Inhibition of KIF20A suppresses the replication of influenza A virus by inhibiting viral entry

Hoyeon Jeon, Younghyun Lim, In Gu Lee, Dong In Kim, Keun Pil Kim, So Hee Hong, Jeongkyu Kim, Youn Sang Jung, Young Jin Seo

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish
Pages (from-to)1113-1121
Number of pages9
JournalJournal of Microbiology
Issue number11
StatePublished - Nov 2022

Bibliographical note

Funding Information:
This study was supported by the National Research Foundation of Korea (NRF) grant funded by the Korean government [grant number: NRF-2018R1A5A1025077, 2021R1F1-A1047001, 2021R1I1A1A01041639].

Publisher Copyright:
© 2022, Author(s).


  • KIF20A
  • influenza A virus
  • paprotrain


Dive into the research topics of 'Inhibition of KIF20A suppresses the replication of influenza A virus by inhibiting viral entry'. Together they form a unique fingerprint.

Cite this