LFA-1 is a key determinant for preferential infection of memory CD4+ T cells by human immunodeficiency virus type 1

Memory CD4(+) T cells are considered a stable latent reservoir for human immunodeficiency virus type I (HIV-1) and a barrier to eradication of this retroviral infection in patients under therapy. It has been shown that memory CD4(+) T cells are preferentially infected with HIV-1, but the exact mechanism(s) responsible for this higher susceptibility remains obscure. Previous findings indicate that incorporation of host-derived intercellular adhesion molecule 1 (ICAM-1) in HIV-1 increases virus infectivity. To measure the putative involvement of virus-anchored ICAM-1 in the preferential infection of memory cells by HIV-1, quiescent and activated naive and memory T-cell subsets were exposed to isogenic virions either lacking or bearing ICAM-1. Memory CD4(+) T cells were found to be more susceptible than naive CD4(+) T cells to infection with ICAM-1-bearing virions, as exemplified by a more important virus replication, an increase in integrated viral DNA copies, and a more efficient entry process. Interactions between virus-associated host ICAM-1 and cell surface LFA-1 under a cluster formation seem to be responsible for the preferential HIV-1 infection of the memory cell subset. Altogether, these data shed light on a potential mechanism by which HIV-1 preferentially targets long-lived memory CD4(+) T cells.