GROSS DEFECTS IN THE VPR AND VPU GENES OF HIV TYPE-1 CANNOT EXPLAIN THE DIFFERENCES IN RNA COPY NUMBER BETWEEN LONG-TERM ASYMPTOMATICS AND PROGRESSORS

Disease progression in HIV-1-infected individuals is strongly associat ed with persistent and high numbers of HIV-1 RNA copies, We previously reported a markedly lower viral RNA load in eight long-term asymptoma tics (LTAs) compared to seven matched progressors (at 1 year after ser oconversion or entry in the study, p < 0.001) (Hogervorst E, et al.: J Infect Dis 1995;171:811-821). Here we extend our study to examine whe ther a difference in viral load can be attributed to infection by viru ses having distinct vpr and vpu genes, Sequencing of vpr and vpu genes from serum samples collected at seroconversion from both long-term as ymptomatics and progressors showed full-length and intact open reading frames of both genes in all subjects, At the protein level, no differ ence was discerned in domains of putative functional importance within Vpr and Vpu between the two groups, Phylogenetic analysis showed no c lustering of LTA sequences, which interdigitated with sequences from p rogressors. We therefore concluded that nonprogression is not likely t o be explained by deletion of vpr and vpu, or by gross sequence abnorm ality in these genes.