The first AIDS cases were diagnosed in 1981 among young homosexual men in the U.S. Although the syndrome was puzzling. it soon became clear that all its victims suffered from a depletion of a specific subset of T cells- T4 cells and that as a result they fell prey to pathogens that would easily be controlled by a healthy immune system. A variety of hypotheses were advanced to explain AIDS. including breakdown of the victims' immune systems following repeated exposure to foreign proteins or even to sperm-during homosexual intercourse. It seemed more plausible. however. to explain a new syndrome by the appearance of a new infectious agent.
To one of us (Gallo) the likeliest agent was a retrovirus. It had already been shown that the AIDS pathogen. like HTLV-I. could be transmitted by sexual intercourse and by blood. Furthermore. Max Essex of the Harvard School of Public Health had shown that a retrovirus of cats called feline leukemia virus (FeLV) could cause either cancer or immune suppression. Since in most species the infectious retroviruses are closely related. it seemed plausible that the same was true in human beings. Hence the initial hypothesis was that the cause of AIDS was a close relative of HTLV-I. That hypothesis. as it turned out. was wrong. Nonetheless, it was fruitful because it stimulated the search that led to the correct solution.
The retrovirus hypothesis for the origin of AIDS reached the other one of us in France in the following way. Almost as soon as AIDS was first diagnosed. a working group on the syndrome had been formed by a circle of young clinicians and researchers in France. One member of the group. Jacques Leibowitch of the Raymond Poincare Hospital in Paris. had had some contact with Gallo's team and carried the HTLV hypothesis back to France. The members of the French group wanted to test that hypothesis. and they had the biological materials to do so because the group included clinicians with patients afflicted by AIDS or pre-AIDS. What they lacked, however, was the collaboration of virologists experienced in work with retroviruses.
The French author of this article and his colleagues Francoise Barre-Sinoussi and Jean-Claude Chermann at the Pasteur Institute fitted that description. They were engaged in several lines of work on cancer and interferon including attempts to find retroviruses in patients with cancer particularly in cultures of lymphocytes. A member of the working group, Willy Rozenbaum of the Salpetriere Hospital, asked whether they were interested in analyzing tissues from a patient with lymphadenopathy. or swollen glands. (Lymphadenopathy can be an early sign of the process that culminates in AIDS. Such a patient was chosen because finding a virus early in the disease seemed more meaningful than finding one later. when AIDS patients were infected with many opportunistic agents.) The answer was yes, and in January, 1983, a specimen from the swollen lymph node of a young homosexual arrived at Montagnier's laboratory.
The specimen was minced. put into tissue culture and analyzed for reverse transcriptase. After two weeks of culture. reverse-transcriptase activity was detected in the culture medium. A retrovirus was present. But which one? The first possibility that had to be tested was whether the virus was one of the known HTLVs. or perhaps a close relative of them. That possibility was tested using specific HTLV-I reagents supplied by Gallo. The virus did not react significantly with the HTLV-I reagents; a similar result was later obtained with HTLV-Il reagents. A strenuous effort was begun to characterize the new agent.
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Add CommentEarly on ciclosporin was used to try and save Rock Hudson just before he died. The Doctors treating him apparently thought what was happening to the immune system resembled rejection or allergic response to self.
Reply | Report Abuse | Link to thisThe response apparently was dramatic. His t-cells skyrocketed in #.
He was too far gone though, for he died very shortly thereafter, and this line of reasoning on how to treat the then unknown viral infection was dropped in favor of pursuing angles the medical establishment favored.
Medical research like all science can be rigid when it comes to trying something new, and trying to re-imagine HIV as a virally induced allergy for experimental treatment's sake just goes against the ingrained accepted notions on what HIV is and how to treat it.
Everything is focused on finding a way to eradicate it from the system or limit its ability to reproduce or a vaccine.
While there were a few incidences of experimentation with ciclosporin beyond Hudson, all were dropped when the patient died. It was considered a "what do you have to lose" option.
Unfortunately, for some odd reason, because ciclosporin did not produce a miracle interested disappeared.
It never was tried in a proper setting where the patients were NOT at death's door, despite evidence that when tried on close to death patients the effects on the immune system was dramatic showing a marked transient jump in T-cells.
Ciclosporin deserves its day in the sun.
Perhaps it can modulate the overactive immune system downward enough so that T-helper cells don't go killing each other confusing each other with HIV, because HIV's coating is a product of the T-Cell outer envelope.
Once slowed down by ciclosporin perhaps the immune system would be more able to appropriately distinguish infected from healthy and properly manage the infection - turning it into a mild chronic infection rather than the killer it still is in many areas.
Of course, the biggest obstacle to even trying this is that ciclosporin is not going to make the big bucks the new anti-virals are, so its in the interest of big pharma to ignore it entirely no matter how positive the evidence is that such medications could play a successful role in managing the HIV infection.