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Access to Polymerized Actin in Migrating T Cells Potentiates HIV Infection

Lymphoid organs are the primary site of HIV-1 replication and CD4+ T cell depletion. T cells are highly migratory in lymph nodes at steady-state, but how their motile behaviors can impact HIV-1 susceptibility during infection has not been examined. Here, we show that T cell infection in 3D collagen matrix, which support robust migration along fibrillar collagen networks, significantly enhanced infection by cell-free R5-tropic lab adapted and transmitted/founder molecular HIV clones in the absence of exogenous cytokines or cationic polymers. Increased HIV infection in collagen was not attributed to differences in CCR5 expression or the activation state, but significantly higher viral DNA integration was observed. Increased infection rates correlated with high T cell migration speeds and fluctuating F-actin content, suggesting that HIV-1 may access cortical actin filaments in motile cells to facilitate viral integration. Collagen gels enhanced total infection rates of activated T cells but did not increase latent infections. Together, our studies demonstrate that the environmental context in which T cells encounter viral particles are important factors that regulate HIV-1 susceptibility and pathogenesis.