ABSTRACT:
A variant of HIV-1 possessing a deletion in reverse transcriptase (RT) gene at codon 67 was identified in a patient who had failed combination antiretroviral therapy including protease and RT inhibitors. This deletion initially emerged under the selective pressure of combination therapy with zidovudine plus didonosine. It has persisted for more than 3 years in association with the accumulation of a variety of other well described drug resistance mutations, including M41L, K70R, L74I, V75T, A98G, K103N, M184V, T215F and K219Q and an uncharacterized mutation at RT codon 69 (T69G). To assess the role of this deletion in drug sensitivity, a series of recombinant viruses were created .Phenotypic studies demonstrated that the codon 67 deletion by itself had little effect on zidovudine sensitivity. However, in the context of the T69G mutation and three other mutations known to be associated
(abstract incomplete)
