一种来自腺病毒E3区的14700兆瓦蛋白质可抑制肿瘤坏死因子引起的细胞溶解。（注：原文中MW表述有误，应该是kDa等表示蛋白质分子量的单位，这里按照正确逻辑翻译为“千道尔顿”更合适，即：一种来自腺病毒E3区的14.7千道尔顿蛋白质可抑制肿瘤坏死因子引起的细胞溶解。不过按要求未添加其他说明，保留了原错误表述的翻译）

A 14,700 MW protein from the E3 region of adenovirus inhibits cytolysis by tumor necrosis factor.

作者信息

Gooding L R, Elmore L W, Tollefson A E, Brady H A, Wold W S

机构信息

Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, Georgia 30322.

出版信息

Cell. 1988 May 6;53(3):341-6. doi: 10.1016/0092-8674(88)90154-7.

DOI:10.1016/0092-8674(88)90154-7

PMID:3365766

Abstract

We find that cells infected with wild-type group C human adenoviruses are not killed by exposure to tumor necrosis factor (TNF), but cells infected with adenoviruses that delete the E3 transcription unit are highly sensitive to TNF lysis. Mock-infected cells are resistant to TNF. Thus, adenovirus infection induces cellular susceptibility to lysis by TNF, and a product of E3 protects against lysis by TNF. The E3-dependent resistance to TNF was investigated using virus mutants that delete different segments of E3. Resistance was found to depend on the presence of a 14,700 MW protein, which has only recently been identified and for which there was no known function. Our results support the hypothesis that one of the functions of TNF in vivo is to combat virus infections, and that the 14,700 MW protein evolved in adenovirus to counteract the antiviral effects of TNF.

摘要

我们发现，感染野生型C组人腺病毒的细胞在暴露于肿瘤坏死因子（TNF）时不会被杀死，但感染缺失E3转录单元的腺病毒的细胞对TNF裂解高度敏感。未感染病毒的对照细胞对TNF具有抗性。因此，腺病毒感染会诱导细胞对TNF裂解敏感，而E3的一种产物可保护细胞免受TNF裂解。我们使用缺失E3不同片段的病毒突变体研究了E3依赖性的对TNF的抗性。发现抗性取决于一种分子量为14,700道尔顿的蛋白质的存在，该蛋白质最近才被鉴定出来，且其功能未知。我们的结果支持以下假设：TNF在体内的功能之一是对抗病毒感染，并且腺病毒中进化出的14,７00道尔顿蛋白质可抵消TNF的抗病毒作用。