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Retrovirusgate

Blog entry posted by JPV, Jan 22, 2010.

New York Native
November 28, 1994

RETROVIRUSGATE
by Neenyah Ostrom


Have all the retroviral findings in Chronic Fatigue Syndrome been derailed because they resemble HIV just a little too closely?

Whatever happened to the "Chronic Fatigue Syndrome retrovirus?" The research, which seemed so promising in 1990 when the virus's discovery was announced at a conference in Kyoto, Japan, seems to have since dwindled into nothingness.

Is that because there was actually no discrete retrovirus to be found? Or is it because the retrovirus that was discovered resembled HIV just a little too closely?

If a form of HIV were identified in CFS patients, that would negate one of the major arguments that CFS is not part of the "AIDS" epidemic.

Is that why the "CFS retrovirus" research has, apparently, been abandoned?

Results from the search for a "CFS retrovirus" were first announced at the 11th International Congress of Neuropathology in Kyoto, Japan, on September 4, 1990. The three scientists announcing the retroviral finding were Elaine DeFreitas, an associate professor at the Wistar Institute (Philadelphia), along with CFS researchers Paul Cheney (Charlotte, North Carolina) and David Bell (Lyndonville, New York).

According to the press release issued by the Wistar Institute, the three scientists announced that "A possible link has been found between the illness known as chronic fatigue syndrome (CFS) and a member of the human T-cell lymphotropic virus (HTLV) family of retroviruses- viruses that use RNA to make DNA."(1)

Noting that the HTLV family of viruses "is linked with" some T-cell cancers like leukemia and lymphoma, as well as with chronic diseases of the central nervous system, the Wistar press release states that the "virus that might be implicated in CFS is similar, but not identical, to HTLV-II, a retrovirus discovered by Dr. Robert C. Gallo."

At the Kyoto conference, DeFreitas and colleagues reported that 82 percent of 11 adult patients and 74 percent of 19 pediatric patients had viral sequences indicative of HTLV-II infection in blood cells. None of 20 healthy control subjects (adults and children) showed evidence of infection.(2)

One of the more disturbing findings reported in Kyoto was that "people who were in relatively close but casual (non-sexual) contact either with the pediatric or adult patients, and who themselves had no symptoms of CFS, nonetheless also showed the HTLV-II-like viral sequences in their blood, with 43 percent of adult exposure controls and 29 percent of pediatric exposure controls testing positively."(3)

At a press conference in San Francisco on September 5, 1990, DeFreitas explained that the research group did not believe their "CFS retrovirus" to be "prototypic HTLV-II." The virus is either a "variant of HTLV-II," DeFreitas said, or "a totally different virus that just shares these particular gene sequences with HTLV-II."(4)

DeFreitas and colleagues had not, at this point, isolated an entire virus, as she pointed out, but only identified viral fragments. She also anticipated difficulty in isolating the whole virus: "One cannot isolate this virus like one can isolate HTLV-I," DeFreitas remarked in San Francisco. "We've tried that, it doesn't work....Many of these patients are infected with a variety of herpes viruses, not the least of which is HHV-6, which really wreak havoc on the cells after two days in culture...."(5)

DeFreitas thought, however, that the virus could be characterized within a year of September 1990.(6)

DeFreitas also addressed the implication of finding the virus in "exposure controls"-that this human retrovirus, unlike any other, might be casually transmitted-by commenting that there are no known human retroviruses that are transmitted casually.(7)

The Kyoto meeting and the San Francisco press conference resulted in major press coverage for CFS in early September 1990, including stories in the New York Times, USA Today, Newsweek, Philadelphia Inquirer, Boston Globe, Toronto Star, Montreal Gazette, San Francisco Chronicle, and the Charlotte Observer, among others.

In April 1991, a formal report of the retroviral findings was published by DeFreitas, Cheney, Bell, and eight colleagues in the Proceedings of the National Academy of Sciences USA.(8)

"Although our data support an association between an HTLV-like agent and CFIDS, we cannot, as yet, define the agent's role in the disease process," DeFreitas and colleagues' PNAS report concludes. "Rather than an etiologic agent, it may be a benign secondary infection to which immunologically compromised patients are susceptible. Alternatively, it may be one of two viruses that, when coinfecting the same hematopoetic cells, induce immune dysfunction. In any case, biological characterization of this agent and its role in the pathogenesis of CFIDS awaits its isolation."(9)

And here the "CFS retrovirus" story appears to have come to a complete halt.

None of the questions raised by DeFreitas and colleagues-or anyone else-about the virus has been answered to date.

What happened?

The Summer 1993 issue of the CFIDS Chronicle attempted to answer that question. K. Kimberly Kenney began an overview of the retroviral research by noting that "CFIDS has been compared to early HIV disease because of similarities between the two illnesses." She continued:

In fact, AIDS is one of the diseases that must be ruled out when making a diagnosis of CFIDS because of the number of shared symptoms including: fatigue, fever, sweats, sore throat, lymph node pain, headache, muscle and joint pain, diarrhea and abdominal discomfort. Cognitive difficulties are also reported by those with these diseases: difficulty concentrating and with word finding and calculating, emotional lability, impaired judgment and memory loss. Neurologic complaints are similar as well: dizziness, visual disturbances, weakness, sensory changes, abnormal gait, parasthesias and sometimes seizures.... The overwhelming similarities between these two diseases add weight to the theory that CFIDS may be caused-in part or whole-by a retrovirus.(10)

Despite the apparent promise of the retroviral theory, efforts to reproduce DeFreitas and colleagues' findings were unsuccessful. A commercial laboratory, Oncore Analytics(Houston), attempted to replicate the discovery of HTLV-II related gene sequences in CFS patients. Oncore's Dr. C.V. Herst was "privately reporting" by summer 1991 that he had "confirmed the presence of a new virus with genes related to the HTLV-II virus or, possibly, a defective or incomplete HTLV-II virus in patients with CFIDS," according to Kenney.(11)

Herst's assay was not identical to DeFreitas's, however, and there was some question about whether Herst's results were "a true confirmation of the Wistar findings," Kenney reports.(12)

Meanwhile, other investigators- including Jay Levy at the University of San Francisco, California, and scientists at the Centers for Disease Control-were unable to duplicate DeFreitas and colleagues' work.(13)

At an October 1992 CFS conference in Albany, New York, CDC's Walter Gunn and Walid Heineine reportd their inability to replicate DeFreitas's work. Heineine summarized the CDC scientists' results by commenting, "Our data indicates that the tested retroviruses do not appear to have an etiological or cofactor role in the chronic fatigue syndrome of our study population."(14)

DeFreitas, who had just relocated to the University of Miami, defended her work and asserted that the CDC investigators had modified her assay in ways that prevented it from working properly. A heated discussion ensued, according to Kenney's report.(15)

In March 1993, the CDC investigators published a formal report of their inability to replicate DeFreitas's findings in the agency's Morbidity and Mortality Weekly Report.(16)

"None of the three assays [used to test for the presence of a retrovirus] could differentiate between case-patients andcontrols in either the combined study population or any of the individual study populations," Walter Gunn and his co-workers reported in the MMWR.(17)

DeFreitas again defended her work in the Summer 1993 CFIDS Chronicle, but was unable to report any more definitive results that would absolutely refute her critics.

DeFreitas and colleagues have not published any further data concerning their retrovirus. During the last year, in fact, the silence surrounding the "CFS retrovirus" has grown almost deafening.

During that period of time, however, an array of "mutant" or "defective" HIVs have been detected. These "defective" HIVs have been blamed for just about every anomaly in the HIV theory of "AIDS," from false results on HIV antibody tests, to long-term survival of HIV-positive individuals, to AZT resistance.

One of the arguments that is generally advanced to explain why CFS cannot be a part of the "AIDS" epidemic is that CFS patients are not infected with HIV.

All "AIDS" patients are not infected with HIV, either, but government scientists are concealing that fact by calling non-HIV "AIDS" by another name, idiopathic CD4-positive lymphocytopenia (ICL).

What would happen if the public realized that not only are there "AIDS" cases in which HIV does not appear, but also that millions of CFS patients are infected with a retrovirus that is related to, or actually a type of, HIV?

Is it possible that the "CFS retrovirus" disappeared from the radar screen because it too closely resembled a "defective"or "mutant" HIV? Could this new retrovirus actually be a previously undetected HIV, like the Group O HIV that is not identified by the standard HIV antibody test?(18) Or might it be a newly-discovered HIV-i.e., HIV-3?

In fact, such a possibility was suggested a couple of years ago by Victoria Brownworth, writing in the now-defunct New York City magazine QW. Brownworth noted that the presence of a retrovirus in some CFS patients tied the epidemic to "AIDS," but not, she argued, in the way the Native suggests. Brownworth asks, "What causes CFIDS?" She then provides an answer, based on the facts selected by her in September 1992:

The hypotheses vary, but only slightly. CFIDS is linked to HIV through CEBV (Chronic Epstein-Barr Virus), CMV(Cytomegalovirus), and HBLV(Human B-Cell Lymphotropic Virus [i.e., HHV-6])-three viruses that are generally believed to play a causal role in the breakdown of the immune system in both AIDS and CFIDS. In fact more than a few researchers theorize that CFIDS is a form of AIDS. This is not to say as the New York Native obsessively suggests, that CFIDS is AIDS, but that the two retroviruses are linked in ways that virologists and immunologists have yet to discover. That CFIDS, like HIV, is retroviral in nature has been extensively studied by the Wistar Institute's Dr. Elaine DeFreitas, who isolated the DNA that is widely viewed as the causative agent. DeFreitas found many commonalities between the HIV virus and the CFIDS virus in terms of both retroviral structure and pathogenesis. But these links, which suggest many possibilities for new research on diagnosis, treatment, and cure for CFIDS, have been virtually ignored bye the CDC...(19)

Although Brownworth is the only writer to report this information, it raises a very interesting question: Did DeFreitas find "many commonalities" between the CFS retrovirus and HIV before the work essentially dropped from sight?

In the Summer 1993 CFIDS Chronicle, DeFreitas suggested that her "HTLV-II like virus" may be "defective," or even "endogenous (i.e. genetically inherited)."(20)

She also suggested that CFS may develop only in people who are co-infected with not only the " CFS retrovirus," but also "a ubiquitous virus such as a herpes-virus such as EBV or HHV-6."(21)

DeFreitas noted the interaction between HHV-6 and retroviruses such as HIV. In early 1992, scientists at Case Western Reserve University (Cleveland) showed that retroviruses like HIV and DNA viruses like HHV-6 are able to exchange genetic material.

Gallo and others have hypothesized that co-infection with HIV and HHV-6 enhances the ability of HIV to cause immune dysfunction.

But in light of the damage that HHV-6 is capable of inflicting on immune system cells- and other types of cells, like those in the nervous system- is the additional presence of HIV or any other virus necessary to produce immune system malfunction?

Is the presence of a retrovirus-HIV, HTLV-II, or something else-just a red herring, in both "AIDS" and CFS?

The Case Western research team, headed by Hsing-Jien Kung, reported the interaction of two viruses common in chicken, one a retrovirus and the other a herpesvirus, in the Proceedings of the National Academy of Sciences USA.(22)

Kung and colleagues concluded, "We would predict integration in other systems where coinfection of the same target cell by both viral types takes place (e.g., HIV and human herpesvirus 6)." Such interactions, they suggest, "may have important clinical implications."(23)

In her report of these findings in New York Newsday, Laurie Garrett interviewed Robert C. Gallo, the National Cancer Institute scientist who claims that both HIV and HHV-6 were isolated in his laboratory.

"Gallo said yesterday that it is 'very, very common' to see cells of AIDS patients that are simultaneously infected with HHV-6 and HIV," Garrett reported.(24)

"It seems wherever HHV-6 is going, you're bound to bump into HIV," Gallo told Garrett. "It's like a cohabitation..."(25)

In his 1991 scientific autobiography, Gallo also discussed how HHV-6 contributes to HIV's pathogenesis:

But it was not just that HHV-6 so efficiently infected the CD4-positive T4 helper lymphocyte that made it of interest. Lusso showed that it killed these cells even more efficiently than HIV when it actively replicated in them. Double infection with HIV plus HHV-6 gave a synergistic effect, killing more T4 cells than the additive effect of each of these viruses alone.(26)

HHV-6, Gallo hypothesized, "is also likely to be a contributing factor to the development of AIDS-not necessary, but perhaps speeding the progressive immune impairment."(27)

But, again, considering the damage HHV-6 is known to inflict, is HIV necessary for serious , even life-threatening, disease to develop in a person with an active HHV-6 infection? Recent research has answered that question with a pretty definitive "no."

All of this rather begs the question of whether the DeFreitas retrovirus is related to HIV-scientifically, at least.

But CFS and "AIDS" do not exist primarily in a scientific environment; they exist, for the most part, in an extremely political environment.

While it might be scientifically advantageous to learn that the retrovirus infecting some CFS patients is a mutant HIV, it would be politically disastrous.

For instance, what behaviors would heterosexual, non-IV drug-using, white men and women and children-the people most likely to be diagnosed with CFS instead of "AIDS"-be told to change?

What would happen if the "risk groups" turned out to be all Americans, and the most dangerous "risk behavior" was one that resulted in accidental exchange of saliva (like eating from an improperly washed fork)?

The "CFS retrovirus" might turn out to be a great deal more hazardous politically than it is clinically-especially if it is identified as a form of HIV.

References

1. Wistar News Release; "Possible Retroviral Link Found in
Patients With Chronic Fatigue Syndrome"; issued September 4,
1990.
2. Ibid.
3. Wistar News Release, op cit.
4. CFIDS Chronicle Special Issue; "Research Breakthrough!";
September 1990.
5. Ibid.
6. CFIDS Chronicle, op cit.
7. CFIDS Chronicle, op cit.
8. DeFreitas, Elaine et al.; "Retroviral Sequences Related to
Human T-Lymphotropic Virus Type II in patients With Chronic
Fatigue Immune Dysfunction Syndrome"; Proceeedings of the
National Academy of Sciences USA 88:2922, April 1991.
9. Ibid.
10. Kenney, K. Kimberly; "The Elusive CFIDS Retroviruses"; CFIDS
Chronicle, Summer 1993.
11. Ibid.
12. Kenney, op cit.
13. Kenney, op cit.
14. Kenney, op cit.
15. Kenney, op cit.
16. Gunn, W.J. et al.; "Inability of Retroviral Tests to Identify
Persons With Chronic Fatigue Syndrome, 1992"; Morbidity and
Mortality Weekly Report, Vol. 42, No. 10, March 19, 1993.
17. Ibid.
18. Schable, Charles et al.; "Sensitivity of United States HIV
Antibody Tests for Detection of HIV-1 Group O Infections"; The
Lancet 344:1333, November 12 1994.
19. Brownworth, Victoria; "CFIDS: The Invisible Health Crisis";
QW, September 13, 1992.
20. DeFreitas, Elaine; "DeFreitas on Her Study Results"; CFIDS
Chronicle, Summer 1993.
21. Ibid.
22. Isfort, Robert, Dan Jones, Rhonda Kost, Richard Witter,
and Hsing-Jien Kung; "Retrovirus Insertion into Herpesvirus
In Vitro and In Vivo"; Proceedings of the National Academy of
Sciences USA 89:991, February 1992.
23. Ibid.
24. Garrett, Laurie; "Viruses Swap Genetics in Cells"; New York
Newsday, February 2, 1992.
25. Ibid.
26. Gallo, Robert: Virus Hunting: AIDS, Cancer, and the Human
Retrovirus: A story of Scientific Discovery; A New Republic
Book (HarperCollins Publishers), 1991.,p.253-4.
27. Ibid.