Maintenance of Long Term γ-Herpesvirus B Cell Latency Is Dependent on CD40-Mediated Development of Memory B Cells | Zendy

In-Jeong Kim | Zendy; Emilio Flaño | Zendy; David L. Woodland | Zendy; Frances E. Lund | Zendy; Troy D. Randall | Zendy; Marcia A. Blackman | Zendy

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Maintenance of Long Term γ-Herpesvirus B Cell Latency Is Dependent on CD40-Mediated Development of Memory B Cells

Author(s) -

In-Jeong Kim,

Emilio Flaño,

David L. Woodland,

Frances E. Lund,

Troy D. Randall,

Marcia A. Blackman

Publication year - 2003

Publication title -

the journal of immunology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.737

H-Index - 372

eISSN - 1550-6606

pISSN - 0022-1767

DOI - 10.4049/jimmunol.171.2.886

Subject(s) - cd40 , b cell , naive b cell , germinal center , microbiology and biotechnology , biology , immunoglobulin class switching , memory b cell , latency (audio) , immunology , antibody , cytotoxic t cell , genetics , in vitro , computer science , telecommunications

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.

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