The T-cell Killer HHV-6 May Not Even Need HIV to Destroy The Cells That Prevent Opportunistic Infections

by Neenyah Ostrom
NEW YORK NATIVE/May 22, 1995

What sets off the cascade of events that results in the destruction of the immune systems of "AIDS" patients? Although the putative causal agent of the syndrome, HIV, is believed to orchestrate the immune system's collapse, no one has been able to explain how it does it. Meanwhile, another virus, Human Herpes Virus 6 (HHV-6), has been found to kill immune system cells directly-including T-cells, the loss of which is the agreed-upon hallmark of the syndrome-without any mystery or putative indirect mechanisms that have been attributed to HIV. Now, new research from Robert Gallo's National Cancer Institute of Tumor Cell Biology reveals that HHV-6 infection is required for HIV to be able to infect some T-cells.
Not only is HHV-6 able to infect and kill these T-cells that HIV is unable to infect, these are the very T-cells that are meant to defend against HHV-6 infection. Therefore, HHV-6 is able to elude detection by the immune system by killing these cells. Furthermore, these particular T-cells killed by HHV-6 are also the ones that protect against specific types of bacteria, including the Mycobacterium that causes tuberculosis.
In other words: According to this new research, HHV-6 is not only able to elude detection by the immune system by killing the cells that are meant to defend against the virus, but HHV-6 infection may also be the driving force behind the tuberculosis epidemic that is sweeping the inner cities of the nation.
This research from the National Cancer Institute italicizes the public health tragedy that has been allowed to develop, as billions have been spent unsuccessfully to fight HIV, and very little attention has been paid to HHV-6. HHV-6 is a treatable infection, when it is caught early; it can be controlled by the readily-available drugs foscarnet and ganciclovir, as well as the experimental (and presumably less toxic) drug Ampligen.
But because of the power of the HIV lobby in doling out grant monies, nearly all the anti-"AIDS" research in the U.S. has focused (unsuccessfully) on HIV and on developing (ineffective) anti-HIV drugs.
A collaboration between Paolo Lusso from Gallo's NCI lab and others at the National Institutes of Health examined the "potential role of HHV-6 in AIDS," which is described in their new research report.(1)
These investigators found that the HHV-6 infects a particular subset of T-cells that is "involved in the protective immune response against specific microorganisms"-including HHV-6 itself.
HHV-6 (Variant A) is not only able to infect this subset of T- cells, infection by HHV-6 results, in laboratory studies, in "massive cell death."
In addition to infecting and killing these T-cells, HHV-6 radically alters them: It causes them to secrete the cell surface protein that turns them into CD4 (T4) cells.
This, according to Lusso and colleagues, renders these T-cells newly "susceptible to productive infection by HIV-1."
In other words: HIV is incapable of infecting these T-cells unless HHV-6 has infected them first. (Because of the damage HHV-6 is capable of causing without HIV, one is tempted to say: So what?)
This subset of T-cells has only recently been described, and is called "gamma/delta T-cells."
"These results demonstrate that gamma/delta T-cells can be directly targeted and killed by a herpesvirus and may have implications for the potential role of HHV-6 in AIDS," Lusso and colleagues reported.
This finding raises the question: What is the primary immunosuppressive infection in "AIDS" patients? Is HHV-6 simply loosening the jar's lid so that HIV can remove it?
Or is HHV-6 actually the primary infection that destroys the immune systems of "AIDS" patients?
And if it is, what is this virus doing in other people with active HHV-6 infections-like Chronic Fatigue Syndrome patients?
Lusso is joined in this investigation by NCI colleagues Alfredo Garzino-Demo and Richard W. Crowley, as well as Mauro S. Malnati from the National Institute of Allergy and Infectious Diseases. Their study is published in the April issue of the Journal of Experimental Medicine.(2)
Lusso and colleagues' investigation delves into an arcane and newly-discovered pocket of immunology. It has recently been discovered, they note, that there are two distinct lineages, or families, of T- cells. One is called alpha/beta; the other is called gamma/delta. These two families of T-cells respond to challenges by infectious agents in different ways, which have not yet been entirely elucidated.(3)
The gamma/delta T-cells appear to be capable of responding to viruses, bacteria, and protozoa. In addition, in the laboratory, these T-cells are activated by proteins created in response to an infection- i.e., by the host response, not simply the invading organism itself.
Lusso and colleagues hypothesize that, in living organisms (as opposed to in the laboratoy), these cells' response "to microorganisms may be, at least in part, secondary to the effects that the infection induces in the host, suggesting a possible role of gamma/delta T-cells in the regulation of the immune response and/or in self-reactive immune phenomena."(4)
In other words: Because these cells react to an organism's response to infection, they may play a role in regulating such immune responses to invaders such as bacteria and viruses.
Additionally, it is primarily the gamma/delta T-cells; so, by killing those cells, HHV-6 can elude attack by the immune system.
Lusso and co-authors point out that HHV-6 was the first "T- lymphotropic human herpesvirus" to be discovered. Unlike its close relative HHV-7, HHV-6 is quite deadly to the cells it infects, not only T-cells but also natural killer (NK) cells, B-cells, and monocytes.
Lusso and co-authos put this all into perspective this way: " In all these cell types, HHV-6 induces dramatic cytopathic changes, suggesting that it may act as an immunosuppressive agent in vivo. Moreover, a series of positive viral interactions has been documented between HHV-6 and HIV, the causative agent of AIDS, leading to the hypothesis that HHV-6 may accelerate the natural course of HIV infection in coinfected patients. This concept has been corroborated by the recent demonstration that HHV-6 infection is active and widespread in terminal AIDS patients. Diverse anomalies of both the cellular and humoral arms of the immune system have been reported in patients with AIDS, including gamma/delta T-cell alterations. In this study, we have investigated the susceptibility of gamma/delta T-cells to infection by HHV-6 and the interactions between HHV-6 and HIV in gamma/delta T-cells.(5)"
In their laboratory studies, Lusso and colleagues separated out a population of gamma/delta T-cells (contamination by alpha/beta T-cells was estimated to be less than one percent) and exposed them to HHV-6. After three days, there were signs that the T-cells were infected. After four to seven days, "a growing proportion of gamma/delta T-cells exibited the typical HHV-6 induced cytomorphological changes, consisting of size enlargement, refractile appearance, and loss of blastic shape with the acquision of an evenly rounded cellular profile," according to Lusso et al. "Eventually, the viral cytopathic effect induced widespread cell destruction, resulting in the extinction of the cultures at day 10-12 after infection."(6)
In about 12 days, then, HHV-6 infection resulted in the total destruction of the cell cultures into which the virus was introduced.
Before killing the infected gamma/delta T-cells, HHV-6 decreased the ability of those cells to kill invaders. This loss of function in the T-cells occurred in two to four days.
In other words: Not only does HHV-6 kill these T-cells, it destroys the immune system mechanism that is supposed to kill other invaders.
Gamma/delta T-cells do not ordinarily have the CD4 protein on their surfaces. HHV-6 infection, however, causes them to express this cell surface protein. After nine days of infection, more than 70 percent of the gamma/delta T-cells were expressing the CD4 protein, according to Lusso and colleagues.
HIV uses the CD4 cell protein to infect T-cells. Gamma/delta T- cells are generally resistant to HIV infection. When Lusso and colleagues exposed the HHV-6 infected gamma/delta T-cells (which were producing the CD4 protein) to HIV, however, "they became susceptible to productive infection by HIV-1," they found. When the cells were treated with a substance that inhibited the production of the CD4 protein, HIV was no longer able to infect the cells, "conclusively demonstrating that the HHV-6 induced CD4 was essential for infection of gamma/delta T-cells by HIV-1."(7)
In other words, HIV couldn't even infect these T-cells unless HHV- 6 already had infected them and begun the process of causing their "extinction."
The infection of gamma/delta T-cells by HHV-6 is particularly diabolical, since those cells help to defend against invasion by the virus. By infecting these cells, Lusso and colleaues write, "HHV-6 may seek to escape the immune control of the host and thereby establish persistent infection." They note that HHV-6 "can infect and kill several critical elements of the immune system," suggesting the virus "may have broad immunosuppressive effects."(8)
And, in what may be an even more sinister development, Lusso and colleagues suggest that it is HHV-6, not HIV, that is driving the tuberculosis epidemic.
While HHV-6 has been shown to be associated with potentially life- threatening conditions such as encephalitis, pneumonitis, and bone marrow suppression, in "AIDS" patients, "HHV-6 has been suggested to play a more substantial pathogenetic role," according to Lusso and co- workers.
For instance, "Diverse clinical and experimental observations indicate that HHV-6 may contribute, directly or indirectly, to the destruction of CD4-positive T-cells, a pathological hallmark of AIDS, and thereby expedite the course of the disease."(9)
In particular, "Damage to gamma/delta T lymphocytes could predispose patients to infection by specific microorganisms that these cells help to control, including some (e.g. Mycobacteria [that causes tuberculosis]) that are in important cause of morbidity and mortality in AIDS."
Lusso, along with Gallo, has previously suggested in the medical literature that HHV-6 may play a more primary role in causing "AIDS" than is generally appreciated.
In the March 5, 1994, issue of The Lancet, Lusso and Gallo wrote an editorial that accompanied a research report by Medical College of Wisconsin researchers Konstance K. Knox and Daniel R. Carrigan. Knox and Carrigan noted that "HHV-6 has been proposed as a cofactor in the pathogenesis of AIDS." They decided to evaluate "the frequency of active HHV-6 infections in patients who died with AIDS."(10)
Knox and Carrigan found that 100 percent (34 of 34) of the autopsy tissues from "AIDS" patients tested were positive for HHV-6 infection, compared to only nine of 34 positive for cytomegalovirus infection.(11)
Knox and Carrigan found HHV-6 infections in the lungs, kidneys, livers, spleens, and lymph nodes of the patients studied. They suggested that HHV-6's ability to infect lymphocytes could not only help spread infection throughout the body, but also contribute to the destruction of lymphocytes in "AIDS" patients: "An HHV-6 infected lymphocyte within an area of inflammation could transfer infection to other lymphocytes newly recruited into the lesion which, when combined with immunosuppressive result of CD4 lymphocyte destruction by the HHV- 6 infection, could perpetuate inflammation and lead to significant systemic consumption of lymphocytes."(12)
In their accompanying editorial, Lusso and Gallo point out "That HHV-6 could contribute to the striking depletion of CD4 T-cells seen in patients with AIDS was suggested by us more than five years ago. We made this proposal after observing that HHV-6, unlike cytomegalovirus or other putative cofactors in AIDS, shares with HIV a primary tropism for CD4 T-cells and can productively coinfect with HIV individual target lymphocytes, causing accelerated cytopathic changes..."(13)
Because of all the destruction HHV-6 is known to be able to inflict on the immune system, Lusso and Gallo suggest that "it may have detrimental effects on the immune sytem and expedite progression of the disease [AIDS]."(14)
Is HHV-6 merely "expediting" the progression of "HIV disease," as these HIV investigators suggest?
Or, as HHV-6 researchers like Knox and Carrigan have been showing, is HHV-6 infection more primary to "AIDS" than has been previously acknowledged?
REFERENCES
  1. Lusso, Paolo, Afredo Garzino-Demo, Richard W. Crowley, and Mauro S. Malnati; "Infection of Gamma/Delta T Lymphocytes by Human Herpesvirus 6: Transcriptional Induction of CD4 and Susceptibility to HIV Infection"; Journal of Experimental Medicine 181:1303, April 1995.
  2. Ibid.
  3. Lusso et al., op cit.
  4. Lusso et al., op cit.
  5. Lusso et al., op cit.6. Lusso et al., op cit.
  6. Lusso et al., op cit.
  7. Lusso et al., op cit.
  8. Lusso et al., op cit.
  9. Knox, Konstance Kehl and Donald R. Carrigan; "Disseminated Active HHV-6 Infections in Patients With AIDS"; The Lancet 343:577, March 5, 1994.
  10. Ibid.
  11. Knox and Carrigan, op cit.
  12. Lusso, Paolo and Robert C. Gallo; "Human Herpesvirus 6 in AIDS"; The Lancet 343:555, March 5, 1994.
  13. Ibid.
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If HHV-6 is the real cause of AIDS, here are some of the implications:

1. HIV is a massive scientific fraud. Something akin to a Ponzi scheme. Scientists who challenged the HIV theory of AIDS (the ones who have been thuggishly censored and silenced) turn out to be on the money.

2. Chronic Fatigue Syndrome and Autism (and many other so-called HHV-6 related mysterious epidemics) are part of the so-called AIDS epidemic.  Chronic Fatigue Syndrome and Autism both are clearly the results of the ravages of HHV-6.

3. AIDS and Chronic Fatigue Syndrome has been artificially and politically separated into two epidemics. We are living in a period of CFS/AIDS apartheid. So-called AIDS patients have to sit in the back of the HHV-6 epidemic bus while the befuddled HHV-6/CFS patients and HHV-6/Autism victims sit up front. Nobody is well-served.

4. AIDS is not a sexually transmitted disease. That paradigm has set a scapegoating and antigay agenda in place that the public thinks is solidly based on science. It is only based on homophobic and racist nosology, epidemiology and virology. The scientists behind the paradigm are charlatans and crooks.

5. The Centers for Disease Control in Atlanta and the Pasteur Institute in Paris have a great deal in common with the institutions of Nazi medicine. For Blacks, everything these institutions have done in the name of AIDS really constitutes a second Tuskegee Syphilis Experiment.

Elements of a Scientific Ponzi Scheme like the Montagnier-Agut HIV Fraud Ponzi Scheme and HHV-6 Cover-up

A scientific Ponzi scheme begins with a central seminal or foundational scientific fraud and is  sometimes built on an infrastructure of smaller scientific frauds. Like the fake dividends issued in a strictly financial Ponzi scheme, a scientific Ponzi scheme issues fake dividends in the form of ongoing fraud-based research often framed as "breakthroughs" and bogus extrapolations which make it look like everything is above board and that what, in reality, is scientific fraud, appears to the rest of the scientific community and the public as good faith progress.

A classic scientific Ponzi scheme like the Montgnier-Agut HIV Fraud Ponzi Scheme and HHV-6 Cover-up include elements like these:

1. Nosological fraud.

2. Epidemiological fraud.

3. Virological fraud.

4. Treatment fraud.

5. Public health policy fraud.

6. Concealment of negative scientific data and paradigm-challenging anomalies.

7.  Use of an elite network of "old boys" and pseudo-activist provocateurs to censor critics and whistleblowers.

8. Chronic obscurantism.

9. If necessary, vigilantism and witch-hunts against any intellectuals, scientists, or citizens who constitute any form of resistance to the Ponzi scheme.

10. A subservient scientific press that is used as a conveyor belt for the Ponzi scheme's propaganda.

Everything always looks like it is working perfectly in a Ponzi scheme, until the moment comes when someone look at the books and blows the whistle.  Hopefully, that game-changing moment for the Montagnier-Agut HIV Fraud Ponzi Scheme and HHV-6 Cover-up is coming soon.



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