ABSTRACT
Kaposi's sarcoma-associated herpesvirus is a human rhadinovirus of the gammaherpesvirus sub-family. Although herpesviruses are well-studied models of capsid formation and its processes, those of KSHV remain unknown. KSHV ORF17 encoding the viral protease precursor (ORF17-prePR) is thought to contribute to capsid formation; however, functional information is largely unknown. Here, we evaluated the role of ORF17 during capsid formation by generating ORF17-deficient and ORF17 protease-dead KSHV. Both mutants showed a decrease in viral production but not DNA replication. ORF17 R-mut, with a point-mutation at the restriction or release site (R-site) by which ORF17-prePR can be functionally cleaved into a protease (ORF17-PR) and an assembly region (ORF17-pAP/-AP), failed to play a role in viral production. Furthermore, wild type KSHV produced a mature capsid, whereas ORF17-deficient and protease-dead KSHV produced a B-capsid, (i.e., a closed body possessing a circular inner structure). Therefore, ORF17 and its protease function are essential for appropriate capsid maturation.
