Impaired Japanese encephalitis virus replication in p62/SQSTM1 deficient mouse embryonic fibroblasts

Area of Science:

• Virology
• Cell Biology
• Molecular Biology

Background:

• Autophagy is a cellular process involved in degrading damaged components.
• p62/SQSTM1 is an autophagy adaptor protein crucial for selective autophagy.
• Japanese encephalitis virus (JEV) causes severe neurological disease.

Purpose of the Study:

• To investigate the role of p62/SQSTM1 in JEV replication.
• To determine if p62 influences JEV RNA and protein production.
• To assess the impact of p62 deficiency on viral titers.

Main Methods:

• Used p62-deficient mouse embryonic fibroblasts (MEFs) and wild-type MEFs.
• Infected cells with JEV.
• Quantified JEV RNA and E protein levels at 24 hours post-infection (p.i.).
• Performed viral plaque assays to determine viral titers.

Main Results:

• JEV RNA and E protein levels were significantly lower in p62-deficient MEFs compared to wild-type MEFs at 24 hr p.i.
• Viral RNA quantitation and plaque assays revealed significantly reduced viral titers in the culture fluid of p62-deficient cells.
• JEV replication was impaired in the absence of p62.

Conclusions:

• p62/SQSTM1 positively regulates JEV replication in host cells.
• p62 deficiency leads to reduced JEV propagation.
• This suggests p62 is a potential host factor for JEV.