期刊
ANTIVIRAL RESEARCH
卷 165, 期 -, 页码 42-46出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.antiviral.2019.03.002
关键词
Antiviral; Stearoyl-CoA desaturase-1; Unsaturated fatty acids; Dengue virus; Flavivirus; Replicon
资金
- JSPS KAKENHI [JP17K08870]
- Research Program on Emerging and Re-emerging Infectious Diseases of the Japan Agency for Medical Research and Development (AMED) [JP18fk0108035]
- National Medical Research Council [NMRC/CBRG/0103/2016]
- National Research Foundation [NRF2016NRF-CRP001-063]
Dengue virus (DENV) is the most prevalent human arthropod-borne virus and causes severe problems worldwide, mainly in tropical and sub-tropical regions. However, there is no specific antiviral drug against DENV infection. We and others recently reported that stearoyl-CoA desaturase-1 (SCD1) inhibitor showed potent suppression of hepatitis C virus replication. In this study, we examined the impact of SCD1 on DENV replication. We found that SCD1 inhibitors (MK8245 and #1716) dramatically suppressed DENV replication in a dose dependent manner without cytotoxicity. This anti-DENV efficacy was observed against all four DENV serotypes and other flaviviruses, including Zika virus and Japanese encephalitis virus. A subgenomic replicon system of DENV was used to confirm that SCD1 inhibitor suppressed viral RNA replication. Interestingly, exogenous supplementation of unsaturated fatty acids resulted in recovery of the DENV titer even in the presence of SCD1 inhibitor, suggesting that fatty acid biosynthesis contributes to DENV genome replication. These findings indicate that SCD1 is a novel host factor required for DENV replication, and SCD1 inhibitor is a potential candidate for treating dengue fever.
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