Alpha interferon enhances TRIM5α-mediated antiviral activities in human and rhesus monkey cells

Dominant, constitutively expressed antiretroviral factors, including TRIN5 alpha and APOBEC3 proteins, are distinguished from the conventional innate immune systems and are classified as intrinsic immunity factors. Here, we demonsirate that interferon alpha (IFN-alpha) treatment upregulates TRIN15 alpha mRNA in rhesus monkey cells, which correlates with the enhanced TRIM5 alpha-mediated pre- and postintegration blocks of human immunodeficiency virus replication. In human cells, IFN-alpha increases the levels of TRIM5 alpha mRNA, resulting in enhanced antiviral activity against N-tropic murine leukemia virus infection. These observations indicate that the TRIN15 alpha-mediated antiviral effects can be orchestrated by the conventional innate immune response. It is conceivable that TRIM5 alpha plays an essential role in controlling both the initial retroviral exposure and the subsequent viral dissemination in vivo.