The cellular activating protein-1 cFos regulates influenza A virus replication.

Area of Science:

• Virology
• Molecular Biology
• Immunology

Background:

• Influenza A virus (IAV) infection activates transcription factors, including activating protein-1 (AP-1), during the antiviral response.
• The specific role of AP-1 family members in IAV pathogenesis requires further elucidation.

Purpose of the Study:

• To investigate the role of cFos, a key AP-1 transcription factor, in the context of IAV infection in human lung cells.
• To determine the mechanisms by which cFos influences IAV replication and host response.

Main Methods:

• Utilized A549 human lung cells for IAV infection experiments.
• Employed cFos knockdown techniques to assess its impact on viral replication.
• Performed fluorescence microscopy and functional assays to analyze cFos localization and function.
• Quantified apoptosis, interferon-beta mRNA levels, and viral gene expression (NA, M2).

Main Results:

• cFos was identified as the most upregulated AP-1 transcription factor during IAV infection.
• Knockdown of cFos significantly impaired IAV replication.
• cFos exerts its proviral function through nuclear localization, not cytoplasmic lipid synthesis regulation.
• cFos knockdown led to increased apoptosis and elevated interferon-beta mRNA levels.
• Reduced viral NA mRNA and late viral protein expression (NA, M2) were observed upon cFos knockdown.

Conclusions:

• cFos acts as a proviral factor that facilitates IAV proliferation.
• cFos modulates innate immunity by suppressing interferon-beta production and enhances cell survival during IAV infection.
• The findings suggest cFos supports viral transcription, contributing to IAV replication.