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痘苗病毒丝氨酸蛋白酶抑制剂B13R和B22R不抑制向I类限制性细胞毒性T淋巴细胞的抗原呈递。

Vaccinia virus serpins B13R and B22R do not inhibit antigen presentation to class I-restricted cytotoxic T lymphocytes.

作者信息

Blake N W, Kettle S, Law K M, Gould K, Bastin J, Townsend A R, Smith G L

机构信息

Sir William Dunn School of Pathology, University of Oxford, UK.

出版信息

J Gen Virol. 1995 Sep;76 ( Pt 9):2393-8. doi: 10.1099/0022-1317-76-9-2393.

Abstract

Vaccinia virus (VV) inhibits the presentation of certain epitopes from influenza virus nucleoprotein (NP), haemagglutinin (HA) and non-structural 1 (NS1) proteins to CD8+ cytotoxic T lymphocytes (CTL) by an unknown mechanism. We have investigated whether VV genes B13R and B22R, which encode proteins with amino acid similarity to serine protease inhibitors (serpins), are involved in this process. Recombinant VVs were constructed which express influenza virus proteins HA, NP or NS1 and which lack serpin gene B13R or both B13R and B22R. The lysis of cells infected with these viruses by influenza virus-specific CD8+ CTL was compared to the lysis of cells infected with viruses expressing both the influenza proteins and the serpin genes. Cytotoxicity assays showed that deletion of the VV serpin genes B13R and B22R and other genes between B13R and B24R did not increase the level of lysis, indicating that these genes are not involved in inhibition of antigen presentation of the epitopes tested.

摘要

痘苗病毒(VV)通过一种未知机制抑制流感病毒核蛋白(NP)、血凝素(HA)和非结构1(NS1)蛋白的某些表位向CD8 + 细胞毒性T淋巴细胞(CTL)的呈递。我们研究了编码与丝氨酸蛋白酶抑制剂(丝氨酸蛋白酶抑制剂)氨基酸相似性蛋白的VV基因B13R和B22R是否参与此过程。构建了表达流感病毒蛋白HA、NP或NS1且缺失丝氨酸蛋白酶抑制剂基因B13R或同时缺失B13R和B22R的重组VV。将流感病毒特异性CD8 + CTL对感染这些病毒的细胞的裂解与感染同时表达流感蛋白和丝氨酸蛋白酶抑制剂基因的病毒的细胞的裂解进行比较。细胞毒性试验表明,VV丝氨酸蛋白酶抑制剂基因B13R和B22R以及B13R和B24R之间的其他基因的缺失并未增加裂解水平,表明这些基因不参与所测试表位的抗原呈递抑制。

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