Abstract
As interferon-γ (IFN-γ) is produced at lower levels by neonatal than adult T cells, we determined whether IFN-γ influences HIV-1 replication in thymocytes. IFN-γ significantly decreased replication of R5 but not X4 viruses, and reduced depletion of CD3hiCD27 (mature) thymocytes, the preferential targets for R5 HIV-1. Thus infection and depletion of functionally mature thymocytes that can produce endogenous IFN-γ may mutually contribute to HIV-1 replication in the thymus and to reduced T-cell output.