OBJECTIVE: To determine whether blood plasma levels of HIV-2 RNA viral loads and immune activation markers differ between persons infected with HIV-2 only and those dually infected with HIV-1 and HIV-2. METHODS: Between September 1996 and February 2000, we collected, analyzed and compared levels of HIV-2 RNA in plasma and immune activation markers among 52 persons infected with HIV-2 alone and 75 with confirmed dual infection. We also compared viral load and immune activation in patients who were infected with HIV-1 only and those who were dually infected. RESULTS: When we conducted a CD4 T-cell count-stratified multivariate analysis of HIV-2 viral load, controlling for difference in CD4 T-cell counts, age and sex: at < 200 x 10 CD4 T cells/l, HIV-2 viral load was 2.0 log10 copies/ml lower in dually infected patients than in HIV-2 only patients (P < 0.0001). At CD4 T-cell counts between 200 x 10 and 500 x 10/l, HIV-2 viral load was 0.3 log10 copies/ml lower in dually infected patients (P = 0.45). However, at CD4 T-cells counts > 500 x 10/l, HIV-2 viral load was 0.9 log10 copies/ml higher in dually infected patients (P < 0.0001). Dually infected persons with undetectable HIV-2 viral loads had significantly higher median levels of CD8 T cells expressing CD38 (P < 0.001) and HLA-DR (P = 0.01) than HIV-2 only infected patients. CONCLUSION: These results suggest that in dual infection, the level of HIV-2 replication depends on the immune status of the patients, with HIV-1 out-replicating HIV-2 as disease progress.
OBJECTIVE: To determine whether blood plasma levels of HIV-2 RNA viral loads and immune activation markers differ between persons infected with HIV-2 only and those dually infected with HIV-1 and HIV-2. METHODS: Between September 1996 and February 2000, we collected, analyzed and compared levels of HIV-2 RNA in plasma and immune activation markers among 52 persons infected with HIV-2 alone and 75 with confirmed dual infection. We also compared viral load and immune activation in patients who were infected with HIV-1 only and those who were dually infected. RESULTS: When we conducted a CD4 T-cell count-stratified multivariate analysis of HIV-2 viral load, controlling for difference in CD4 T-cell counts, age and sex: at < 200 x 10 CD4 T cells/l, HIV-2 viral load was 2.0 log10 copies/ml lower in dually infected patients than in HIV-2 only patients (P < 0.0001). At CD4 T-cell counts between 200 x 10 and 500 x 10/l, HIV-2 viral load was 0.3 log10 copies/ml lower in dually infected patients (P = 0.45). However, at CD4 T-cells counts > 500 x 10/l, HIV-2 viral load was 0.9 log10 copies/ml higher in dually infected patients (P < 0.0001). Dually infected persons with undetectable HIV-2 viral loads had significantly higher median levels of CD8 T cells expressing CD38 (P < 0.001) and HLA-DR (P = 0.01) than HIV-2 only infectedpatients. CONCLUSION: These results suggest that in dual infection, the level of HIV-2 replication depends on the immune status of the patients, with HIV-1 out-replicating HIV-2 as disease progress.
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