Conversely, introduction of wild-type PRMT2 markedly increased the proportion of latent infection in Jurkat T cells transduced with HIV-1GKO virus while the proportions of latently and actively infected cells are largely unaffected by the expression of a methylase-inactive PRMT2 (Fig. 3c), indicating that PRMT2 promotes latency establishment during viral infection in a methylase-dependent manner. This evidence concerns the gene PRMT2 and viral infectious disease.