Our laboratory has been working on the molecular and cellular biology of HIV-1 replication, mutagenesis, evolution and viral escape for more than two decades. We do so by employing both biochemical and virological approaches. Our recent research focuses on HIV-1 infection to nondividing myeloid cells that serve as long-living HIV-1 reservoirs, contributing to HIV-1 persistence. We have found that HIV-1 replication in nondividing target cells harbors various distinct features, compared with activated CD4+ T cells. Our research claims differences between replication in these cell types in terms of host restriction, viral replication kinetics and cell biology/signaling responses can contribute to viral evolution and pathogenesis. The current topics studied in the Kim laboratory include:

• Mechanistic understanding for HIV-1 mutagenesis, escape and evolution
• Cell type-specific factors that control viral replication kinetics and mutagenesis
• Cellular and immunological responses of macrophages to HIV-1 infection
• Cellular dNTP regulation by myeloid specific anti-HIV restriction factor, SAMHD1
• Mechanisms that other lentiviruses employ for achieving efficient replication in nondividing target cell types