Protein kinases conserved in herpesviruses potentially share a function mimicking the cellular protein kinase cdc2.

Abstract

Herpesviruses encode protein kinases. A subset of these proteins, represented by HSV-1 UL13, are conserved throughout all members of the Herpesviridae, and here, are designated CHPKs (conserved herpesvirus protein kinases). In addition to conserved gene products like CHPKs, herpesviruses encode genes specific to respective herpesviruses. When acting upon conserved viral gene products or cellular factors, CHPKs may play conserved roles in the life cycles of herpesviruses. CHPKs may also express unique functions within the infectious process of individual herpesviruses when specific viral gene products are targeted. CHPKs demonstrate specific activity in multiple herpesvirus infections, functioning in the regulation of viral gene expression in HSV-1, tissue tropism in VZV, and viral DNA synthesis, encapsidation and egress from the nucleus in HCMV. The HCMV CHPK, however, can partially substitute for the HSV-1 CHPK. Representative CHPKs from all Herpesviridae subfamilies can also facilitate the hyperphosphorylation of the cellular translation factor, EF-1delta. This indicates that CHPKs have conserved functions. Recent data have shown that both CHPKs and a cellular protein kinase, cdc2, phosphorylate the same amino acid residues of target proteins. Thus, CHPKs may mimic cdc2 function in infected cells.