Abstract
BACKGROUND: Although the interactions of cellular cytidine deaminase A3G and viral infection factor (vif) of human immunodeficiency virus (HIV) were reported, regulation of A3G after in vivo HIV infection and disease progression is not known. METHODS: Time courses of plasma virus, CD4(+) T lymphocyte Macaca levels, and concentrations of A3G and vif transcripts were determined in infant macaques infected with HIV-2(287) . These in vivo results were compared with those collected in vitro in HIV-2-infected T cells. RESULTS: Human immunodeficiency virus-infected macaques exhibited plasma viremia (≥10(8) copies/ml) followed by a precipitous CD4(+) T-cell (from 40-70 to ≤5%) decline. An initial increase in A3G transcripts coincides with early increases in virus and vif RNA. As virus load continues to increase, A3G RNA decreases but recovers at a later phase as virus level stabilizes. Pearson correlation analysis revealed strong interactions of A3G-CD4, vif-CD4, and A3G-vif. CONCLUSIONS: There is a time-dependent A3G and vif RNA interaction throughout the course of HIV infection.