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Influenza A virus induces p53 accumulation in a biphasic pattern
Yang Shen1, Xiaodu Wang, Lin Guo
1Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Science, Shanghai, PR China.
Biochemical and Biophysical Research Communications
|March 12, 2009
Summary
Tumor suppressor p53, crucial for preventing tumors, also aids antiviral defense. This study reveals p53
Area of Science:
- Virology
- Molecular Biology
- Immunology
Background:
- The tumor suppressor p53 is a key factor in cellular defense against tumor development.
- p53 has been recognized for its role in host antiviral defense mechanisms.
- Prior research indicated p53 induction during the apoptotic stage of influenza virus infection.
Purpose of the Study:
- To investigate the temporal pattern of p53 accumulation during influenza virus infection.
- To determine the mechanisms regulating p53 up-regulation in response to influenza virus.
- To assess the functional activity of p53 during influenza virus infection.
Main Methods:
- Influenza virus infection in cell culture models.
- Western blot analysis to detect p53 protein levels.
- Quantitative PCR to assess p53 mRNA transcription.
- Reporter assays to measure p53 transactivation activity.
- Analysis of downstream target gene expression (IRF9, Bax).
Main Results:
- p53 exhibited a biphasic accumulation pattern in influenza virus-infected cells: an early transient elevation and a later, more sustained increase.
- p53 up-regulation was independent of transcriptional changes but dependent on virus adsorption and replication.
- The accumulated p53 was functionally active, evidenced by the transactivation of target genes like IRF9 and Bax.
- This biphasic p53 response is a novel finding in the context of influenza virus infection.
Conclusions:
- Influenza virus infection induces a biphasic accumulation of the tumor suppressor p53.
- p53 up-regulation is regulated post-transcriptionally and linked to viral processes.
- Activated p53 plays a role in the cellular response to influenza virus infection by transactivating key genes.
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