| Title | Inhibition of KIF20A suppresses the replication of influenza A virus by inhibiting viral entry |
|---|---|
| Author | Hoyeon Jeon1, Younghyun Lim1, In-Gu Lee1, Dong-In Kim1, Keun Pil Kim1, So-Hee Hong2, Jeongkyu Kim1*, Youn-Sang Jung1*, and Young-Jin Seo1* |
| Address | 1Department of Life Science, Chung-Ang University, Seoul 06974, Republic of Korea, 2Department of Microbiology, College of Medicine, Ewha Womans University, Seoul 07804, Republic of Korea |
| Bibliography | Journal of Microbiology, 60(11),1113-1121, 2022, |
| DOI | 10.1007/s12275-022-2436-x |
| Key Words | influenza A virus, KIF20A, paprotrain |
| Abstract | The influenza A virus (IAV) has caused several pandemics, and therefore there are many ongoing efforts to identify novel antiviral therapeutic strategies including vaccines and antiviral drugs. However, influenza viruses continuously undergo antigenic drift and shift, resulting in the emergence of mutated viruses. In turn, this decreases the efficiency of existing vaccines and antiviral drugs to control IAV infection. Therefore, this study sought to identify alternative therapeutic strategies targeting host cell factors rather than viruses to avoid infection by mutated viruses. Particularly, we investigated the role of KIF20A that is one of kinesin superfamily proteins in the replication of IAV. The KIF20A increased viral protein levels in IAV-infected cells by regulating the initial entry stage during viral infection. Furthermore, the KIF20A inhibitor significantly suppressed viral replication, which protected mice from morbidity and mortality. Therefore, our findings demonstrated that KIF20A is highly involved in the viral replication process and viral propagation both in vitro and in vivo, and could thus be used as a target for the development of novel antiviral drugs. |