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The Journal of Immunology, 2000, 165: 1074-1081.
Copyright © 2000 by The American Association of Immunologists

Latent Murine {gamma}-Herpesvirus Infection Is Established in Activated B Cells, Dendritic Cells, and Macrophages1

Emilio Flaño2,*,{ddagger}, S. Mazher Husain{dagger},{ddagger}, Jeffery T. Sample{dagger},{ddagger}, David L. Woodland2,*,{ddagger} and Marcia A. Blackman2,3,*,{ddagger}

Departments of * Immunology and {dagger} Virology and Molecular Biology, and {ddagger} Program in Viral Oncogenesis and Tumor Immunology, St. Jude Children’s Research Hospital, Memphis, TN 38105; and § Department of Pathology, University of Tennessee, Memphis, TN 38163

Intranasal infection of mice with the murine {gamma}-herpesvirus MHV-68 results in an acute lytic infection in the lung, followed by the establishment of lifelong latency. Development of an infectious mononucleosis-like syndrome correlates with the establishment of latency and is characterized by splenomegaly and the appearance of activated CD8+ T cells in the peripheral blood. Interestingly, a large population of activated CD8+ T cells in the peripheral blood expresses the Vß4+ element in their TCR. In this report we show that MHV-68 latency in the spleen after intranasal infection is harbored in three APC types: B cells, macrophages, and dendritic cells. Surprisingly, since latency has not previously been described in dendritic cells, these cells harbored the highest frequency of latent virus. Among B cells, latency was preferentially associated with activated B cells expressing the phenotype of germinal center B cells, thus formally linking the previously reported association of latency gene expression and germinal centers to germinal center B cells. Germinal center formation, however, was not required for the establishment of latency. Significantly, although three cell types were latently infected, the ability to stimulate Vß4+CD8+ T cell hybridomas was limited to latently infected, activated B cells.




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