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KAP1 Positively Modulates Influenza A Virus Replication by Interacting with PB2 and NS1 Proteins in Human Lung
Huapeng Feng1, Ruonan Yi1, Shixiang Wu1
1Department of Biopharmacy, College of Life Sciences and Medicine, Zhejiang Sci-Tech University, Hangzhou 310018, China.
Abstract:
Influenza virus only encodes a dozen of viral proteins, which need to use host machinery to complete the viral life cycle. Previously, KAP1 was identified as one host protein that potentially interacts with influenza viral proteins in HEK 293 cells. However, the role of KAP1 in influenza virus replication in human lung alveolar epithelial cells and the underlying mechanism remains unclear. In this study, we first generated KAP1 KO A549 cells by CRISPR/Cas9 gene editing. KAP1 deletion had no significant effect on the cell viability and lack of KAP1 expression significantly reduced the influenza A virus replication. Moreover, we demonstrated that KAP1 is involved in the influenza virus entry, transcription/replication of viral genome, and viral protein synthesis in human lung epithelial cells and confirmed that KAP1 interacted with PB2 and NS1 viral proteins during the virus infection. Further study showed that KAP1 inhibited the production of type I IFN and overexpression of KAP1 significantly reduced the IFN-β production. In addition, influenza virus infection induces the deSUMOylation and enhanced phosphorylation of KAP1. Our results suggested that KAP1 is required for the replication of influenza A virus and mediates the replication of influenza A virus by facilitating viral infectivity and synthesis of viral proteins, enhancing viral polymerase activity, and inhibiting the type I IFN production.
Insights
Kaplan-adult-protein 1 (KAP1) is essential for influenza A virus replication in human lung cells. KAP1 facilitates viral entry, replication, protein synthesis, and inhibits the host
Area of Science:
- Virology
- Molecular Biology
- Immunology
Background:
- Influenza A virus relies on host cell machinery for replication.
- Kaplan-adult-protein 1 (KAP1) was previously suggested to interact with influenza viral proteins.
- The specific role and mechanism of KAP1 in influenza virus replication in lung epithelial cells were unknown.
Purpose of the Study:
- To investigate the role of KAP1 in influenza A virus replication in human lung alveolar epithelial cells.
- To elucidate the underlying mechanisms by which KAP1 influences viral replication.
- To determine KAP1's interaction with viral proteins and its effect on host immune response.
Main Methods:
- Generated KAP1 knockout (KO) A549 cells using CRISPR/Cas9 gene editing.
- Assessed influenza A virus replication in wild-type and KAP1 KO cells.
- Confirmed KAP1 interaction with viral proteins (PB2, NS1) and analyzed its effect on type I Interferon (IFN) production.
Main Results:
- KAP1 deletion significantly reduced influenza A virus replication without affecting cell viability.
- KAP1 was found to be involved in viral entry, genome transcription/replication, and protein synthesis.
- KAP1 interacted with PB2 and NS1 viral proteins, inhibited type I IFN production, and its phosphorylation/deSUMOylation was induced by viral infection.
Conclusions:
- KAP1 is essential for efficient influenza A virus replication in human lung epithelial cells.
- KAP1 facilitates viral infectivity, protein synthesis, and polymerase activity while suppressing the type I IFN response.
- KAP1 represents a potential host-targeting strategy for antiviral therapies against influenza A virus.
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