Selenomethionine Inhibited RSV Infection-Induced Apoptosis and Inflammatory Response through ROS-Mediated Signaling...

Area of Science:

• Virology
• Immunology
• Biochemistry

Background:

• Respiratory syncytial virus (RSV) is a major cause of severe lower respiratory tract infections in young children globally.
• Current treatment options for RSV are limited, highlighting the need for new antiviral therapies.
• Selenomethionine (SeMet), a component of selenium supplements, possesses known antioxidant, antiviral, and immunomodulatory properties.

Purpose of the Study:

• To investigate the antiviral mechanism of SeMet against RSV.
• To assess SeMet's effects on apoptosis, DNA damage, cytokine and ROS production, and mitochondrial membrane potential.
• To evaluate SeMet's binding affinity and dynamic interactions with RSV target proteins.

Main Methods:

• Detection of apoptotic markers, DNA damage, cytokine and reactive oxygen species (ROS) levels, and mitochondrial membrane potential.
• Screening of SeMet's affinity for common RSV target proteins.
• Molecular dynamics simulations to explore interactions between SeMet and RSV polymerase.

Main Results:

• SeMet inhibited apoptosis and inflammatory responses by modulating ROS-mediated PARP/Bcl-2 and NF-κB/JAK1-STAT3 signaling pathways.
• SeMet demonstrated a stable interaction with RSV polymerase.
• Hydrogen bonding was identified as the primary interaction between SeMet and key amino acid residues of RSV polymerase.

Conclusions:

• SeMet exhibits antiviral activity against RSV by suppressing apoptosis and inflammation through specific signaling pathways.
• SeMet's stable binding to RSV polymerase suggests its potential as a direct-acting antiviral agent.
• Further research into SeMet as an anti-RSV therapeutic is warranted.