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The oncogenic  gammaherpesviruses , Epstein–Barr virus (EBV) and Kaposi’s sarcoma herpesvirus (KSHV), are etiologically associated with a variety of human cancers, including Burkitt’s lymphoma (BL), Hodgkin lymphoma (HL), Kaposi’s sarcoma (KS), and primary effusion lymphoma (PEL). Recently, we demonstrated KSHV infection of B- and endothelial cells to significantly upregulate the expression of interferon induced transmembrane protein 1 (IFITM1) which in turn enhances virus entry. This is an extension of the above study. In here, we determined EBV infection of cells to trigger IFITM1 expression,  in vitro . Silencing IFITM1 expression using siRNA specifically lowered  gammaherpesvirus  infection of cells at a post binding stage of entry. A natural model system to explore the effect of IFITM1 on  gammaherpesvirus  infection  in vivo  is infection of BALB/c mice with murine  gammaherpesvirus  68 (MHV-68). Priming mice with siRNA specific to IFITM1 significantly lowered MHV-68 titers in the lung specimens compared to priming with (NS)siRNA or PBS. MHV-68 titers were monitored by plaque assay and qPCR. Taken together, for the first time, this study provides insight into the critical role of IFITM1 to promoting  in vivo gammaherpesvirus  infections.

IFITM1 expression is crucial to gammaherpesvirus infection, in vivo