HIV without AIDS for knowsomethingabout...

Cause Someone said; "It must also be stated that the only common denominator between people who develop AIDS (drug addicted prostitutes living on the streets to wealthy, yoga loving corporate CEO) is an acute infection with HIV. LET ME BE CLEAR. NO PERSON HAS EVER DEVELOPED AIDS WITHOUT BEING INFECTED BY HIV. EVER. If 25 years of the most groundbreaking, indesputable science are not enough to convince you I don't know what will."

The Enigma That Won't Disappear: The Recurring Problem of Non-HIV AIDSby Neenyah Ostrom
(NONYN@aol.com)


New York Native, issue #639, July 17, 1995

When the first cases of "AIDS" without HIV were revealed at the Ninth International Conference on AIDS in Amsterdam, American public health officials moved quickly to contain world-wide speculation as well as public concern in the United States. Although potentially hundreds of cases of "non-HIV AIDS" were reported by the group of international researchers gathered in Amsterdam in July 1992, U.S. health authorities declared the condition to be a non-phenomenon almost immediately upon returning home.

However, researchers who'd been tracking "AIDS"-associated conditions occurring in people not infected with HIV--such as Kaposi's sarcoma and Pneumocystis carinii pneumonia (PCP)

--began reporting those cases in international journals like The Lancet.

The "non-HIV AIDS" cases raised fundamental questions about the syndrome.

For instance, the hallmark of "non-HIV AIDS," just like regular "AIDS," was the near-disappearance of a type of immune system cell. These are the CD4-positive T-lymphocytes, also called T4 cells (or simply CD4 cells).

It was widely assumed in 1992 that HIV was causing the destruction of the T4 cells observed in "AIDS," either by directly killing them or by setting in motion an indirect mechanism through which the cells were killed.

But if serious CD4 cell depletion could occur in the absence of HIV, was HIV really responsible for the deaths of those cells in "AIDS" patients?

Similarly, if "AIDS"-associated conditions like KS and PCP could occur in the absence of the "AIDS virus," then what role was HIV really playing in causing those manifestations of the syndrome?

A report of some non-HIV retroviral particles being found in some "non-HIV AIDS" patients raised one of the questions asked most frequently in media reports about the phenomenon: Is there another virus capable of causing "AIDS?"

If so, is it a retrovirus? Or could it be another type of virus altogether?

Is there another virus that could create life-threatening immunosuppression by destroying CD4 cells?


It was in the shadow of these questions that a meeting was held at the U.S. Centers for Disease Control in Atlanta on August 14, 1992, to examine the data collected on the "non-HIV AIDS cases." Included was some information indicating that a type of retroviral particle, unrelated to HIV, might be present in the patients who had "non-HIV AIDS."

What emerged from that meeting was a statement from the CDC asserting that there was no new "AIDS" agent lose in the world--even though, in part, it was the CDC's initial statement about the "non-HIV AIDS" cases that had raised the question in the first place.

The abstract (#Q347) presented to the international "AIDS" meeting in Amsterdam by CDC scientists Thomas J. Spira and Bonnie M. Jones reported that CDC had "identified six persons with persistently low CD4 count (less than 250/cubic millimeter) who are repeatedly HIV-seronegative."

These patients had developed "AIDS"-related conditions, including (but not limited to) PCP, cryptococcal meningitis, oral and vaginal candidiasis, Kaposi's sarcoma, as well as atypical pneumonias caused by mycobacteria (an organism related to the one that causes tuberculosis).

After providing a few more clinical details in their abstract in Amsterdam, Spira and Jones concluded, "In summary, we have identified six persons with low CD4 counts without evidence of HIV infection with clinical manifestations of opportunistic infections or tumors of varying severity. This suggests that HIV may not be the only infectious cause of immunosuppression in man."

About a month later, at the August meeting in Atlanta, CDC researchers an-nounced that there was no new "AIDS virus," that the people with "non-HIV AIDS" appeared to have nothing in common--therefore, they concluded, it was not an emerging epidemic.

A report of the meeting published in the British journal The Lancet August 22 announced that the phenomenon of "HIV-negative AIDS" had also had a tongue-twister of a name conferred upon it: "idiopathic CD4-positive T lymphocytopenia," abbreviated ICL.

That means, in short, an unexplained loss of T4 (CD4) cells.

The Lancet's correspondents were John P. Moore and David D. Ho from the Aaron Diamond AIDS Research Center in New York City, where some of the ICL cases were being studied.

Moore and Ho suggested, in concluding their report, that "Whether a [new] retrovirus is really involved will emerge only after a period of careful research. But investigators should remove the retroviral blinkers and look more broadly at these cases, especially to define their immunological profile."

U.S. government researchers had no intention of removing those blinkers. In early 1993, Dr. Anthony Fauci, Director of the National Institute of Allergy and Infectious Diseases, wrote an editorial assessing the public health implications of the "non-HIV AIDS" cases.

He concluded, not surprisingly, that the cases were not "AIDS" because they were not caused by HIV and furthermore, that they were not particularly important.

"We can reasonably conclude that ICL is a rare syndrome, is not new, and is not caused by HIV-1 or -2 or human T lymphotropic virus (HTLV)-I or -II nor by a transmissible agent," Fauci wrote in the February 11 issue of the New England Journal of Medicine. "Furthermore, the syndrome is heterogeneous in that it affects a demographically diverse population and has different clinical manifestations, both of which make it dissimilar from HIV infection and AIDS."

All this time, it was known by government and private-sector researchers that there was, in fact, a second virus that preferentially infects and kills CD4 cells: Human Herpes Virus 6.

In 1992, scientists were just beginning to learn how important active HHV-6 infection is in destroying "AIDS" patients' health.

It was known at that time, however, that another group of patients also had active HHV-6 infections: Chronic Fatigue Syndrome patients.

And further research into the ICL phenomenon by non-governmental scientists was yielding evidence that the ICL cases were emerging in part from that other group of patients: those with Chronic Fatigue Syndrome.


One of the physicians who'd broken open the "non-HIV AIDS" story was Dr. Sidhur Gupta of the University of California, Irvine. Gupta was studying Chronic Fatigue Syndrome patients when he discovered some cases of CD4 cell depletion in the absence of HIV.

Other CFS researchers also came forward to report they had CFS patients with severely depleted CD4 cell counts, but who were not infected with HIV. Among them was Dr. Paul Cheney, one of the physicians who discovered CFS in 1984.

Cheney told Newsweek's Geoffrey Cowley that his CFS patients "suffer an array of illnesses--some mild, some devastating--that come and go for years." Some of his patients are even infected with "what appear to be HIV-like viruses," Cowley reported in the September 7, 1992, Newsweek.

"Cheney says 30 to 40 percent of his patients report having a close associate with a similar illness, but he has never managed to identify `a behavior pattern that places people at risk,'" Cowley wrote.

Cowley noted that not only Cheney, whom he described as "the nation's best-known chronic fatigue syndrome specialist," but also Harvard University researcher Dr. Anthony Komaroff, had numerous patients with dangerously low CD4 cell counts. These include not only patients with T4 cell counts below 300--the ICL cut-off point--but also numerous patients with T4 cell counts below 500, a level considered to be dangerous to "AIDS" patients. Any count below 800, according to Cowley, is abnormally low.

All of these findings, it is important to point out, came from the private sector.

Finally, the government's own CFS researcher, Dr. Stephen Straus at the National Institute of Allergy and Infec-tious Diseases, admitted in early 1993 that his studies of CFS patients' T4 cell counts showed a serious depletion in some cases.

Straus stressed, however, that the CD4 cell depletion seen in CFS patients was totally different from that seen in "AIDS" patients. In CFS patients, the T4 cells were not destroyed, Straus hypothesized--based on no evidence--they were just "hiding" in the lymph nodes.

Unfortunately for Straus, an "AIDS" researcher almost simultaneously suggested the same mechanism for the disappearance of CD4 cells in "AIDS" patients.


Although major U.S. public health officials like NIAID's Fauci have continued to scoff at the idea of "AIDS" without HIV--since they gave the syndrome a circular definition, requiring the presence of HIV in the first place--something is still happening that requires government scientists to deny the existence of "non-HIV AIDS" over and over.

In fact, a brand-new report published by scientists at the Centers for Disease Control and Prevention emphasizes that unexplained, exceptionally low CD4 cell counts among children is nothing to be concerned about.

The report examining inexplicable, low CD4 cell counts in children was published by Dr. Mark N. Lobato and colleagues from the CDC in the June 1995 Pediatric Infectious Disease Journal. The study was a follow-up to the 1992 report of "non-HIV AIDS" cases at the international meeting in Amsterdam.

Lobato and co-authors castigated the researchers who made the original "non-HIV AIDS" cases public--cases, it turned out, that government scientists had known about since 1983--for suggesting a new, undetected virus might be causing them.

"Investigators describing these cases suggested that a new human retrovirus or other new infectious agent may have caused the low CD4 T lymphocyte counts, a theory that produced public alarm and considerable news media attention," Lobato and co-authors wrote in the Pediatric Infectious Disease Journal.

"In response to these concerns, the CDC and state health departments initiated surveillance in July, 1992, to detect HIV-seronegative adults and children who had low CD4 lymphocyte counts or percentages," they explained.

According to a report by Salynn Boyles in the July 3 AIDS Weekly, Lobato and co-workers "investigated children identified through surveillance to determine if a retrovirus or other infectious organism was the cause of low CD4 T lymphocyte counts, to estimate the extent of this condition, to learn risk factors if the condition was transmissible, and to describe longitudinal CD4 T lymphocyte measurements in relation to possible opportunistic infections."

Eighteen children were studied; ten were boys, and 14 were black. All had been observed to have a low CD4 cell count in infancy (median age, ten months). According to Boyles, "Three children had opportunistic infections and two still had low CD4 T lymphocyte counts five and seven years later."

In other words, this was not a time-limited condition that had no ill effect upon the children's health.

While 11 of the 18 children with low CD4 cell counts were born to HIV-infected mothers, none was infected with HIV.

Additionally, no other family member (other than, presumably, the mothers) had what Lobato and colleagues determined to be immunosuppressive diseases.

"We conclude that negative retroviral tests and lack of illness among their family members do not support the hypothesis that a retrovirus causes CD4 T lymphocytopenia among these children," Lobato and colleagues wrote in the Pediatric Infectious Disease Journal. "Persistent CD4 T lymphocytopenia well beyond recovery from an opportunistic infection suggests that the immunosuppression may not be the result of the acute infection."

These statements raise a few unanswered questions. For instance: Since when are retroviral infections considered to occur in family clusters, so that the lack of retroviral infections in family members rules out the presence of a new virus?

And which comes first, the chicken or the egg: the "acute infection" or the "opportunistic infection?"

The conventional wisdom about "AIDS" is that the "acute infection," generally assumed to be HIV, weakens the immune system so that "opportunistic infections" can take hold.

Lobato and colleagues, however, are suggesting that what they are calling "opportunistic infections" are causing immunosuppression--not the other way around, as is generally assumed.

Follow-up, Lobato and colleagues conclude, is needed.