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轮状病毒特异性蛋白合成对于病毒特异性细胞毒性T淋巴细胞识别受感染细胞并非必要。

Rotavirus-specific protein synthesis is not necessary for recognition of infected cells by virus-specific cytotoxic T lymphocytes.

作者信息

Offit P A, Greenberg H B, Dudzik K I

机构信息

Division of Infectious Diseases, Children's Hospital of Philadelphia, Pennsylvania 19104.

出版信息

J Virol. 1989 Aug;63(8):3279-83. doi: 10.1128/JVI.63.8.3279-3283.1989.

Abstract

We found that rotavirus-specific protein synthesis was not necessary for recognition by virus-specific cytotoxic T lymphocytes (CTLs). In addition, CTLs lysed rotavirus-infected target cells prior to production of infectious virus. Target cell processing of rotavirus antigens for presentation to CTLs was enhanced by treatment of rotavirus with trypsin prior to infection; trypsin-induced cleavage of the viral hemagglutinin (vp4) has previously been found to facilitate rotavirus entry into target cells by direct penetration of virions through the plasma membrane. We conclude that sufficient quantities of exogenous viral proteins may be introduced into the cytoplasm for processing by target cells. The mechanism by which rotavirus proteins are processed for presentation to the target cell surface remains to be determined.

摘要

我们发现,轮状病毒特异性蛋白质合成对于病毒特异性细胞毒性T淋巴细胞(CTL)的识别并非必需。此外,CTL在感染性病毒产生之前就裂解了轮状病毒感染的靶细胞。在感染前用胰蛋白酶处理轮状病毒可增强靶细胞对轮状病毒抗原的处理,以呈递给CTL;先前已发现胰蛋白酶诱导的病毒血凝素(vp4)裂解可促进轮状病毒通过病毒粒子直接穿透质膜进入靶细胞。我们得出结论,可能有足够量的外源性病毒蛋白被引入细胞质中以供靶细胞处理。轮状病毒蛋白被处理以呈递到靶细胞表面的机制仍有待确定。

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Rotaviruses: a review.轮状病毒:综述
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Pathogenesis of rotavirus infection in mice.小鼠轮状病毒感染的发病机制。
Infect Immun. 1982 Nov;38(2):755-63. doi: 10.1128/iai.38.2.755-763.1982.

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