bovine herpesvirus type 1 (bhv-1) ul49.5 luminal domain residues 30 to 32 are critical for mhc-i down-regulation in virus-infected cells牛疱疹病毒1型(bhv-1)ul49.5腔的域残留30 - 32是至关重要的mhc i下调在感染病毒的细胞.pdfVIP

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bovine herpesvirus type 1 (bhv-1) ul49.5 luminal domain residues 30 to 32 are critical for mhc-i down-regulation in virus-infected cells牛疱疹病毒1型(bhv-1)ul49.5腔的域残留30 - 32是至关重要的mhc i下调在感染病毒的细胞.pdf

bovine herpesvirus type 1 (bhv-1) ul49.5 luminal domain residues 30 to 32 are critical for mhc-i down-regulation in virus-infected cells牛疱疹病毒1型(bhv-1)ul49.5腔的域残留30 - 32是至关重要的mhc i下调在感染病毒的细胞

Bovine Herpesvirus Type 1 (BHV-1) U 49.5 Luminal L Domain Residues 30 to 32 Are Critical for MHC-I Down-Regulation in Virus-Infected Cells Huiyong Wei, Ying Wang, Shafiqul I. Chowdhury* Department of Pathobiological Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, Louisiana, United States of America Abstract Bovine herpesvirus type 1 (BHV-1) U 49.5 inhibits transporter associated with antigen processing (TAP) and down-regulates L cell-surface expression of major histocompatibility complex (MHC) class I molecules to promote immune evasion. We have constructed a BHV-1 U 49.5 cytoplasmic tail (CT) null and several U 49.5 luminal domain mutants in the backbone of wild- L L type BHV-1 or BHV-1 U 49.5 CT- null viruses and determined their relative TAP mediated peptide transport inhibition and L MHC-1 down-regulation properties compared with BHV-1 wt. Based on our results, the UL49.5 luminal domain residues 30– 32 and UL49.5 CT residues, together, promote efficient TAP inhibition and MHC-I down-regulation functions. In vitro, BHV-1 U 49.5 D30–32 CT-null virus growth property was similar to that of BHV-1 wt and like the wt U 49.5, the mutant U 49.5 was L L L incorporated in the virion envelope and it formed a complex with gM in the infected cells. Citation: Wei H, Wang Y, Chowdhury SI (2011) Bovine Herpesvirus Type 1 (BHV-1) U 49.5 Luminal Domain Residues 30 to 32 Are Critical for MHC-I

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