Kim In-Jeong, Flaño Emilio, Woodland David L, Lund Frances E, Randall Troy D, Blackman Marcia A
Trudeau Institute, Saranac Lake, NY 12983, USA.
J Immunol. 2003 Jul 15;171(2):886-92. doi: 10.4049/jimmunol.171.2.886.
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.
有人提出，γ-疱疹病毒通过进入记忆B细胞池并利用宿主维持这些细胞的机制，在B细胞中维持终身潜伏。我们通过动态监测感染鼠γ-疱疹病毒MHV-68后的CD40(+)CD40(-)混合骨髓嵌合小鼠的CD40(+)和CD40(-)B细胞中的病毒潜伏情况，直接验证了这一假设。CD40(+)B细胞选择性地进入生发中心并分化为记忆B细胞。重要的是，CD40(-)B细胞中的潜伏性逐渐丧失，而在长寿的、同种型转换的CD40(+)B细胞中优先维持。这些数据直接证明了病毒利用正常B细胞分化途径来维持潜伏性。
