FOLLICULAR DENDRITIC CELLS AND HIV PATHOGENESIS

描述：(改编自调查人员摘要)大量的艾滋病毒 被困在毛囊树突状细胞(FDC)上的生发中心 次级淋巴组织。在整个临床潜伏期内CD+4 T细胞 持续下降，这些带有病毒的生发中心FDC，高度 被激活的CD+4T细胞和高细胞激活状态是 活跃的艾滋病毒复制的主要地点。调查人员假设 FDC在HIV的发病机制中起主要作用：(1)作为HIV的储存库 传染性HIV；(2)加强新进入者的新感染 细胞和潜伏感染细胞进入生发中心；以及 (3)允许在存在高水平中和的情况下感染 抗体。他们还假设，FDC的特征是促进感染 可能会被抑制。为了支持这一假设，他们有 最近发现FDC捕获的HIV免疫复合体具有很强的传染性 他们有数据表明，FDC即使在 没有病毒复制。他们还有证据表明，民革联会推动了 新的和新的艾滋病毒感染率显著增加 潜伏感染的T细胞。最后，他们发现FDC允许感染 即使在大量中和抗体存在的情况下。 研究人员认为，他们的假设令人兴奋，而且 了解FDC在HIV致病中的作用将是至关重要的 设计干预策略，以攻击这一水库 传染性病毒。目前阻止病毒复制的策略并不奏效 锁定FDC储水池，直到细胞被摧毁和 艾滋病发作前的淋巴转移。因此，对 FDC的贡献可能使他们能够成功地瞄准这个重要的细胞 以及它的病毒库。

DESCRIPTION: (Adapted from investigator's abstract) Large amounts of HIV are trapped on follicular dendritic cells (FDC) in the germinal centers of secondary lymphoid tissues. throughout clinical latency when CD+4 T cells continually decline, these germinal centers with virus-laden FDC, highly activated, CD+4 T cells and a state of high cellular activation are the primary sites of active HIV replication. The investigators hypothesize that FDC play a major role in HIv pathogenesis by: (1) serving as a reservoir of infectious HIV; (2) potentiating both de novo infection of newly entering cells and of latently infected cells coming into the germinal center; and (3) by permitting infection in the presence of high levels of neutralizing antibody. They also hypothesize that FDC features that promote infection may be able to be inhibited. In support of the hypothesis, they have recently shown that FDC trapped HIV immune complexes are highly infectious and they have data suggesting that FDC maintain HIV infectivity even in the absence of viral replication. They also have evidence that FDC promote a significant increase in the amount of HIV infection in both newly and latently infected T cells. Lastly they have found that FDC permit infection even in the presence of a vast excess of neutralizing antibody. The investigators believe that their hypothesis is exciting and that an understanding of FDC contributions to HIV pathogenesis will be critical in designing intervention strategies that can attack this reservoir of infectious virus. Current strategies to stop viral replication do not target the FDC reservoir which remains until the cells are destroyed and the lymph node involutes prior to the onset of AIDS. thus an understanding of FDC contributions may allow them to successfully target this important cell and its viral reservoir.