 1998;12:197-203; Gray et al., Am J Obstet Gynecol 2001;185:1209-17; Gray et al., Lancet 2005;366:1182-8). Drug abusers very often test “HIV-positive”. That the Centers for Disease Control and Prevention included increasing numbers of conditions as “AIDS-defining” after “HIV-positive” became a criterion reflects the fact that many illnesses induce oxidative stress and the resulting “HIV-positive” status.

Here is a simple way of Rethinking AIDS:
There are two hypotheses.
1. AIDS is caused by a previously unknown retrovirus that first infected gay men simultaneously in several large metropolitan areas in the United States even though it had first crossed into humans in Africa. No vaccine or microbicide against it has been found after more than two decades of concentrated effort. Transmitted sexually, it is however very difficult to transmit, which is why it has remained within the original risk groups of promiscuous drug-abusing gay men and other drug abusers, except in Africa where 20-40% of the adult population has several sexual partners simultaneously and changes them frequently (James Chin, The AIDS Pandemic); however, the retrovirus has never actually been observed, in prospective studies, to be transmitted sexually. It kills T-cells by some unknown but certainly indirect as well as obscure mechanism. Though transmitted by breastfeeding, it is transmitted less, the greater the degree of exclusive breastfeeding. The presence of antibodies denotes active infection even when no actual virus can be detected. Some significant proportion of those infected remain healthy, even as no reason for this immunity has been discovered. One of the three original salient AIDS diseases supposedly caused by this retrovirus, Kaposi’s sarcoma, turns out not to be caused by it after all. Antibodies to the retrovirus appear after vaccination against flu, or after an anti-tetanus shot, and in a host of illnesses as well as natural conditions of some physiological stress like pregnancy. In an appreciable number of AIDS cases, no antibodies or retrovirus could be found, but this could be explained away as another new disease, idiopathic CD4-T-cell lymphopenia. Drugs that kill the virus do not correlate with restoration of the immune system nor with improved health. Indeed, purported restoration of the immune system with these drugs brings on another new ailment, “immune restoration syndrome”, a worsening of clinical condition with symptoms that mimic AIDS. The retrovirus mutates at unprecedented speed, so that infected individuals harbor not a single variant but a swarm of variants; and all variants and strains appear to be pathogenic to similar extents. Antiretroviral treatment is by toxic drugs whose side effects are so severe that non-compliance by patients has been observed or estimated at nearly 50%. Deaths from AIDS continue to occur in the same age-range as before, roughly mid-30s to late 40s. Although the retrovirus is latent for an average of a decade before causing illness, the age of first infection, of first AIDS diagnosis, and of death are all in that same age range.
2. AIDS is caused by oxidative stress. Proof: dietary supplements of antioxidants and essential minerals and vitamins restore health and extend life without dangerous side effects.

Posted in Alternative AIDS treatments, HIV absurdities, HIV as stress, HIV does not cause AIDS, HIV skepticism, HIV tests, HIV transmission, sexual transmission, vaccines | Tagged: , , , , , , , , , , , | 45 Comments »

Spontaneous generation of “HIV”

Posted by Henry Bauer on 2009/10/25

In places where claimed outbreaks of “HIV” have had “infected needles” as the only possible source of the supposedly infecting agent, the large but unaddressed question is, how did those needles become infected in the first place? And then remain infected long enough to pass on that infection when the purported contagious agent is supposed to survive for only a brief time outside bodily fluids? [HIV/AIDS in Italy — and “NEEDLE ZERO”, 11 October 2008; “Needle ZERO” again; or, HIV pops up magically out of nowhere, 15 November 2008].
It’s as though this “HIV” were spontaneously generating itself. That would not have seemed absurd a couple of centuries ago, when spontaneous generation of living organisms was an acceptable theory, but HIV/AIDS theory is supposed to be scientifically up-to-date.

An even more direct instance of “HIV-positive” in absence of “HIV” is that of certain elite controllers who have no detectable “viral load” (Compounding HIV/AIDS absurdities, 11 October 2009).

There are at least two other situations where “HIV-positive” pops up without any sign that “HIV” was present in the first place: In clinical trials of circumcision as a means of preventing “HIV-positive” status, and in a prospective study of acquisition of “HIV” by pregnant women.

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Two clinical trials of circumcision both reported that participants in both control and intervention groups acquired “HIV-positive” status during the trial even while abstaining from intercourse:

“there were seven early seroconverters . . . : four in the circumcision group and three in the control group. Three of the four in the circumcision group reported no sexual activity in the month after circumcision. We cannot exclude the possibility that any of these individuals were actually HIV positive at baseline, and that their infection was not detected. Two of the three early seroconverters in the control group also denied sexual activity in the period before seroconversion” [emphases added; Bailey et al., “Male circumcision for HIV prevention in young men in Kisumu, Kenya: a randomised controlled trial”, Lancet, 369 (2007) 643-56].

circumcision  was not protective against HIV acquisition in the few men  who  reported  no  sexual  activity in  a  given  follow-up  interval. There were six incident cases (three in each group)  during periods of reported abstinence. None of these six  participants reported receipt of injections or transfusions  during the follow-up interval of HIV seroconversion; these  participants probably under-reported their sexual activity” [emphases added; Gray et al., “Male circumcision for HIV prevention in men in Rakai, Uganda: a randomised trial”, Lancet, 369 (2007) 657-66].

The mainstream explanation, then, is that the individuals concerned lied, or that they had been “HIV-positive” at enrolment but failed to be detected by those highly specific “HIV” tests. Sherlock Homes might have agreed in general that when all the likely possibilities have been excluded, one must accept those of high improbability — but Holmes would never have come to believe HIV/AIDS theory in the first place. What a coincidence, that about the same number of men in all four groups became “HIV-positive” in absence of sexual activity. Or, alternatively, what a coincidence that the number who not only lied about sexual activity but also became “HIV-positive” should be the same in all four groups.

HIV Skeptics and AIDS Rethinkers, however, understand that “HIV-positive” does not necessarily bespeak an infection transmitted sexually or by other means. These facts are perfectly compatible with the copious data that show “HIV-positive” to be a condition inducible by any number of stimulating influences. Moreover, the tendency to test “HIV-positive” increases with age from the teens into middle age:

agevariations

Therefore it is only to be expected that in any group of young men observed for any substantial length of time, a few will become “HIV-positive” — perhaps as a result of flu, or malaria, or a vaccination, etc.

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Consistent with these occasional real-time observations of “HIV-positive” incidence among people who have had no sexual activity, no blood transfusions, and no injections is the finding in a large clinical trial carried out over many years that pregnant women become “HIV-positive” at a greater rate than do those who have already given birth and are lactating or those who are neither pregnant nor breastfeeding:

CondomsPregnantGray

Lest one attempt to explain this away by postulating, counter to common sense, that pregnant women have more sex or more unsafe sex than do non-pregnant women, Gray et al. note that
“The  mean  monthly  frequency  of  intercourse  was  lower  during  pregnancy  (6·7  acts  per month) than during breastfeeding (7·5 acts per month) and  during  non-pregnant  and  non-lactating  intervals (8·0 per month; p<0·05). Therefore, we also estimated the  rate  of  HIV  acquisition  per  coital  act,  which  was higher during pregnancy than in the non-pregnant and non-lactating group (incidence rate ratio 1·42, 95% CI 0·37-3·82). . . . [P]regnant women were  significantly  less  likely  to  report  multiple  sexual partners  than  were  non-pregnant  and  non-lactating women,  and   in   married   couples   the   husbands   of pregnant  women  reported  significantly  fewer  sexual partners  than  husbands  of  non-pregnant  and  non- lactating women. Although there could be misreporting of  sexual  behaviours,  the  results  are  unlikely  to  differ between the three exposure groups, so both female and male  sexual  behaviours  are  unlikely  to  account  for  the excess risk of HIV during pregnancy. . . . [W]e  conclude  that  behavioural  factors  are unlikely  to  explain  why  the  HIV  incidence  rate  is increased  during  pregnancy,  and  we  speculate  that biological factors might have a role. . . . . Hormonal  contraception  has  been  associated  with  increased  risks  of  HIV acquisition   in   some   but   not   all   epidemiological studies” [emphases added].
In overall summary, Gray et al. state:
“Interpretation The risk of HIV acquisition rises during pregnancy. This change is unlikely to be due to sexual risk behaviours, but might be attributable to hormonal changes affecting the genital tract mucosa or immune responses. HIV prevention efforts are needed during pregnancy to protect mothers and their infants.”

How close they come to recognizing the fact of the matter, that “HIV-positive” signifies any one or more of a wide range of physiological conditions, of which pregnancy has long been known to be one. They even cite a study from Malawi that reported higher incidence of “HIV-positive” in pregnancy than post-partum, by a factor of 2.19, and another from Rwanda that reported higher incidence of “HIV-positive” early post-partum compared to later. In South Africa, “HIV-positive” prevalence is persistently higher among pregnant women than among women as a whole [HIV demographics are predictable; HIV is not a contagious infection, 27 August 2008].

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But perhaps most remarkable of all is the quite direct evidence in the Gray article that “HIV” can be “caught” in absence of “HIV”. During the study, 338 seroconversions were observed: 23 among pregnant women, 40 among lactating women, and 275 among the others. The article also reports on discordant couples — male partner “HIV-positive”, wife “HIV”-negative — and in those cases there were 77 seroconversions: 6 among pregnant women, 11 among lactating women, and 60 among the rest. The inference is clear that 261 (338-77) seroconversions occurred among couples not known to be discordant — in other words, one partner “caught” “HIV” though the other partner didn’t have it.

Of course, “partners not known to be ‘HIV-positive’” is not the same as “partners known not to be ‘HIV-positive’”. But since the investigators explicitly sought to ascertain the “HIV” status of partners, and were confident enough of their data that they reported separately on “transmission” among discordant couples, it seems unlikely that they would have missed a large enough number to explain all the seroconversions observed in the study; therefore it does seem that as many as 77% (261/338) of the women in the study who became “HIV-positive” did so without any evidence of sexual intercourse with an “HIV-positive” male, indeed, with implicit evidence of LACK of such contact.

Lest this line of inference not be convincing, consider this clear statement in the article’s Summary:
“In married pregnant women who had a sexual relationship with their male spouses, the HIV incidence rate ratio was 1·36  (0·63-2·93).  In  married  pregnant  women  in  HIV-discordant  relationships  (ie,  with  HIV-positive  men)  the incidence rate ratio was 1·76 (0·62-4·03).”
Thus the rate of seroconversions in discordant relationships was very little higher than overall; evidently the rate of seroconversion in non-discordant relationships was appreciable. “HIV” was appearing in absence of “HIV”.

AGAIN: The obvious inference, consistent with large amounts of other data, is that pregnancy per se is a condition that conduces to testing “HIV-positive”. Pregnancy is one of many conditions that conduce to testing “HIV-positive” (see Why pregnant women tend to test “HIV-positive”, 5 October 2009).

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Under mainstream HIV/AIDS theory, then,

“HIV” is sometimes SPONTANEOUSLY GENERATED.

An irreverent observer might express this as

“HIV” is IMMACULATELY CONCEIVED

or as Axel put it,

the virgin birth of “HIV”

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P.S. re condoms:
Alert and wary consumers of data will have noted in the Table above not only that pregnant women become “HIV”-positive more often than others, but also that women who used condoms (regularly or irregularly) became “HIV”-positive more often than those who never used condoms.
Just another unacknowledged self-contradiction in HIV/AIDS theory.

Posted in clinical trials, experts, HIV absurdities, HIV as stress, HIV does not cause AIDS, HIV risk groups, HIV skepticism, HIV tests, HIV transmission, HIV varies with age, HIV/AIDS numbers, sexual transmission | Tagged: , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , | 11 Comments »

Why pregnant women tend to test “HIV-positive”

Posted by Henry Bauer on 2009/10/05

Sabine Kalitzkus drew to my attention this plausible explanation for the tendency of pregnant women to test “HIV-positive”:
1. Pregnancy brings a Th1→Th2 shift in the immune system.
2. “HIV-positive” is associated with a Th1→Th2 shift.

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It is vital to bear in mind — always, not only in this connection! — that testing “HIV-positive” does not signify the presence of a specific agent, still less the presence of an human immunodeficiency virus. There are several lines of proof for that:
First: a great variety of conditions can bring about an “HIV-positive” test-result. For empirical proof, see Christine Johnson, “Factors known to cause false positive HIV antibody test results”, Continuum 4 #3, Sept/Oct 1996, www.healtoronto.com/testcross.html or www.virsumyth.com/aids/hiv/cjtestfp.htm); or The Origin, Persistence and Failings of HIV/AIDS Theory; or a large number of posts on this blog in the category “HIV tests”. (Quite recently, a correspondent told me of testing “HIV-positive” after having abused steroids, which I have not seen mentioned elsewhere as inducing “HIV-positive”. After changing his lifestyle, he now tests negative again. Was Magic Johnson perhaps one of the many athletes who [ab]used steroids?)
Second: For a priori proof, note that the ELISA and Western Blot tests respond to many combinations and magnitudes of 2 or more among 10 separate proteins, none of which has been proven to be unique to the hypothesized “HIV” — virions of which have never been isolated directly from “HIV-positive” people or from AIDS patients, even though the latter are postulated to experience overwhelming viremia in the later stages of their illnesses [HIV tests: Danger to life and liberty, 16 November 2007].
Third: Again empirical and entirely consistent with and illustrative of the first two: Surveys of “HIV” “prevalence” show a continuum of rates of “HIV-positive” test-results among different groups. The progression from low to high rates appears to correlate with the likelihood that some sort of health challenge is present. Note in particular that pregnant women (pre-natal clinics) test positive at a higher rate than the general average of the population (National Health and Nutrition Survey), and quite significantly more often than women at family planning clinics:

groupcomparison

Not only do surveys of “HIV” prevalence find it higher among pregnant women, a full-scale prospective clinical trial in Africa actually found a higher incidence of “HIV-positive” during pregnancy [Gray et al., “Increased risk of incident HIV during pregnancy in Rakai, Uganda: a prospective study”, Lancet 366 (2005) 1182-8].

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Among the variety of circumstances that can stimulate an “HIV-positive” response is “AIDS”, and in AIDS, “A gradual shift from Th1- to Th2-dominance is observed. . . . This Th1-to-Th2 shift perfectly explains some of the major conundrums of the AIDS clinical syndrome. . . . Furthermore, elevated levels of antibodies, including autoantibodies, are characteristic of all AIDS patients — a finding consistent with a decrease in the Th1 subset coincident with an increase in the Th2 subset. . . . HIV is expressed primarily in Th0 and Th2 cells, and is scarcely to be found in the Th1 subset. 38-40 This is curious indeed, since it is the Th1 cells that decline, whereas the cells in which HIV prefers to reside do not decrease” [Culshaw, “Mathematical Modeling of AIDS Progression: Limitations, Expectations, and Future Directions”, Journal of American Physicians and Surgeons 11 (#4, Winter 2006) 101-5].

Notoriously, gay men are more likely than others to suffer an “AIDS” condition, and — independently — they are more likely to test “HIV-positive” without necessarily becoming ill: many “HIV-positive” gay men have remained healthy for upwards of two decades. As Tony Lance has pointed out, much evidence indicates that gut dysbiosis can induce gut leakage, testing “HIV-positive”, and in severe cases the most characteristic of the AIDS illnesses, namely, the fungal infections Pneumocystis carinii pneumonia and candidiasis; and gut dysbiosis is also associated with a shift in the Th1-Th2 balance:
“T-cell abnormalities — There appears to be a connection to be elucidated between gut dysbiosis, glutathione deficiency, and T-cell anomalies thought to be characteristic of HIV/AIDS. . . . A direct connection between the composition of gut microflora and the balance of Th-type cells has been reported by several authors: . . . ‘What typically happens in a person with gut dysbiosis is that two major arms of their immune system, Th1 and Th2, get out of balance with underactive Th1 and overactive Th2. . . ’ (35)” [emphases added; Tony Lance, “GRID = Gay Related Intestinal Dysbiosis?
Explaining HIV/AIDS Paradoxes in Terms of Intestinal Dysbiosis”, pdf at “What really caused AIDS: Slicing through the Gordian Knot”, 20 February 2008].

Testing “HIV-positive”, then, correlates with a Th1→Th2 shift, under some circumstances at least.
The immune system is of course much more complicated than just these two categories of cells. There are a variety of Th1 cells and of Th2 cells, so a shift in the overall balance might mask more specific differences; in other words, a given Th1/Th2 ratio in healthy gay men may bespeak functionally different circumstances than the same numerical ratio in AIDS patients, or in TB patients, or in pregnant women. The mere fact of a Th1→Th2 shift does not necessarily signify a dangerous health condition, any more than an “HIV-positive” test necessarily signifies a dangerous health condition or that an “HIV-positive” test always signifies the presence of the same combination of two or more of those ten proteins.

So: the fact that pregnant women are more likely to test “HIV-positive” does not necessarily signify a health challenge more serious than normal pregnancy.
As to a Th1→Th2 shift in pregnancy, Sabine Kalitzkus sent a link to impfreport, Zeitschrift für unabhängige Impfaufklärung, 56/57, July/August 2009 [vaccination report, magazine for independent vaccination education; editor, Hans U. P. Tolzin]. Pages 4-5 report information for doctors and pharmacists that was issued by the Paul Ehrlich Institute on 4 September 2009. What follows is free translation from German:

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Vaccinating pregnant women during the swine-flu pandemic
The immune system has broadly speaking two arms. Cellular immunity is mediated largely by Th1 “killer” cells which attack “foreign” cells, i.e. those not recognized by their protein coating as belonging to the host. The other arm is mediated by Th2 cells which are responsible for generating antibodies to foreign proteins.
A fetus is at least partly “foreign” to the mother since its genes, and consequently the generated proteins, come partly from the father. To prevent aborting of the fetus, pregnancy causes a partial Th1→Th2 switch. [In other words, such a shift is perfectly normal in healthy pregnancies, but it will also tend to be associated with an “HIV-positive” test]
The [European] swine-flu vaccine contains adjuvants to stimulate the Th1 arm, which may increase the risk of spontaneous abortion. Indeed, it is known that spontaneous abortion is associated with a shift towards Th1.
The Paul Ehrlich Institute’s release minimizes this risk in bureaucratic weasel-word fashion:
Altogether, a harmful effect on pregnancy of adjuvant-containing vaccines seems rather unlikely. But since data from clinical trials are lacking, such an effect is not impossible.
[Insgesamt erscheint ein negativer Effekt von squalenhaltigen Influenzaimpfstoffen auf die Schwangerschaft eher unwahrscheinlich. Da jedoch umfangreiche Daten bei Schwangeren in klinischen Studien fehlen, kann ein Effekt auch nicht vollständig ausgeschlossen werden.]

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To paraphrase this “conclusion”: We have no relevant data, hence no evidence. What we know about the immune system and pregnancy would incline one to be concerned. However, in our opinion the risk is negligible, though we can offer no evidentiary basis for that judgment.

That evidence is totally lacking for this Micawber-ish, Panglossian or Pollyanna-ish failure to be concerned is obvious, since pregnant women are (at least in developed countries) not eligible for enrolment in clinical trials — except, of course, in the case of HIV/AIDS and the attempt to find out how high a dose of antiretroviral drugs can be tolerated by “HIV-positive” pregnant women [Celia Farber, “Out of control: AIDS and the corruption of medical science”, HARPER’S MAGAZINE, March 2006, 37-52].

To recapitulate:
Empirical fact: Pregnant women test “HIV-positive” more frequently than others.
Empirical fact: In several groups, Th1→Th2 shift is associated with a tendency to test “HIV-positive”.
Empirical fact: Normal, healthy pregnancy induces a Th1→Th2 shift.

The higher frequency of “HIV-positive” tests among pregnant women
may be nothing more than a natural consequence of pregnancy

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