Identification of chicken CAR homology as a cellular receptor for the emerging highly pathogenic fowl adenovirus 4 via unique binding mechanism

文献类型： 外文期刊

第一作者： Pan, Qing

作者： Pan, Qing;Wang, Jing;Gao, Yulong;Wang, Qi;Cui, Hongyu;Liu, Changjun;Qi, Xiaole;Zhang, Yanping;Wang, Yongqiang;Li, Kai;Gao, Li;Liu, Aijing;Wang, Xiaomei;Wang, Xiaomei

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关键词： Emerging FAdV-4; novel binding mechanism; cell receptor; chicken CAR; D2 domain; short fibre

期刊名称：EMERGING MICROBES & INFECTIONS （ 影响因子：7.163； 五年影响因子：7.329 ）

ISSN：

年卷期： 2020 年 9 卷 1 期

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收录情况： SCI

摘要： Since 2015, the prevalence of severe hepatitis-hydropericardium syndrome, which is caused by the novel genotype fowl adenovirus serotype 4 (FAdV-4), has increased in China and led to considerable economic losses. The replication cycle of FAdV-4, especially the emerging highly pathogenic novel genotype FAdV-4, remains largely unknown. The adenovirus fibre interacts with the cellular receptor as the initial step in adenovirus (AdV) infection. In our previous studies, the complete genome sequence showed that the fibre patterns of FAdV-4 were distinct from all other AdVs. Here, protein-blockage and antibody-neutralization assays were performed to confirm that the novel FAdV-4 short fibre was critical for binding to susceptible leghorn male hepatocellular (LMH) cells. Subsequently, fibre 1 was used as bait to investigate the receptor on LMH cells via mass spectrometry. The chicken coxsackie and adenovirus receptor (CAR) protein was confirmed as the novel FAdV-4 receptor in competition assays. We further identified the D2 domain of CAR (D2-CAR) as the active domain responsible for binding to the short fibre of the novel FAdV-4. Taken together, these findings demonstrate for the first time that the chicken CAR homolog is a cellular receptor for the novel FAdV-4, which facilitates viral entry by interacting with the viral short fibre through the D2 domain. Collectively, these findings provide an in-depth understanding of the mechanisms of the emerging novel genotype FAdV-4 invasion and pathogenesis.

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