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Inhibition of natural killer cells by a cytomegalovirus MHC class I homologue in vivo

机译：巨细胞病毒MHC I类同源物在体内抑制自然杀伤细胞

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摘要

Herpesviruses, such as murine and human cytomegalovirus (MCMV and HCMV), can establish a persistent infection within the host and have diverse mechanisms as protection from host immune defences. Several herpesvirus genes that are homologous to host immune modulators have been identified, and are implicated in viral evasion of the host immune response. The discovery of a viral major histocompatibility complex (MHC) class I homologue, encoded by HCMV, led to speculation that it might function as an immune modulator and disrupt presentation of peptides by MHC class I to cytotoxic T cells. However, there is no evidence concerning the biological significance of this gene during viral infection. Recent analysis of the MCMV genome has also demonstrated the presence of a MHC class I homologue. Here we show that a recombinant MCMV, in which the gene encoding the class I homologue has been disrupted, has severely restricted replication during the acute stage of infection compared with wild-type MCMV. We demonstrate by in vivo depletion studies that natural killer (NK) cells are responsible for the attenuated phenotype of the mutant. Thus the viral MHC class I homologue contributes to immune evasion through interference with NK cell-mediated clearance.
机译：诸如鼠和人巨细胞病毒（MCMV和HCMV）之类的疱疹病毒可以在宿主内建立持续感染，并具有多种机制来保护免受宿主免疫防御。已经鉴定出几种与宿主免疫调节剂同源的疱疹病毒基因，并与宿主免疫反应的病毒逃逸有关。由HCMV编码的I类病毒主要组织相容性复合物（MHC）同源物的发现，导致人们猜测它可能起免疫调节剂的作用，并破坏I类MHC向细胞毒性T细胞的肽呈递。但是，没有证据表明该基因在病毒感染期间具有生物学意义。最近对MCMV基因组的分析也表明存在MHC I类同源物。在这里我们显示，与野生型MCMV相比，重组MCMV在感染的急性期严重复制受到限制，其中编码I类同源物的基因已被破坏。我们通过体内耗竭研究证明自然杀手（NK）细胞负责突变体的减毒表型。因此，病毒MHC I类同源物通过干扰NK细胞介导的清除而有助于免疫逃逸。

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