Important note: Information in this article was accurate in 1995. The state of the art may have changed since the publication date.
Resistance: how HIV evolves to survive. Clearinghouse, P.O. Box 6003, Rockville, MD 20849-6003. 800-458-5231 ext. 5023.
Common Factor. 1995 Apr;(no 10):13-4. Unique Identifier : AIDSLINE AIDS/95700366 Colvin R
Abstract:
Drug resistance, the biggest problem facing medicine today, has caused recent views of anti-HIV therapies to be pessimistic. Resistance arises in HIV due to an evolutionary process involving mutations, which are passed on to viral offspring. Continuous use of antiviral agents, such as AZT, in combination with the slow course of the disease, provides time for the virus to evolve and become more resistant. There is dispute over the level of cross-resistance (how resistance to one drug affects the action of another drug). Non-nucleoside analog reverse transcriptase inhibitors (RTI's) are more prone to becoming ineffective compared to other classes of anti-HIV drugs since RTI's, while significantly reducing blood viral load, still allow enough virus to survive, thus encouraging resistance to develop. Some evidence suggests that the inhibitors MK-639, saquinavir, and the Abbott inhibitor, can be combined with each other in order to achieve greater reductions in the viral load. Merck reports, however, that a year's treatment with MK-639 has created a virus that is resistant to all protease inhibitors thus far tested. Clinical trials, designed to find other anti-HIV drugs and to avoid resistance, are beginning soon.
Keywords: Antiviral Agents/PHARMACOLOGY Drug Resistance, Microbial/GENETICS Evolution HIV/DRUG EFFECTS/*GENETICS HIV Protease Inhibitors/PHARMACOLOGY Mutation RNA-Directed DNA Polymerase/ANTAGONISTS & INHIB Virus Replication/DRUG EFFECTS NEWSLETTER ARTICLE
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