Centre des Innovations Thérapeutiques en Oncologie et Hématologie, CHU Saint-Louis, Paris, France.
Stem Cells. 2011 Nov;29(11):1656-60. doi: 10.1002/stem.725.
Most of the viruses known to be associated with anemia in human tend to persistently infect their host and are noncytopathic or poorly cytopathic for blood cell progenitors. Infections with Epstein-Barr virus, cytomegalovirus, varicella-zoster virus, human herpes virus 6 (HHV-6), B19 parvovirus, human immunodeficiency virus, hepatitis A and C viruses and the putative viral agent associated with non-A-G post-hepatitis aplastic anemia have been reported in association with anemia. Nevertheless, a direct cytotoxic effect on erythroid progenitors has been clearly demonstrated only for human parvovirus B19 and evocated for HHV-6. A major role for destructive immunity is strongly suspected in the pathogenesis of anemia associated with the other viral infections. Host genes play a role in the occurrence of virus-induced anemia in animal models, and there are some evidences that genetic background could also influence the occurrence of virus-associated anemia in human.
大多数已知与人类贫血相关的病毒往往会持续感染宿主,并且对血细胞祖细胞无细胞毒性或毒性较弱。已报道与贫血相关的病毒感染包括 Epstein-Barr 病毒、巨细胞病毒、水痘-带状疱疹病毒、人类疱疹病毒 6(HHV-6)、细小 B19 病毒、人类免疫缺陷病毒、甲型和丙型肝炎病毒以及与非 A-G 后肝炎后再生障碍性贫血相关的假定病毒因子。然而,只有人类细小 B19 病毒和 HHV-6 被明确证明对红系祖细胞具有直接细胞毒性作用。其他病毒感染引起的贫血发病机制中强烈怀疑存在破坏性免疫的主要作用。宿主基因在动物模型中病毒诱导性贫血的发生中起作用,并且有一些证据表明遗传背景也可能影响人类病毒相关性贫血的发生。