We can hypothesize that differential viral methylation may alter host responses to infection, in that depending on the host or cell type, as well as the genomic context of methylation, presence or absence of m5C may either allow detection by and/or provide a mechanism of escape from RNA-binding proteins (e.g., Dicer, RIG-I, MDA5, TLRs, APOBEC3) involved in virus restriction or non-self RNA recognition that trigger downstream immune signaling and interferon production [43]. Here, DICER1 is linked to infection.