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

نویسندگان

  • In-Jeong Kim
  • Emilio Flaño
  • David L Woodland
  • Frances E Lund
  • Troy D Randall
  • Marcia A Blackman
چکیده

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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عنوان ژورنال:
  • Journal of immunology

دوره 171 2  شماره 

صفحات  -

تاریخ انتشار 2003