HIV: IT MUST HAVE BEEN TRANSMITTED BY BITE!

The unshakable belief that testing “HIV-positive” denotes infection by a virus transmitted from another “HIV-positive” individual sometimes makes it necessary to draw inferences that outsiders and lay people might find hard to accept, indeed outlandish. So it is with the “evidence” that a man infected his daughter by biting her finger.

The following piece (”Rare causes of HIV transmission“)  comes from Professor Courtenay Bartholomew, Executive Director of the Medical Research Foundation in Trinidad & Tobago.

“Our case report on human bites: a rare risk factor for HIV transmission was published last year. . . . in the American Journal of AIDS, which . . . accepts only about one in 20 submissions. . . . In a review of such cases . . . Richman and Rickman . . . stated that ‘transmission of HIV through human bites is biologically possible but remains epidemiologically insignificant and as yet not well documented.’”

However, in June 2004 a heterosexual man with “very late stage AIDS” was found to be HIV-positive; he died in September 2007. He had a history of “dental caries and bleeding gums”. His wife was found to be HIV-negative, but their 7-year-old child tested positive. The wife was assumed to have remained negative “because sexual intercourse was infrequent”.

“Problem! How could the child be HIV-positive when the mother was HIV-negative seeing that childhood infection is usually from mother to child? We tested and retested the blood from the mother and the child but the results were the same. We also excluded any history of sexual abuse by the father and of blood transfusion to the child. It was then that the mother recalled an incident when at age three the child was bitten on her finger by her father, who was in a tantrum. Since we excluded all other modes of HIV transmission, her HIV infection had to be a direct result of the bite from her father four years ago.”

BABIES INFECT MOTHERS; CRAZY THEORY RUINS LIVES

What can one say about tragedies like these?

“Kyrgyz Babies Pass HIV to Mothers
OSH, Kyrgyzstan (AP) — Not long ago, she was a wife, mother and teacher. Now Dilfuza Mustafakulova is HIV-positive and has lost her husband and her job. Mustafakulova’s baby son was among 72 children infected with the virus at two Kyrgyz hospitals. Sixteen mothers also have contracted it — in some cases by breast-feeding their children. . . .
The scandal has led to charges of negligence against 14 medical workers in the impoverished former Soviet republic, where investigators suspect the children were infected by tainted blood and the reuse of needles. . . . Although HIV infection from breast-feeding is rare, it is possible, usually when the baby has mouth sores and the mother has lesions on her nipples, according to AIDS experts. Mustafakulova, whose son was 7 months old at the time, said her breasts were cracked and bleeding. . . . Some 1,600 people are infected with HIV in the Central Asian nation of 5 million people, according to official figures — 15 times more than in 2002. AIDS experts estimate the real number is closer to 6,000. The majority of cases stem from intravenous drug use. . . .
Mustafakulova’s troubles began in June, when her son developed a high fever. She took him to the Nookat hospital, where she said doctors put him on an intravenous drip. When he did not get better, she took him to the hospital in Osh, the country’s second-largest city. After more than a month in the hospital, her son still was not well and she was also feeling weak, so they returned to their village . . . . In October, they both tested positive for HIV. . . . It has not been established where the infection originated. Of the 72 children infected, some were treated only in Nookat and others only in Osh, so both hospitals are suspected. ‘Where else could my child and I become infected if I don’t use narcotics and don’t live an immoral life?’ Mustafakulova said during a recent visit to the Rainbow center. ‘This could only be the irresponsibility of doctors.’ She was abandoned by her husband . . . .  No longer welcome in her in-laws’ home, she and her children moved in with her parents. She sold her only possession, a small plot of land, to pay for her son’s medical treatment. . . .  The story of Mustafakulova’s fellow villager, Zarifa Shamshiyeva, is remarkably similar. “

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On what evidence do the experts rely for the view that mothers can be infected in this way?

Even the higher estimate of 6000 infected in a country of 5 million makes the rate only 1.2 per 1000, which is typical for low-risk populations in non-African countries where there has been no epidemic during the two decades of the AIDS era, despite continual prediction of such epidemics by “AIDS experts”.

Here’s an assignment:

In 2002, only about 100 people were infected.
Most new infections have come via needles.
Construct a plausible scenario to account for how this mechanism brought a 15-fold increase in infections in half-a-dozen years.

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The tragedies here are not only the wrongly diagnosed babies and mothers. What about the doctors and other medical personnel who are being charged with negligence, when they did nothing to bring about this situation?

“Four health officials from southern Kyrgyzstan were fired for their alleged roles in the outbreak, including the directors of the two hospitals. The Kyrgyz General Prosecutor’s office has opened a criminal investigation into the incident.”

“Kyrgyz medical workers charged with infecting children with HIV”  [Associated Press, March 20, 2008]
“BISHKEK, Kyrgyzstan: Fourteen health professionals in Kyrgyzstan will face trial for allegedly infecting children with HIV”

REGULAR AS CLOCKWORK: HIV, THE TRULY UNIQUE “INFECTION”

Astonishment, disbelief, incredulity would merely begin to describe my feelings when I began collecting published data about HIV a few years ago.

I got started because I couldn’t believe the assertion, in Harvey Bialy’s book about Peter Duesberg’s work, that (in the mid-1980s, no less) teenage females from every part of the United States were as likely as teenage males to be “HIV”-positive. But I verified the correctness of the assertion in the original source; whereupon I expected to find contradictions in other studies, and so I kept looking. I jotted notes on how rates of testing positive varied with all the factors mentioned in the various reports. And my head swam, or spun, or rebelled, because it made no sense: testing “HIV”-positive seemed to be as regular as clockwork, not at all like the incidence of something infectious or contagious, which sweeps back and forth, here and there, as the opportunity offers itself.

—“HIV”-positive was always greater among men than among women: except in the teenage years, where it was often higher among females.
—“HIV”-positive always increased with age from the teens into the 30s or 40s, and then declined again.
—Most extraordinary of all, so far as age was concerned: children below teenage tested “HIV”-positive more than teenagers did, and increasingly so, the younger they were! The rate of testing positive among newborns rivaled the highest rates among adults in their 30s and 40s!

I was looking at the wealth of data based on tests in the United States, but also came across some reports from elsewhere, published by the same reliable researchers. That strange variation with age, including young children, had been reported also from Africa!

US data of all sorts are typically reported by racial category. Regular as clockwork, rates of testing “HIV”-positive always increased from among Asians to among white Americans to among Hispanic Americans to among black Americans. Whether it was blood donors or gay men, injecting drug users or newborns or their mothers; whether it was military personnel or prisoners, people at STD clinics or women at pre-natal clinics—there were simply no reports that did not fit into that progression of testing “HIV”-positive according to racial category. What sort of infection is it that discriminates consistently and regularly by race?

Whenever there’s discussion of racial disparities between blacks and whites in the USA, the first resort is to explanations based on slavery, Jim Crow laws, racial discrimination in general and their lingering after-effects: high rates of poverty, unemployment, drug abuse, criminality, and so on. But analogous circumstances have been the lot of Native Americans, displaced from their homelands, traditional practices disrupted, never integrated into the American mainstream. So one would expect that Native Americans might test “HIV”-positive about as often as African Americans. But they don’t. Every published study finds that Native Americans test “HIV”-positive at rates closer to those of white Americans than to those of any other group; somewhere between the rates of whites and those for Hispanics, but generally closer to those of whites. HIV is very race-sensitive indeed, and it discriminates by broad racial genetic category as no other infection does.

In South Africa, the same racial disparities in testing “HIV”-positive were reported as in the United States. Whites always much lower than blacks, and coloreds—mulattos—tested in between. “HIV”-positive rates even reflect miscegenation!

Similarly, within the United States, the ethnic category of Hispanic delivers “HIV”-positive rates that are distinctly higher in the East than in the West—in the same manner as the racial proportions among Hispanics differ, higher proportion of Caribbean and African descent in the East than in the West. HIV is adept at recognizing human racial genetics.

HIV is regular as clockwork in other respects, too. The same number of Americans has been “HIV”-positive from when testing began in the mid-1980s right up to the present; about 1 million, give or take whatever uncertainty the Centers for Disease Control and Prevention (CDC) is prepared to admit at any give time.

Who dies of “HIV disease”, the latest obfuscating term devised by CDC? Always the highest rate is among adults in their 30s and 40s, steadily from 1987 to date; no sign of any change in the distribution of deaths by age, no sign that treatments have had any effect, that they have shifted deaths to later ages (“HIV DISEASE” IS NOT AN ILLNESS, 19 March 2008). HIV is regular as clockwork. You can bet on it.

HIV is distributed in the United States in a pattern that hasn’t changed in two decades. Just as the total number of “HIV”-positive Americans has remained the same, so their geographic location hasn’t changed. It’s highest in the Northeast, next highest in the Southeast, and lowest in the North Central and Midwest. That applies to military personnel, new mothers and their infants, members of the Job Corps, blood donors—every tested group shows that same geographic distribution. Like no other infectious agent, HIV knows its place and sticks to it. Regular as clockwork. You can bet on it.

I put one and one together. Constant geographic distribution, constant racial disparities—maybe the geographic distribution merely reflects the racial proportions of the American population in the different parts of the country?
Yes. Calculate what the geographic distribution of HIV would be if it depended only on the racial make-up of the population and the relative rates at which the different races test positive, and you get a very good fit with the maps of “HIV”-positive rates.

There was one regularity in the data I collected that was, if possible, even more puzzling than the others. Quite a few reports made a point of noting that “HIV”-positive rates were higher in urban areas than in rural regions; always that same progression, and always higher, too, in the large urban areas than in the smaller ones. So regular was this that it seemed quantitative: in the largest metropolitan areas, rates of testing “HIV”-positive were about 4 times as high as in rural areas, and in “semi-urban” regions the rates were about half those in the largest cities.
Leave aside “why”, I thought. Clearly, the calculation of geographic distribution should be modified by taking also this factor into account. Doing that, the fit between the calculated and the actual geographic distributions of HIV is even better.

So HIV is this unique, unprecedented, even magical infection that hides itself not only in human bodies (because none of it has never been isolated in live form from an “HIV”-positive person), it hides itself also in its demographic characteristics, by behaving just like something endemic! It doesn’t go up and down in incidence like other infections or contagions. It doesn’t skip, hop, and jump around regions and countries and the world like other viruses or bacteria. It’s just there. It mimics DNA, in fact, because it distributes itself according to racial category. It mimics physiology: it varies according to the age of its host— regular as clockwork, it’s lowest in the teens and highest at birth and in middle age. You can bet on it.

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I’ve mentioned before, on this blog (for instance, HIV DEMOGRAPHICS FURTHER CONFIRMED…, 26 February 2008), how reassuring it has been to find that these regularities, described and documented in my 2007 book (The Origin, Persistence and Failings of HIV/AIDS Theory), continue to be reported in newer studies. Reassuring because it emphasizes that the regularities I had discerned were not artefacts of those particular samples—which was unlikely a priori, in any case, given that those “samples” included just about all the published data and represented upwards of 60 million tests; including some, like blood donors and military cohorts, in which all members of those groups were tested, not just sampled; and moreover tested regularly throughout the era of AIDS.

The present little essay was stimulated by finding confirmation of that most puzzling of the regularities, the variation of “HIV”-positive rates with population density. In gathering data for my book, I had not come across a piece in the Journal of Rural Health by Steinberg and Fleming of the CDC, “The geographic distribution of AIDS in the United States: Is there a rural epidemic?” (16 [2000] 11-19). Maybe I had missed it because I focused my searches on “HIV”, not “AIDS”.

Despite its title, that paper is about the distribution of “HIV”. CDC has added to its many sins by conflating, since the late 1990s, HIV and AIDS in such a manner as to make it difficult if not impossible to know what their statistics refer to. In this instance, “AIDS” is said to include “HIV-related severe immunodeficiency”—healthy, asymptomatic people who test “HIV”-positive and have low CD4 counts. So the numbers given in this publication represent “HIV”-positive rates. The article reports specifically on data for 1996; and it confirms rather strikingly the regular trends, including the variation with population density, that are published in my book, for data collated from the mid-1980s to the later 1990s.

Geographic distribution:
Northeast > South > West > Midwest  (49.4 to 34.2 to 28.6 to 13.5 per 100,000)

Black-to-white ratio, 7.2 (in my book, 5.5 ± 3.4)
Hispanic-to-white ratio, 3.4 (in my book, 2.7 ± 2.1)

Variation with population density:
Metropolitan statistical area (MSA) >500,000, 41.6;  50,000 - 500,000, 17.7; non-MSA, 10.1
In my book, 4 to 2 to 1

Regular as a clock that keeps good time.

AIDS AS INTESTINAL DYSBIOSIS

The article by Tony Lance posted in WHAT REALLY CAUSED AIDS . . . [20 February 2008] is powerfully persuasive that the outbreaks of “AIDS” in the 1980s were really outbreaks of intestinal dysbiosis among people whose lifestyle was conducive to such dysbiosis. It is further support for Lance’s thesis that some doctors have been successfully treating “AIDS” patients for intestinal dysbiosis, or something very like it, from the very beginning of the “epidemic”.

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Dissenters from orthodox HIV/AIDS theory differ among themselves over what really caused AIDS. John Scythes, for example, believes that undiagnosed syphilis played and perhaps continues to play a significant role (for details, see the website maintained by his colleague Colman Jones ). But Scythes doesn’t claim to have all the answers, and he was an outstandingly objective and helpful reader of drafts of my book. He has met a number of people in various parts of the world who are involved in HIV/AIDS in one way or another, and recently he mentioned to me Dr. Juliane Sacher in Germany as someone who has successfully treated “AIDS” patients without resort to antiretrovirals. I asked Dr. Sacher for published accounts of her work, and she sent me 3 articles published in 2006 in the German periodical Raum & Zeit (141: 34-38: AIDS—Chronology of the mistakes; 142: 18-23: II. AIDS—The virus that doesn’t exist; III. 143: 60-62: “AIDS”—How alternative therapies can help [titles translated by Henry Bauer]). It turns out that Dr. Sacher’s practical clinical experience with AIDS patients and with HIV-positive people affords convincing support for Tony Lance’s hypothesis of intestinal dysbiosis.

Sacher had served as a physician with Lufthansa and had noted already in the 1970s that male flight-crews often had reduced lymphocyte counts, were often homosexual, and indeed were among the first AIDS cases in Germany. In the 1980s, Sacher was in a medical group in Frankfurt that treated many AIDS patients, and she noted their high, sometimes extreme levels of immunoglobulins and antibodies: from 35 to 40 or 45% as against the normal 18%. But T4-cells, which HIV supposedly destroys, are instrumental in the production by B-cells of these globulins; so how could patients supposedly low in T4-cells be producing excess globulins? The answer, shown by research in the early 1990s, is that the low counts of T4-cells in the blood, characteristic of AIDS, does not mark destruction of those cells but rather reflects that they move elsewhere—in particular, into the lymph system. They act against inflammation of the lymph nodes, and return into the blood once the inflammation subsides.

Sacher also notes that the balance between two types of T4 cells is shifted in AIDS patients: typically they display a relative dearth of Th1 and an excess of Th2 cells.
In 1987, Germany funded research to asses the efficacy of antiretroviral treatment of AIDS patients. Dr. Sacher had the largest or second-largest group of HIV/AIDS patients in Germany enrolled in the study. Results after one year showed that in patients treated with AZT the T4-cell counts had decreased by 70%, whereas in those treated by Sacher using alternative treatments–80-90% of all her patients–the decrease had been an average of only 7.5%! Most of these patients had had full-blown AIDS, though a few were HIV-positive but asymptomatic. This result was described in the Ärzte-Zeitung (Physicians Newsletter), 6/7 October 1989, #189, page 15: some 50 patients treated by alternative means did better than 56 patients treated with AZT (Sacher’s Raum & Zeit article no. I includes a photocopy of that publication in the Ärzte-Zeitung).

Sacher’s “alternative” approach to treatment of AIDS patients is informed by the views of Dr. Heinrich Kremer; his 2005 book, “Die stille Revolution von Krebs- und AIDS-Medizin” (The quiet revolution in cancer and AIDS medicine), Ehlers Verlag, Wolfratshausen, is to appear in English translation in the near future. The key is recognition that glutathione is a most important antioxidant which also regulates the Th1/Th2 balance: deficiency of glutathione shifts the balance in the direction of Th2. HIV-positive patients invariably have a glutathione deficiency, and their health improves when this is rectified. In addition, Dr. Sacher monitors carefully and corrects deficiencies in vitamins and minerals; she encourages a healthy lifestyle—exercise, minimizing stress—and uses a number of dietary supplements as indicated in individual cases.

In Part III of her articles in Raum & Zeit, Sacher offers more details of how she treats specific conditions that AIDS patients often experience—diarrhea, bronchitis, bladder and kidney problems. She also recommends preventive measures including specific laboratory tests. A brief professional biography of Dr. Sacher is included in these articles:
Dr. Sacher has been in private medical practice since 1983. She worked with the German Federal HIV Study between 1987 and 1993; served in 1988 on the Parliamentary HIV/AIDS Commission; and was co-recipient in 1990 of a prize of 100,000 Deutschmark for her work with HIV/AIDS patients. Between 1975 and 1993 she served under contract with Lufthansa. From 2000 to 2002 she worked part-time in the biostatistics unit of Wuppertal University. She takes a special interest in all aspects of chronic illnesses, and in complementary as well as mainstream medicine.

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I’ve often been struck by how frequently I come across, “by chance” or from unexpected quarters, material relevant to what I’m thinking about at some given moment. Here it is again. Dr. Sacher’s clinical experience with “AIDS” patients is fully in line with Tony Lance’s intestinal-dysbiosis theory, in particular the role of glutathione and of Th1-Th2 shifts. Dr. Sacher’s work shows the salience of those factors; Lance’s theory explains why so notable a proportion of gay men display glutathione deficiency and Th1/Th2 imbalance and therefore benefit from Dr. Sacher’s approach to medical care.

HIV-POSITIVE BABIES ARE NOT VIRUS-INFECTED

MacDonald reminded me that the Perth Group have documented in devastating fashion that “HIV-positive” data on mothers and babies proves that testing HIV-positive does not signify an infection.

I really should have emphasized that when commenting on the self-contradictions regarding “HIV” and breastfeeding (HIV and BREASTFEEDING AGAIN, 13 February 2008; FIRST: DO NO HARM!, 19 December 2007; MORE HIV, LESS INFECTION: THE BREASTFEEDING CONUNDRUM, 21 November 2007) and claims of mother-to-child transmission generally (for instance, TWINS ATTRACT THEIR MOTHER’S HIV, 12 January 2008; HIV-POSITIVE CHILDREN, HIV-NEGATIVE MOTHERS, 25 November 2007).

The Perth Group’s website has two comprehensive discussions available as links: “Monograph on mother-to-child transmission”, and “BMJ Online Debate”.

MacDonald cited (from the latter) this concise yet fully documented argument by the Perth Group in response to orthodox viewpoints pressed by a certain Peter Flegg:

“In regard to ‘HIV’ seropositive mothers, their infants and antibody specificity, we would be grateful for Peter Flegg’s view on the following:

In 1987 the CDC advised: ‘Most of the [CDC] consultants believed that passively transferred maternal HIV antibody could sometimes persist for up to 15 months’. (18 ) In 1991 the CDC extended the time to 18 months 13 and by 1995 ‘…the range of WB seroconversions might eventually extend beyond 30 months’, (14) that is, at double the age ‘believed’ eight years earlier. Before the AIDS era the evidence was that transplacental maternal antibody in offspring did not persist beyond nine months.(15) In 1993, Parekh from the CDC developed ‘a human immunodeficiency virus type 1 (HIV-1)-specific 1gG-Fc capture enzyme immunoassay (1gG-CEIA) to elucidate the dynamics of HIV-1 maternal antibody decay and de novo synthesis of HIV-1 antibodies in infants’. He and his colleagues demonstrated a rapid decay of maternal ‘HIV’ antibody ‘with decline to background levels by 6 months’. (16 ) In other words, if the ‘HIV’ antibody test is specific, any child who has a positive ‘HIV’ antibody test beyond 9 months should remain positive for the remainder of his or her life. In the only study providing a detailed analysis of post partum loss of infant HIV seropositivity, the European Collaborative Study, (17) approximately 23% of the children became seronegative between birth and 9 months. However, 59% became seronegative between 9 and 22 months. Since the latter cannot be due to loss of maternal antibodies, the only explanation is that either: (i) the antibody test is non-specific or; (ii) the children managed to clear ‘HIV’ infection without treatment. If 23% of children test positive because of maternal antibodies and in 59% the test is non-specific, how certain can Peter Flegg be that in the remaining 18% of children the test will not also serorevert after 22 months? Or if the test remains positive, is it a true positive? May we ask, what does Peter Flegg tell the mother of a child who tests positive between 9 and 30 months and what is his approach to the clinical management of this child?”

The cited references are

14. Chantry CJ, Cooper ER, Pelton SI, Zorilla C, Hillyer GV, Diaz C. Seroreversion in human immunodeficiency virus-exposed but uninfected infants. Pediatr Infect Dis J 1995;14(5):382-7.

15. Stiehm ER. Immunologic diseases in infants and children. 3rd ed. Philadelphia: WB Saunders Company, 1973.

16. Parekh BS, Shaffer N, Coughlin R, Hung CH, Krasinski K, Abrams E, et al. Dynamics of maternal IgG antibody decay and HIV-specific antibody synthesis in infants born to seropositive mothers. The NYC Perinatal HIV Transmission Study Group. AIDS Res Hum Retroviruses 1993;9:907-12.

17. Epidemiology, clinical features, and prognostic factors of paediatric HIV infection. Italian Multicentre Study. Lancet 1988;ii:1043-6.

18. CDC. Current Trends Classification System for Human Immunodeficiency Virus (HIV) Infection in Children Under 13 Years of Age. Morb Mortal Wkly Rep 1987;36:225-30, 235-6.

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One can hardly ask for better grounded reasons for recognizing that “HIV-positive” does not signify permanent infection; and that consequently all the claims of mother-to-child transmission of a virus — be it perinatally or as a result of breastfeeding — cannot be taken as valid, based as they are on the most dubious grounds.

Given these facts, how could anyone recommend the administering of toxic antiretroviral drugs to pregnant women and babies? Yet now we have studies exploring how longer exposure to these drugs might influence the spurious indications of the presence of “HIV” (HIV and BREASTFEEDING AGAIN, 13 February 2008).