Medical Research Council Centre for Immune Regulation, University of Birmingham, Birmingham, United Kingdom.
PLoS One. 2011;6(9):e25789. doi: 10.1371/journal.pone.0025789. Epub 2011 Sep 30.
Hepatitis C virus (HCV) infected patients with vasculitis are often treated with the B-cell-depleting anti-CD20 antibody rituximab. Treatment reduces the cryoglobulins that cause vasculitis, yet it also leads to a transient increase in liver enzymes and HCV genomic RNA in the periphery. The mechanism underlying the increased viral load is unclear and both direct and indirect roles have been proposed for B cells in HCV infection. We previously reported that HCV can associate with B cells and can trans-infect hepatocytes. We established an in vitro assay to study the effect(s) of rituximab on B cell-associated HCV infectivity. Rituximab-mediated lysis of B cells in vitro increases the level of infectious HCV released from B cells. Our results, using a model where virus does not replicate in B cells, recapitulate observations seen in patients and may explain in part the rapid increase in blood HCV RNA observed after rituximab treatment.
丙型肝炎病毒（HCV）感染伴有血管炎的患者通常使用 B 细胞耗竭性抗 CD20 抗体利妥昔单抗进行治疗。该治疗可降低导致血管炎的冷球蛋白，但也会导致外周血肝酶和 HCV 基因组 RNA 一过性升高。病毒载量增加的机制尚不清楚，B 细胞在 HCV 感染中可能发挥直接和间接作用。我们之前报道过 HCV 可以与 B 细胞结合并可转染肝细胞。我们建立了体外测定法来研究利妥昔单抗对 B 细胞相关 HCV 感染性的影响。体外利妥昔单抗介导的 B 细胞裂解增加了从 B 细胞释放的感染性 HCV 的水平。我们的结果使用了病毒不能在 B 细胞中复制的模型，再现了患者中的观察结果，并部分解释了利妥昔单抗治疗后血液 HCV RNA 快速增加的原因。
