NEWS: Rare Drug-Resistant HIV Found in N.Y., page 1
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Topic started on 11-2-2005 @ 10:11 PM by GradyPhilpott
A rare strain of HIV has been discovered in New York. It is the only known case in the world. What makes this strain unique is that, not only is it resistant to three drug regimens, the course of infection to AIDS is measured in months, not years or decades.




www.comcast.net
New York's first diagnosed case of highly drug-resistant HIV in a person never before treated for the virus is "a wake up call" to anyone who has unprotected sex, the city's health commissioner said Friday.

The patient, a man in his mid-40s who had unprotected sex with other men, contracted a strain of HIV that is "difficult or impossible to treat and which appears to progress rapidly to AIDS," said the Health Commissioner Dr. Thomas Frieden.

The diagnosis "is a wake up call to men who have sex with men," Frieden said at a news conference.

The commissioner said the city's health authorities are working with the federal Centers for Disease Control in Atlanta to find other possible cases of the drug-resistant HIV strain that quickly turns into AIDS.




Please visit the link provided for the complete story.


I have been saying to anyone who will listen to me that HIV is the "smartest" virus ever known, in that it mutates so rapidly and, seemingly so specifically, and that efforts to eradicate it seem to have only one effect --to expedite mutation. That's why I feel that throwing money at the epidemic in Africa is a monumental waste. The only way known to control this virus is to alter behavior. Drug cocktails that cost tens of thousands of dollars per year are only hastening the mutation of the virus. I don't mean to sound cold, but it seems that the only way to conquer AIDS is to get everyone who doesn't have it to alter their behavior to reduce the likelihood of infection to nearly nil (nothing is absolute) and for those who have it to die, not murdered, but allowed to live out their days without extreme intervention.


[edit on 05/2/15 by GradyPhilpott]


reply posted on 11-2-2005 @ 10:51 PM by GradyPhilpott
Fred

Here is an article published in December that illustrates just what I mean. In the world of organisms and bacteria, mutant strains come and go perhaps without much notice. Bad mutations may die out and good mutations may have to wait for some mutation in another species or some other disaster to ever be known. Cockroaches become immune to insecticides because only the immune cockroaches are left to reproduce and someone has to come up with a better insecticide.

This article tells how a strain of HIV has arisen that requires an HIV drug to replicate. I have never heard of a cockroach that needs diazinon to reproduce.



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."



[edit on 05/2/11 by GradyPhilpott]


reply posted on 12-2-2005 @ 12:10 AM by soficrow
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FYI - A few articles to consider re: the appearance of this new form of AIDS.

[Note: Infectious prions are proteins - and capable of infecting viruses, bacteria and other microbes, not just animals.]


This 1986 paper describes how "proteinaceous capsids" (prions) use viruses as vehicles of transmission...
* "Viral influences on aflatoxin formation by Aspergillus flavus." Appl Microbiol Biotechnol 24:248-252. Schmidt FR, Lemke PA, Esser K (1986)


"Epidemiological observations indicate that a microbial vector is responsible for the transmission of natural prion disease in sheep and goats … ...It is proposed that many microbial proteins may be capable of replicating themselves in mammalian cells eliciting and sustaining thereby degenerative and/or autoimmune reactions subsequent to infections with microorganisms."
* Med Hypotheses. 1999 Aug;53(2):91-102. Is the pathogen of prion disease a microbial protein? Fuzi M. Budapest Institute of National Public Health and Medical Officer Service, Hungary. PMID: 10532698


* Dangerous liaisons between a microbe and the prion protein. J Exp Med. 2003 Jul 7;198(1):1-4. Aguzzi A, Hardt WD. PMID: 12847133




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





"According to a study from France, "...the human PrPc was shown to possess nucleic acid binding and chaperoning properties similar to human immunodeficiency virus type 1 (HIV-1) nucleocapsid protein, a key viral factor in virus structure and replication. These findings prompted us to determine if PrPc could influence HIV-1 replication." "
J Mol Biol. 2004 Apr 2;337(4):1035-51. "Analysis of the interactions between HIV-1 and the cellular prion protein in a human cell line"

[S52.008] Detection of Prion Amyloid Deposits In Vivo
Category - Infections/AIDS/Prion diseases



Barring the door to HIV: The prion propagates Host-virus battle
(This article available free to registered subscribers)


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