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Possible involvement of double-stranded RNA-activated protein kinase in cell death by influenza virus infection
T Takizawa1, K Ohashi, Y Nakanishi
1Department of Biochemistry, Institute for Developmental Research, Aichi Human Service Center, Kasugai, Japan.
Abstract:
We reported previously that influenza virus infection induces the apoptotic death of HeLa cells associated with activation of the Fas gene. In this report, we show that transfection with a PKR having a point mutation in the catalytic domain of K at 296 to R suppressed both the augmented expression of Fas and cell death by influenza virus infection. These results suggested the involvement of PKR in influenza virus-induced cell death.
Insights
Influenza virus causes cell death by activating the Fas gene. A mutated PKR protein blocked this Fas gene activation and subsequent cell death, indicating PKR
Area of Science:
- Virology
- Cell Biology
- Molecular Biology
Background:
- Influenza virus infection is known to induce apoptotic cell death in host cells.
- Previous studies linked this cell death to the activation of the Fas gene.
- Protein kinase R (PKR) is a key mediator of cellular responses to viral infections.
Purpose of the Study:
- To investigate the role of Protein kinase R (PKR) in influenza virus-induced apoptosis.
- To determine if PKR modulates Fas gene expression during influenza virus infection.
Main Methods:
- Transfection of HeLa cells with a mutated form of PKR (catalytic domain mutation K296R).
- Infection of transfected cells with influenza virus.
- Analysis of Fas gene expression and cell viability.
Main Results:
- Transfection with mutated PKR significantly suppressed the augmented expression of the Fas gene induced by influenza virus.
- The mutated PKR also suppressed influenza virus-induced cell death in HeLa cells.
- These findings highlight a critical role for PKR in the apoptotic pathway.
Conclusions:
- Protein kinase R (PKR) is involved in mediating influenza virus-induced apoptotic cell death.
- PKR appears to regulate Fas gene expression, contributing to viral pathogenesis.
- Targeting PKR could be a potential strategy to mitigate influenza virus-induced cell damage.