Murid Herpesvirus 4 Strain 68 M2 Protein Is a B-Cell-Associated Antigen Important for Latency but Not Lymphocytosis

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Abstract
This work describes analyses of the function of the murid herpesvirus 4 strain 68 (MHV-68)M2gene. A frameshift mutation was made in theM2open reading frame that caused premature termination of translation of M2 after amino acid residue 90. TheM2mutant showed no defect in productive replication in vitro or in lungs after infection of mice. Likewise, the characteristic transient increase in spleen cell number, Vβ4 T-cell-receptor-positive CD8+T-cell mononucleosis, and establishment of latency were unaffected. However, theM2mutant virus was defective in its ability to cause the transient sharp rise in latently infected cells normally seen in the spleen after infection of mice. We also demonstrate that expression ofM2is restricted to B cells in the spleen and thatM2encodes a 30-kDa protein localizing predominantly in the cytoplasm and plasma membrane of B cells.