Journal
JOURNAL OF IMMUNOLOGY
Volume 165, Issue 2, Pages 1074-1081Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.165.2.1074
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- NCI NIH HHS [CA56639, P30CA21765] Funding Source: Medline
- NIAID NIH HHS [AI42927] Funding Source: Medline
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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 V beta 4(+) 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 V beta b4(+)CD8(+) T cell hybridomas was limited to latently infected, activated B cells.
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