Fig. 6
Schematic presentation of the molecular mechanism of m6A mediated regulation of the interferon signaling pathway in response to lytic EBV infection and reactivation
Latently infected EBV cells produce a basal level of interferon that bind to the interferon receptors and trigger the downstream signaling that involves TYK2 and ISGF3 which drives the innate antiviral response. During reactivation the virus inhibits the activity of eraser molecule, ALKBH5. This leads to retention of methylation in some host transcripts including TYK2 and DTX4. Methylated TYK2 transcripts are rapidly degraded while methylated DTX4 are translocated to the cytosol to promote degradation of TBK1. These events lead to dampened IFN response and results in an abrogated antiviral response