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DOI 10.1038/srep15575

Медицинская библиотека · Scientific reports · 2015

Heme Oxygenase-1 Suppresses Bovine Viral Diarrhoea Virus Replication in vitro.

Zhang Chong, Pu Fengxing, Zhang Angke, Xu Lele, Li Na, Yan Yunhuan, Gao Jiming, Liu Hongliang, Zhang Gaiping, Goodfellow Ian G, Zhou En-Min, Xiao Shuqi

СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАПеревод в очереди

Аннотация

Viral cycle progression depends upon host-cell processes in infected cells, and this is true for bovine viral diarrhoea virus (BVDV), the causative agent of BVD that is a worldwide threat to the bovine industry. Heme oxygenase-1 (HO-1) is a ubiquitously expressed inducible isoform of the first and rate-limiting enzyme for heme degradation. Recent studies have demonstrated that HO-1 has significant antiviral properties, inhibiting the replication of viruses such as ebola virus, human immunodeficiency virus, hepatitis C virus, and porcine reproductive and respiratory syndrome virus. However, the function of HO-1 in BVDV infection is unclear. In the present study, the relationship between HO-1 and BVDV was investigated. In vitro analysis of HO-1 expression in BVDV-infected MDBK cells demonstrated that a decrease in HO-1 as BVDV replication increased. Increasing HO-1 expression through adenoviral-mediated overexpression or induction with cobalt protoporphyrin (CoPP, a potent HO-1 inducer), pre- and postinfection, effectively inhibited BVDV replication. In contrast, HO-1 siRNA knockdown in BVDV-infected cells increased BVDV replication. Therefore, the data were consistent with HO-1 acting as an anti-viral factor and these findings suggested that induction of HO-1 may be a useful prevention and treatment strategy against BVDV infection.

Для цитирования: Zhang Chong, Pu Fengxing, Zhang Angke, Xu Lele, Li Na, Yan Yunhuan, Gao Jiming, Liu Hongliang, Zhang Gaiping, Goodfellow Ian G, Zhou En-Min, Xiao Shuqi. Heme Oxygenase-1 Suppresses Bovine Viral Diarrhoea Virus Replication in vitro.. Scientific reports. 2015. DOI: 10.1038/srep15575.

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