Consistent with the notion that HIV-1 cell-cell spread is an active, cytoskeletal-dependent process and that virus infection drives this process (Jolly et al., 2004), we found dynamic phosphorylation changes to many actin regulators (PAK1, CFL, PALLD, MYH10, VIM, and WAS), polarity proteins (SCRIB) and components of vesicle trafficking and fusion (SNAP23) (Table S2), most of which that have not been previously described as host cofactors for HIV-1 replication and spread. This evidence concerns the gene CFL1 and viral infectious disease.