Immunological features of murine gammaherpesvirus infection
Abstract Murine gammaherpesvirus (MHV-68) represents a unique opportunity to explore the detailed interaction of a gammaherpesvirus with its natural host. In particular the immunological events occurring in the primary infection and in the establishment of latency are poorly understood. The virus infects experimental mice, replicating in the lung. Spread then occurs to the B-cell compartment resulting in splenomegaly, a process reminiscent of infectious mononucleosis in humans. The virus then becomes latent in B cells and persists. In addition, long-term infection is associated with the development of lymphoproliferative disease. We show here that CD8 T cells are key cells in resolving the primary infection and in maintaining the numbers of latently-infected B cells. A critical interplay exists between B cells and CD4 T cells in the genesis of splenomegaly and in the numbers of latently infected B cells. Cytokines are probably involved here and serve to induce cell expansion in the spleen. A number of genes have been identified and probes for the lytic and latent cycle are being developed. The use of recombinant proteins, recombinant viruses and knockout mice will facilitate the use of this model in the exploration of immunotherapeutic strategies to target lytic and latent infections by gammaherpesvirus.
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