tetano
Editor, Senior Moderator
J Microbiol
. 2022 Nov;60(11):1113-1121.
doi: 10.1007/s12275-022-2436-x. Epub 2022 Nov 1.
Inhibition of KIF20A suppresses the replication of influenza A virus by inhibiting viral entry
Hoyeon Jeon[SUP] 1 [/SUP], Younghyun Lim[SUP] 1 [/SUP], In-Gu Lee[SUP] 1 [/SUP], Dong-In Kim[SUP] 1 [/SUP], Keun Pil Kim[SUP] 1 [/SUP], So-Hee Hong[SUP] 2 [/SUP], Jeongkyu Kim[SUP] 3 [/SUP], Youn-Sang Jung[SUP] 4 [/SUP], Young-Jin Seo[SUP] 5 [/SUP]
Affiliations
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.
Keywords: KIF20A; influenza A virus; paprotrain.
. 2022 Nov;60(11):1113-1121.
doi: 10.1007/s12275-022-2436-x. Epub 2022 Nov 1.
Inhibition of KIF20A suppresses the replication of influenza A virus by inhibiting viral entry
Hoyeon Jeon[SUP] 1 [/SUP], Younghyun Lim[SUP] 1 [/SUP], In-Gu Lee[SUP] 1 [/SUP], Dong-In Kim[SUP] 1 [/SUP], Keun Pil Kim[SUP] 1 [/SUP], So-Hee Hong[SUP] 2 [/SUP], Jeongkyu Kim[SUP] 3 [/SUP], Youn-Sang Jung[SUP] 4 [/SUP], Young-Jin Seo[SUP] 5 [/SUP]
Affiliations
- PMID: 36318360
- DOI: 10.1007/s12275-022-2436-x
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.
Keywords: KIF20A; influenza A virus; paprotrain.