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June 24, 1998

Drug-Resistant HIV-1The Virus Strikes Back

Author Affiliations

From the Naval Medical Research Institute, Bethesda, Md. Dr Mayers is moving to the Henry Ford Hospital, Detroit, Mich.

JAMA. 1998;279(24):2000-2002. doi:10.1001/jama.279.24.2000

The human immunodeficiency virus (HIV) has developed elaborate mechanisms to escape the immune system. Since the reverse transcriptase of HIV makes, on average, 1 error per 10000 bases copied, and the virus has a 9200-base genome, each virus produced is slightly different from its forebear. Over time each patient develops a swarm of virus variants (quasi species) with all possible 1-base and most 2-base variants represented. Additionally, if 2 viruses infect 1 cell or 2 infected cells get fused by HIV infection to form a syncytium, 2 different viral genomes can be packaged into the virus produced. When these viruses with 2 different HIV genomes infect the next cell, the reverse transcriptase enzyme can switch back and forth between the 2 genomes to form a recombinant virus with portions of genes from both parent viruses. The mechanisms of mutation and recombination, which the virus uses to escape immune pressure, are readily used to escape pressure exerted by antiviral drugs, resulting in emergence of drug-resistant virus.1

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