Analysis of mRNA and protein expression, as well as assays mapping viral miRNA binding sites in infected cells, showed that endogenous HSV-1 miR-H2 binds to viral ICP0 mRNA and inhibits its expression,while endogenous miR-H4 inhibits the expression of the viral ICP34.5 gene. In contrast, no viral mRNA target for miR-H3 could be detected, even though miR-H3, like miR-H4, is perfectly complementary to ICP34.5 mRNA.
In addition to miR-H2-3p lying antisense to ICP0, HSV-1 miR-H3 and miR-H4 also lie antisense to the gene encoding the pathogenicity factor ICP34.5 and, based on genetic data, were proposed to inhibit ICP34.5 expression in latently infected neurons.
