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Article

Transportin-3 Facilitates Uncoating of Influenza A Virus

1
State Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan 430070, China
2
Key Laboratory of Preventive Veterinary Medicine in Hubei Province, The Cooperative Innovation Center for Sustainable Pig Production, Wuhan 430070, China
3
Key Laboratory of Agricultural Animal Genetics, Breeding and Reproduction of Ministry of Education & Key Lab of Swine Genetics and Breeding of Ministry of Agriculture and Rural Affairs, Huazhong Agricultural University, Wuhan 430070, China
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Academic Editors: Joan Puig-Barberà, María Lourdes Guerrero, Anna Sominina, Svetlana V. Trushakova and F. Xavier López-Labrador
Int. J. Mol. Sci. 2022, 23(8), 4128; https://doi.org/10.3390/ijms23084128
Received: 5 March 2022 / Revised: 25 March 2022 / Accepted: 2 April 2022 / Published: 8 April 2022
(This article belongs to the Topic Acute Respiratory Viruses Molecular Epidemiology)
Influenza A viruses (IAVs) are a major global health threat and in the future, may cause the next pandemic. Although studies have partly uncovered the molecular mechanism of IAV–host interaction, it requires further research. In this study, we explored the roles of transportin-3 (TNPO3) in IAV infection. We found that TNPO3-deficient cells inhibited infection with four different IAV strains, whereas restoration of TNPO3 expression in knockout (KO) cells restored IAV infection. TNPO3 overexpression in wild-type (WT) cells promoted IAV infection, suggesting that TNPO3 is involved in the IAV replication. Furthermore, we found that TNPO3 depletion restrained the uncoating in the IAV life cycle, thereby inhibiting the process of viral ribonucleoprotein (vRNP) entry into the nucleus. However, KO of TNPO3 did not affect the virus attachment, endocytosis, or endosomal acidification processes. Subsequently, we found that TNPO3 can colocalize and interact with viral proteins M1 and M2. Taken together, the depletion of TNPO3 inhibits IAV uncoating, thereby inhibiting IAV replication. Our study provides new insights and potential therapeutic targets for unraveling the mechanism of IAV replication and treating influenza disease. View Full-Text
Keywords: TNPO3; CRISPR/Cas9; influenza virus; uncoating TNPO3; CRISPR/Cas9; influenza virus; uncoating
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MDPI and ACS Style

Zou, J.; Yu, L.; Zhu, Y.; Yang, S.; Zhao, J.; Zhao, Y.; Jiang, M.; Xie, S.; Liu, H.; Zhao, C.; Zhou, H. Transportin-3 Facilitates Uncoating of Influenza A Virus. Int. J. Mol. Sci. 2022, 23, 4128. https://doi.org/10.3390/ijms23084128

AMA Style

Zou J, Yu L, Zhu Y, Yang S, Zhao J, Zhao Y, Jiang M, Xie S, Liu H, Zhao C, Zhou H. Transportin-3 Facilitates Uncoating of Influenza A Virus. International Journal of Molecular Sciences. 2022; 23(8):4128. https://doi.org/10.3390/ijms23084128

Chicago/Turabian Style

Zou, Jiahui, Luyao Yu, Yinxing Zhu, Shuaike Yang, Jiachang Zhao, Yaxin Zhao, Meijun Jiang, Shengsong Xie, Hailong Liu, Changzhi Zhao, and Hongbo Zhou. 2022. "Transportin-3 Facilitates Uncoating of Influenza A Virus" International Journal of Molecular Sciences 23, no. 8: 4128. https://doi.org/10.3390/ijms23084128

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