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Herpes simplex virus turns off the TAP to evade host immunity.

机译:单纯疱疹病毒会关闭TAP,以逃避宿主的免疫力。

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摘要

Many viruses have evolved mechanisms to avoid detection by the host immune system. Herpes simplex virus (HSV) expresses an immediate early protein, ICP47, which blocks presentation of viral peptides to MHC class I-restricted cells. The properties of the newly synthesized class I molecules in HSV-infected cells resemble those of cell lines deficient in the transporter associated with antigen processing (TAP) in that class I molecules are retained in the endoplasmic reticulum, and the heavy chain and beta 2-microglobulin subunits dissociate in detergent extracts but the complex can be stabilized by peptides. We show here that ICP47 binds to TAP and prevents peptide translocation into the endoplasmic reticulum.
机译:许多病毒已经进化出避免宿主免疫系统检测的机制。单纯疱疹病毒(HSV)表达一种即时早期蛋白ICP47,该蛋白阻止病毒肽向MHC I类限制性细胞的呈递。 HSV感染细胞中新合成的I类分子的特性类似于缺乏与抗原加工(TAP)相关的转运蛋白的细胞系的特性,因为I类分子保留在内质网中,并且重链和β2-微球蛋白亚基在去污剂提取物中解离,但复合物可通过肽稳定。我们在这里显示ICP47与TAP结合并防止肽易位进入内质网。

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