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HIV is notorious for its ability to change, or mutate, and thereby evade the effects of drugs. Many drugs used to treat HIV interfere with the virus' reverse transcriptase (RT) enzyme, slowing the viral growth rate. Mutations in HIV's RT gene produce an RT enzyme uninhibited by the drugs, allowing the virus to begin growing again.
These mutations result in the exchange of one of RT's many amino-acid building blocks for another. Because such mutations typically enable the virus to resist only one specific RT-inhibiting drug, the patient can still take other RT inhibitors.
Originally posted by GradyPhilpott
You're a nurse, Fred, and I'm a Social Worker, so I'm obviously outgunned here, but the infections you named are bacteria and HIV is a virus.
HIV mutation depends on Fuzeon for replication
Last Updated: 2004-12-02 15:36:19 -0400 (Reuters Health)
NEW YORK (Reuters Health) - In an HIV-infected patient undergoing treatment with the fusion inhibitor T20 (enfuvirtide; Fuzeon), researchers have documented the development of HIV resistance mutations that actually depend on T20 for replication.
In the November issue of the Journal of Virology, Dr. Chris E. Baldwin of the University of Amsterdam and colleagues performed a genetic analysis on the entire HIV-1 envelope glycoprotein 41 ectodomain from a patient who failed T20 therapy.
The investigators discovered T20 resistance mutations in both the HR1 and HR2 domains of the envelope glycoprotein. "Surprisingly," the authors report, "we demonstrate that an HR1-HR2 double mutant (GIA-SKY), which dominates the viral populations after 32 weeks of therapy, is not only highly resistant to T20 but also critically dependent on the T20 peptide for its replication."
The researchers propose several mechanisms for T20-dependent viral entry. The most likely explanation for the T20-dependent mutant, they believe, is that it is "more prone to undergo the conformational switch that results in the formation of the fusogenic six-helix bundle structure in the envelope glycoprotein 41."
Originally posted by swintersVT
A great fear of mine is that hiv will become airborne and spread via airport infrastructure.
"If HIV underwent all the necessary changes allowing it to infect through aerosolized droplets, he [Howard M. Temin of the University of Wisconsin, Madison] asserted, "then we might have a virus that could spread by a respiratory route, but it would no longer cause AIDS. So it would be worse in the sense that it might be more contagious, but it might just be another cold virus."
"I don't share your confidence about what can and cannot happen," Lederberg replied. Blood-borne HIV commonly infects macrophages, a kind of white blood cell often present in the lungs, he noted. Even a minor mutation might enable HIV to infect those cells directly via the respiratory tract.
Temin shook his head. Anything may happen in the future, he conceded, but "you don't have to stay up nigths worrying about it."
Replied Lederberg, somewhat ominously: "I'm glad I worry enough for both of us, Howard."
The Spongifrom Encephalopathy (SE) is a lesion, described for the human beings in the Creutzfeldt Jacob disease (CJD), the Gerstmann-Straüssler-Scheinker syndrome, the fatal familial insomnia, the Kuru, and for the animals, particularly in the frame of the epidemy of Bovine Spongiform Encephalopathy (BSE), responsible for the actual crisis of mad cow. The pathologic form of prion (mutated form) would be the causal agent of these SE (SB. Prusiner, 1981). Other authors (L. Manuelidis, 1995) have suggested that a retrovirus (not yet identified) could intervene as a causal agent.
SE lesions have been described on histological sections from the brain of a patient suffering from AIDS dementia (J. Schwenk, 1987). These lesions have been since described (J. Artigas, 1989) for 5 other HIV+ patients. However, a publication recently reported 67 cases of SE on 200 autopsies of patients dead of AIDS (AJ Martinez et coll., Path. Res. Pract. 191, 427-443, 1995).
This lesion appears not to be an epiphenomenon, but maybe a major component of AIDS.
Mad Cow Lesions in AIDS
Originally posted by GradyPhilpott
I'm not disagreeing with Soficrow. I just would like to know how this came to be such an interest for him and whether or not he works in a field that puts him in a position to have such an well-organized overview of the problem and a generally pessimistic view of all things prion.
Originally posted by DrHoracid
Hey, leatherneck, the more you research prions, the more you become pessimistic. I've been working on a way to kill them for years. Ebola is easier to kill. It's like a "hidden" epidemic already.