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首页> 外文期刊>AIDS Research and Human Retroviruses >A Novel HIV-1 Nef Mutation in a Primary Pediatric Isolate Impairs MHC-Class I Downregulation and Cytopathicity
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A Novel HIV-1 Nef Mutation in a Primary Pediatric Isolate Impairs MHC-Class I Downregulation and Cytopathicity

机译：小儿小儿分离物中的新型HIV-1 NEF突变损害MHC-A类下调和细胞病变

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摘要

HIV-1-induced cytopathicity of thymocytes is a major cause of reduced peripheral T cells and rapid disease progression observed in HIV-1-infected infants. Understanding the virulence factors responsible for thymocyte depletion has paramount importance in addressing the pathogenesis of disease progression in children. In this study, thymocyte depletion was analyzed following infection with two primary CXCR4-tropic HIV-1 pediatric isolates (PI), PI-2 and PI-2.1, which were serially derived from an in utero-infected infant. Although highly similar to each other, PI-2 showed markedly decreased thymocyte depletion in vitro compared with PI-2.1. Further analysis showed a novel deletion in the Nef protein (Nef Delta K7S) of PI-2, which was absent in PI-2.1. This deletion inhibited Nef-mediated major histocompatibility complex class I (MHC-I) downregulation in infected thymocytes in vitro and in vivo; in contrast, the mutated Nef continued to downregulate CD4 surface expression in vitro. These results suggest that HIV-1 Nef contributes to thymic damage in infants through selective functions.
机译：HIV-1诱导的胸腺细胞病变性是在HIV-1感染的婴儿中观察到周围T细胞和快速疾病进展的主要原因。理解负责胸腺细胞消耗的毒力因子在解决儿童疾病进展的发病机制方面具有至关重要的重要性。在该研究中，在用两个主要CXCR4-热带HIV-1儿科（PI），PI-2和PI-2.1的感染后分析胸腺细胞耗尽，其源自在子宫感染的婴儿中。尽管彼此高度相似，但PI-2与PI-2.1相比，体外显着降低胸腺细胞耗尽。进一步的分析表明，在PI-2.1中不存在于PI-2的NEF蛋白（NEF DELTA K7s）中的新缺失。该缺失抑制了Nef介导的主要组织相容性复合体I（MHC-I）在体外和体内的受感染的胸腺细胞下调;相反，突变的NEF继续在体外下调CD4表面表达。这些结果表明，HIV-1 NEF通过选择性功能导致婴儿的胸腺损伤。

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