Abstract
It has been proposed that the gamma-herpesviruses maintain lifelong latency in B cells by gaining entry into the memory B cell pool and taking advantage of host mechanisms for maintaining these cells. We directly tested this hypothesis by kinetically monitoring viral latency in CD40(+) and CD40(-) B cells from CD40(+)CD40(-) mixed bone marrow chimera mice after infection with a murine gamma-herpesvirus, MHV-68. CD40(+) B cells selectively entered germinal centers and differentiated into memory B cells. Importantly, latency was progressively lost in the CD40(-) B cells and preferentially maintained in the long-lived, isotype-switched CD40(+) B cells. These data directly demonstrate viral exploitation of the normal B cell differentiation pathway to maintain latency.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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3T3 Cells
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Animals
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B-Lymphocyte Subsets / cytology*
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B-Lymphocyte Subsets / immunology
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B-Lymphocyte Subsets / metabolism
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B-Lymphocyte Subsets / virology*
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Bone Marrow Cells / immunology
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Bone Marrow Cells / radiation effects
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Bone Marrow Transplantation
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CD40 Antigens / biosynthesis
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CD40 Antigens / genetics
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CD40 Antigens / physiology*
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Cell Differentiation / genetics
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Cell Differentiation / immunology
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Cell Survival / genetics
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Gammaherpesvirinae / immunology*
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Germinal Center / cytology
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Germinal Center / immunology
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Germinal Center / metabolism
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Germinal Center / virology
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Herpesviridae Infections / immunology*
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Herpesviridae Infections / virology*
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Immunoglobulin Class Switching
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Immunologic Memory* / genetics
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Lymphocyte Activation / genetics
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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Radiation Chimera
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Virus Latency / genetics
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Virus Latency / immunology*