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Background HIV resistance to the integrase inhibitor raltegravir (RAL) in treated patients is characterized by three main distinct resistance pathways, for which the primary mutations are: N155H, Q148H/K/R, or Y143R/H/C. These genotypes may emerge sequentially, always carried by distinct viral genomes. The mechanism explaining the sequential emergence and in vivo dynamics along with viral escape from RAL treatment are poorly understood. We hypothesize that differences in the in vivo dynamics of HIV resistance to RAL, which must be a direct consequence of the phenotypic expression of viral resistance and/or of viral fitness, are due to the genetic context of the integrase carried by viral variants infecting individual patient.

Impact of the HIV integrase genetic context on the phenotypic expression and in vivo dynamics of integrase inhibitor resistance mutations