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dc.contributor.authorTseng, Chin-Kaien_US
dc.contributor.authorLin, Chun-Kuangen_US
dc.contributor.authorWu, Yu-Hsuanen_US
dc.contributor.authorChen, Yen-Hsuen_US
dc.contributor.authorChen, Wei-Chunen_US
dc.contributor.authorYoung, Kung-Chiaen_US
dc.contributor.authorLee, Jin-Chingen_US
dc.date.accessioned2019-04-03T06:40:07Z-
dc.date.available2019-04-03T06:40:07Z-
dc.date.issued2016-08-24en_US
dc.identifier.issn2045-2322en_US
dc.identifier.urihttp://dx.doi.org/10.1038/srep32176en_US
dc.identifier.urihttp://hdl.handle.net/11536/134078-
dc.description.abstractDengue virus (DENV) infection and replication induces oxidative stress, which further contributes to the progression and pathogenesis of the DENV infection. Modulation of host antioxidant molecules may be a useful strategy for interfering with DENV replication. In this study, we showed that induction or exogenous overexpression of heme oxygenase-1 (HO-1), an antioxidant enzyme, effectively inhibited DENV replication in DENV-infected Huh-7 cells. This antiviral effect of HO-1 was attenuated by its inhibitor tin protoporphyrin (SnPP), suggesting that HO-1 was an important cellular factor against DENV replication. Biliverdin but not carbon monoxide and ferrous ions, which are products of the HO-1 on heme, mediated the HO-1-induced anti-DENV effect by non-competitively inhibiting DENV protease, with an inhibition constant (Ki) of 8.55 +/- 0.38 mu M. Moreover, HO-1 induction or its exogenous overexpression, rescued DENV-suppressed antiviral interferon response. Moreover, we showed that HO-1 induction by cobalt protoporphyrin (CoPP) and andrographolide, a natural product, as evidenced by a significant delay in the onset of disease and mortality, and virus load in the infected mice's brains. These findings clearly revealed that a drug or therapy that induced the HO-1 signal pathway was a promising strategy for treating DENV infection.en_US
dc.language.isoen_USen_US
dc.titleHuman heme oxygenase 1 is a potential host cell factor against dengue virus replicationen_US
dc.typeArticleen_US
dc.identifier.doi10.1038/srep32176en_US
dc.identifier.journalSCIENTIFIC REPORTSen_US
dc.citation.volume6en_US
dc.citation.spage0en_US
dc.citation.epage0en_US
dc.contributor.department生醫工程研究所zh_TW
dc.contributor.departmentInstitute of Biomedical Engineeringen_US
dc.identifier.wosnumberWOS:000381853800001en_US
dc.citation.woscount17en_US
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