KIF11 inhibition decreases cytopathogenesis and replication of influenza A virus

Background Seasonal flu is an infectious disease of the respiratory tract caused by influenza viruses. The development of anti-influenza drugs has significantly reduced the threat from the influenza virus; however, frequent mutations of this negative RNA virus result in antiviral-resistant strains,...

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Bibliographic Details
Published in:Molecular & cellular toxicology 2021, 17(2), , pp.201-212
Main Authors: Kim, Dong-In, Kang, Ji-Hun, Kim, Eui-Ho, Seo, Young-Jin
Format: Article
Language:English
Subjects:
Antiviral agents
Biomedical and Life Sciences
Cell Biology
Cytopathogenesis
Cytotoxicity
Drug development
Infectious diseases
Influenza
Influenza A
Kinesin
Life Sciences
Original Article
Pharmacology/Toxicology
Replication
Respiratory tract diseases
RNA viruses
Therapeutic applications
Viruses
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Summary:Background Seasonal flu is an infectious disease of the respiratory tract caused by influenza viruses. The development of anti-influenza drugs has significantly reduced the threat from the influenza virus; however, frequent mutations of this negative RNA virus result in antiviral-resistant strains, and constantly intimidate the human race. Thus, identifying novel therapeutic targets for the prevention and treatment of influenza virus infections is critical. Objective We aimed to determine whether the kinesin superfamily protein 11 (KIF11) inhibitors, monastrol and K858, inhibit viral cytopathogenesis and influenza A virus (IAV) replication. Result When MDCK or HEK293 cells were treated with monastrol and K858 that did not induce significant cytotoxicity, IAV-induced cytopathic effect was attenuated significantly. Furthermore, these inhibitors effectively suppressed the production of viral RNA, proteins, and infectious viral particles. Conclusion Inhibition of KIF11 activity effectively attenuates virus-mediated cytopathic effect and suppresses viral replication. Hence, KIF11 is a potential therapeutic target against the influenza virus.
ISSN:1738-642X
2092-8467
DOI:10.1007/s13273-021-00126-9