Gerry, I didn't intend the post as a attack on Neenyah's personal choices rather her objectivity. Follows find a pertinant article from THE INFECTIOUS DISEASE WEEKLY.
Towards the end is a discussion with AID's researcher Steve Strauss, indicating his different opinion from Neenyah. I believe Neenyah is a journalist writing for the magizine New York Native (not sure of their content and platform) and not a researcher. Apparently Ablashi one of the discoverers of HHV-6 cites in vitro (I think it means in a test tube) studies from his time with Gallo at NIH. However according to Strauss CDC studies failed to bear out the theories that have been put out their.
Copyright 1996 Information Access Company,
a Thomson Corporation Company
IAC (SM) Newsletter Database (TM)
Charles W Henderson
Infectious Disease Weekly
January 15, 1996
SECTION: ISSN: 1065-6073
LENGTH: 1093 words
HEADLINE: Cofactors (HHV-6) AZT Enhances HHV-6 Cell Killing, Scientist Tells Magazine
BODY:
The co-discoverer of human herpesvirus type 6 (HHV-6) says zidovudine (AZT) enhances the growth and T-cell killing activity of the virus.
Dharam V. Ablashi and Syed Zaki Salahuddin discovered HHV-6 in 1986 while working in Robert Gallo's laboratory at the National Cancer Institute. Ablashi, now with Advanced Biotechnologies Inc., Columbia, Maryland, made the remarks in an interview published in the magazine The New York Native.
According to the transcript of the interview with Native writer Neenyah Ostrom, Ablashi said, "Now, AZT in fact enhances the growth of HHV-6 rather than stopping it."
Closely related to human cytomegalovirus (CMV), HHV-6 preferentially infects - and is capable of destroying - CD4(+) T cells. This cytopathic effect is dramatically increased in cells coinfected with HIV; HHV-6 is also capable of upregulating HIV expression. There is also evidence that HHV-6 not only infects natural killer (NK) cells, but also renders them susceptible to HIV superinfection.
According to the transcript of the interview with Ablashi, Ostrom asked:
"I haven't heard that before - AZT enhances the growth of HHV-6?"
Ablashi replied, "We have some evidence, in vitro, that if you take AZT and put it onto HHV-6 infected cells, it will enhance their growth, and their cytopathic effects become faster, rather than becoming blocked."
Ostrom asked, "So AZT actually makes HHV-6 kill cells faster?"
Ablashi replied, "Yes. So that hypothesis works this way: if the AZT kills those cells that are CD4 positive, carrying the HIV virus, and those cells, if they also carry HHV-6 - when they get killed, then there's more HHV-6 now freed from the cells in the body."
Ostrom asked, "Because the HHV-6 is released by the cells, when the cells die?"
Ablashi replied, "Yes. Then what happens to that cell-free virus in the body is that it stimulates the immune system. Then you see more antibodies produced against HHV-6."
Ablashi went on to describe experiments he credited to Mark Kaplan of North Shore University Hospital, New York. In these experiments, Ablashi said, Kaplan measured HHV-6 antibody titers in 20 AIDS patients prior to initiation of AZT therapy. After therapy, Ablashi said, the HHV-6 titers went from baseline values of 160 to 320 to values as high as 10,000.
"So that explains what is happening there," Ablashi told Ostrom.
Ostrom later asked whether anyone in Gallo's Laboratory of Tumor Cell Biology had studied the purported AZT/HHV-6 interaction.
Ablashi replied: "That work was done in Dr. Gallo's lab by myself and Dr. Howard Streicher. He was the one who was doing the work on AZT, and found that it did not show any inhibition of HHV-6. And we saw, instead of inhibition, a modest increase in the cytopathic effect of HHV-6."
Ablashi subsequently said that a 1988 paper published by Streicher and himself described these experiments but did not report enhancement of HHV-6. As Ablashi noted, none of the experiments purported to show AZT enhancement of HHV-6 growth or cytopathicity have been published in the scientific literature.
A remarkable fact about HHV-6 is that at least nine out of 10 adults have been exposed to one or both of the two known subtypes of HHV-6.
Nearly all immunocompetent people exposed to the virus appear capable of mounting an effective immune response. Indeed, the virus cannot be regularly cultivated except during acute infection or from immunocompromised patients.
In immunocompromised patients, reactivation of latent HHV-6 can be a major problem, although the extent of HHV-6 associated pathology in transplant patients remains controversial.
A recent series of autopsies demonstrated that HHV-6 is widely disseminated in late-stage AIDS; indeed, one patient was shown to have died of HHV-6 pneumonitis similar to that seen in a bone-marrow-transplant patient.
Studies presented at the 1994 X International Conference on AIDS provided evidence that 1) HHV-6 is reactivated in people with HIV infection, 2) that the degree of reactivation increases with HIV disease progression, 3) that HHV-6 makes a major contribution to AIDS by activating latent HIV and contributing to lymphadenopathy, and 4) that HHV-6 may contribute to AIDS retinitis.
HHV-6 also has been associated with atypical lymphoproliferation, unclassified collagen vascular disease, chronic fatigue syndrome, rheumatoid arthritis, and systemic lupus erythematosus. It is unclear whether HHV-6 is involved in the etiology or pathogenesis of these conditions, or whether it is reactivated by an underlying immunodeficiency.
In an address to a session on emerging diseases at the 1995 Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC), NIAID researcher Stephen Strauss discussed HHV-6 in a lecture titled "The New Lymphotropic Herpesviruses."
Strauss noted that the two subtypes of HHV-6 are more closely related than herpes simplex virus types 1 and 2, sharing 75 to 90 percent of the same DNA sequences.
"They are very similar agents and there is yet to be a decision as to whether these should be split off," he said. "These two types have different epidemiological relationships as well. It's possible that these will be renamed and that herpes 7, herpes 8, herpes 9 and things like that may emerge."
While noting that HHV-6 co-infection of lymphocytes enhances HIV infection, Strauss doubted that the herpesvirus could play a major role in AIDS pathogenesis.
"HIV and HHV-6 can infect the same CD4(+) T-cell, but prospective studies have not shown the kinds of epidemiologic association one would think would be seen if these viruses had an intimate relationship in the progression of HIV," he said. "There has not been a good correlation between HHV-6 antibody titers and HIV disease progression, and levels of HHV-6 in the blood has not been increasing as CD4 counts fall. So this remains a purely theoretical issue."
Strauss also doubted whether HHV-6 is implicated in the pathogenesis of chronic fatigue syndrome, a theory favored by Ablashi and championed by Ostrom and by the editorial policy of the New York Native.
"There have been two or three reports arguing that chronic fatigue syndrome is associated with active HHV-6 infection, and there was an article to this effect in the Annals of Internal Medicine about three years ago," Strauss said at the 1995 ICAAC. "A very good, prospective, well-controlled study by the CDC and by some other groups failed to bear any of that out." - by Daniel J. DeNoon, Senior Editor
COPYRIGHT 1996 Charles W Henderson
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