Relation between HIV-2 proviral load and CD4+ lymphocyte count differs in monotypic and dual HIV infections

Objective: To explore and compare the relations between proviral DNA load and CD4(+) lymphocyte counts in both HIV-2 monotypic and HN dual infection. Study Design/Methods: In Dakar, Senegal, where the HN-I and HIV-2 epidemics overlap, serum and peripheral blood mononuclear cell (PBMC) DNA samples were collected from registered female sex workers and hospitalized patients. Sera were evaluated for reactivity to antigens of HIV-1 and HIV-2 by immunoblot; dual reactivity was confirmed with recombinant envelope peptides for HIV-I and HIV-2. These samples were then subjected to HN-1 and HIV-2 proviral DNA polymerase chain reaction (PCR). To evaluate the HIV-2 cellular proviral DNA loads, a quantitative competitive PCR (QC-PCR) was developed using nested primers to amplify the gag region of HIV-2. This assay used an internal competitor generated by inserting 25 bp in the first-round PCR target sequence. T-lymphocyte subset counts were estimated by flow cytometry for both HIV-2 monotypic and dually infected persons. Results: 35 HIV-2-infected and 33 dually seroreactive samples were evaluated in this study. The CD4(+) lymphocyte counts were similar ill both groups, with mean values of 449 +/- 390 cells/mm(3) for the HIV-2 monotypic infected persons and 476 +/- 308 cells/mm3 among the dually infected persons. However, the median proviral loads differed significantly, with those in the HIV-2 group ranging from 63.2 to 669.8 copies/10(5) CD4(+) cells and demonstrating an inverse correlation with CD4(+) lymphocyte count. The HIV dually infected persons showed less variation in viral load, ranging from 9.9 to 43.3 copies/10(5) CD4(+) cells. Among the HN dually infected persons, low HIV-2 proviral load was correlated with low CD4(+) lymphocyte counts. Conclusions: The HIV-2 proviral loads in HIV dually infected persons were significantly lower than those in HIV-2 mono-typically infected individuals (P <.0001), despite comparable CD4(+) lymphocyte counts. These results suggest that different HIV-2 proviral dynamics prevail in HIV dual infection.