Important note: Information in this article was accurate in May 2001. The state of the art may have changed since the publication date.AIDSWEEKLY Plus; Monday, May 14, 2001
Michael Greer, Staff Medical Writer
NewsRx - Drug-resistant HIV strains remain dangerous even when mutations seem to degrade their ability to proliferate, researchers in Switzerland warn.
"[HIV-1] variants resistant to protease (PR) and reverse transcriptase (RT) inhibitors may display impaired infectivity and replication capacity," G. Bleiber and colleagues explained in the Journal of Virology.
After comparing the total fitness of mutant and wild-type strains, however, Bleiber et al. found that drug-resistant strains maintained a high degree of fitness even with apparent functional deficits.
Mutant HIV variants had markedly lower replication rates than their normal counterparts, according to the researchers. Viral strains resistant to reverse transcriptase inhibitors replicated roughly 27% slower than normal, while those with recombinant protease had replication rates almost 40% lower than wild-type viruses.
Despite this replication deficit, and impaired Pol protein packaging by recombinant reverse transcriptase strains, several drug-resistant variations maintained fitness comparable to that of normal HIV. This may be the result of other compensating mutations away from the protease and/or reverse transcriptase areas of the HIV genome, Bleiber et al. noted.
The genomes of mutant viral offspring showed only a limited reversion back to wild-type amino acid positions, underscoring the relatively high fitness of these mutants ("Individual contributions of mutant protease and reverse transcriptase to viral infectivity, replication, and protein maturation of antiretroviral drug-resistant human immunodeficiency virus type 1," J Virol 2001 Apr;75(7):3291-300.
"These data underscore the complex relationship between PR and RT adaptive changes and viral evolution in antiretroviral drug-resistant HIV-1," Bleiber and colleagues concluded.
The corresponding author for this report is A. Telenti, Centre Hospitalier Universitaire (CHU) Vaudois, Division of Infectious Diseases, CH-1011 Lausanne, Switzerland.
Key points reported in this study include:
This article was prepared by AIDS Weekly editors from staff and other reports.
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