Niclosamide inhibits hepatitis E virus through suppression of NF-kappaB signalling

Yunlong Li, Pengfei Li, Qiyu He, Ruyi Zhang, Yang Li, Nassim Kamar, Maikel P. Peppelenbosch, Robert A. de Man, Lin Wang, Qiuwei Pan*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

7 Citations (Scopus)
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Hepatitis E virus (HEV) infection can cause severe acute hepatitis in pregnant women and chronic infection in immunocompromised patients, promoting the development of effective antiviral therapies. In this study, we identified niclosamide, a widely used anthelmintic drug, as a potent inhibitor of HEV replication in a range of subgenomic and full-length HEV models, which are based on human cell lines and liver organoids harbouring genotype 1 and 3 HEV strains. Niclosamide is known to have multiple cellular targets including the inhibition of STAT3 and NFκB signaling pathways. Although HEV activates STAT3, we excluded its involvement in the anti-HEV activity of niclosamide. Interestingly, HEV infection activated NFκB and activation of NFκB promoted viral replication. Consistently, stable silencing of NFκB by lentiviral RNAi inhibited HEV replication. By targeting NFκB signaling, we further revealed its role in mediating the anti-HEV action of niclosamide. These results demonstrated that niclosamide potently inhibits HEV replication by inhibiting NFκB signaling but independent of STAT3. Our findings support the potential of repurposing niclosamide for treating HEV infection.

Original languageEnglish
Article number105228
JournalAntiviral Research
Publication statusPublished - 1 Jan 2022

Bibliographical note

Funding Information:
This study is supported by a VIDI grant (No. 91719300 ) from the Netherlands Organisation for Scientific Research (NWO) to Q. Pan, and the China Scholarship Council for funding PhD fellowship to Yunlong L (No. 201708530243 ), P.L (No. 201808370170 ), R.Z. (No. 201808530490 ), and Yang. L (No. 201703250073 ).

Publisher Copyright:
© 2021 The Authors


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