Generation of an infectious clone of AMDV and identification of capsid residues essential for infectivity in cell culture

文献类型： 外文期刊

第一作者： Xi, Ji

作者： Xi, Ji;Wang, Jigui;Yu, Yongle;Zhang, Xiaomei;Li, Zhaoda;Liu, Weiquan;Zhang, Yanlong;Cui, Shangjin;Cui, Shangjin

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关键词： Aleutian mink disease virus;Infectious molecular clone;VP2 protein;Functional residues

期刊名称：VIRUS RESEARCH （ 影响因子：3.303； 五年影响因子：3.445 ）

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收录情况： SCI

摘要： Highlights ? Pathogenic strains of AMDV, such as Utah-1, do not replicate in cell culture. ? In this study, we constructed a full-length infectious clone (pADV-G). ? Four virulence-associated residues of pADV-G VP2 were studied by mutagenesis. ? Mutation of H92 or Q94 decreased transcription and replication. ? VP2 residues 92 and 94 are critical for AMDV replication in vitro . Abstract Pathogenic strains of Aleutian mink disease virus (AMDV) such as Utah-1 do not replicate in cell culture (e.g., Crandell Rees feline kidney cells) while the in vitro- adapted AMDV strain ADV-Gorham (ADV-G) is not pathogenic. Here, we constructed a full-length infectious clone (pADV-G). Alignment of the VP2 gene of ADV-G with that of other AMDV strains revealed many amino acid (a.a.) residues conserved among pathogenic isolates that differed in ADV-G. Four virulence-associated, conserved residues of pADV-G VP2 were studied by site-directed mutagenesis (H92A, Q94S, Y115F, and I116L). Mutation of residue 92 or 94 decreased viral-transcription and viral-infectivity levels, whereas mutation of residue 115 or 116 did not affect viral-infectivity in CRFK cells. These results indicated that VP2 residues 92 and 94, both located on the surface of the viral capsid, are critical for AMDV infectivity in vitro .

分类号： R37

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