| Literature DB >> 25086213 |
Shuqi Xiao1, Angke Zhang1, Chong Zhang1, Huaibo Ni1, Jiming Gao1, Chengbao Wang1, Qin Zhao1, Xiangpeng Wang1, Xue Wang1, Chao Ma1, Hongliang Liu1, Na Li1, Yang Mu1, Yani Sun1, Gaiping Zhang2, Julian A Hiscox3, Walter H Hsu4, En-Min Zhou5.
Abstract
Virus replication depends upon host-cell processes in infected cells, and this is true for porcine reproductive and respiratory syndrome virus (PRRSV), the causative agent of PRRS that is a worldwide threat to the swine industry. Heme oxygenase-1 (HO-1) is a ubiquitously expressed inducible isoform of the first and rate-limiting enzyme for heme degradation. Our previous research suggested that HO-1 may play an important role in PRRSV infection. However, the function of HO-1 in PRRSV infection is unclear. In the present study, Marc-145, PK-15(CD163) cell lines and porcine alveolar macrophages (PAMs) were used to evaluate the effects of HO-1 induction and over-expression on the replication of two different PRRSV strains. Induction of HO-1 markedly decreased the replication of PRRSV strains in the different cells. Similarly, adenoviral-mediated over-expression of HO-1 also greatly decreased the replication of PRRSV. In contrast, ablation of HO-1 using small interfering RNA concomitantly increased PRRSV replication. Therefore, the data were consistent with HO-1 acting as an antiviral factor and these findings suggested that over-expression or induction of HO-1 may provide a potential therapeutic strategy against PRRSV infection.Entities:
Keywords: Antivirus factor; HO-1; Highly pathogenic PRRSV; PRRSV; siRNA
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Year: 2014 PMID: 25086213 DOI: 10.1016/j.antiviral.2014.07.011
Source DB: PubMed Journal: Antiviral Res ISSN: 0166-3542 Impact factor: 5.970