Maintenance of long term gamma-herpesvirus B cell latency is dependent on CD40-mediated development of memory B cells

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...

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Bibliographic Details
Published in:The Journal of immunology (1950) 2003-07, Vol.171 (2), p.886-892
Main Authors: Kim, In-Jeong, Flaño, Emilio, Woodland, David L, Lund, Frances E, Randall, Troy D, Blackman, Marcia A
Format: Article
Language:English
Subjects:
3T3 Cells
Animals
B-Lymphocyte Subsets - cytology
B-Lymphocyte Subsets - immunology
B-Lymphocyte Subsets - metabolism
B-Lymphocyte Subsets - virology
Bone Marrow Cells - immunology
Bone Marrow Cells - radiation effects
Bone Marrow Transplantation
CD40 Antigens - biosynthesis
CD40 Antigens - genetics
CD40 Antigens - physiology
Cell Differentiation - genetics
Cell Differentiation - immunology
Cell Survival - genetics
Gammaherpesvirinae - immunology
Germinal Center - cytology
Germinal Center - immunology
Germinal Center - metabolism
Germinal Center - virology
Herpesviridae Infections - immunology
Herpesviridae Infections - virology
Immunoglobulin Class Switching
Immunologic Memory - genetics
Lymphocyte Activation - genetics
Mice
Mice, Inbred C57BL
Mice, Knockout
Radiation Chimera
Virus Latency - genetics
Virus Latency - immunology
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Summary: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.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.171.2.886