Host cell autophagy promotes BK virus infection

Area of Science:

• Virology
• Cell Biology
• Molecular Biology

Background:

• Autophagy, a cellular degradation process, plays a role in various viral life cycles.
• The specific role of autophagy in human BK polyomavirus (BKPyV) infection remains largely uncharacterized.

Purpose of the Study:

• To investigate the role of autophagy in the replication and lifecycle of human BK polyomavirus (BKPyV).

Main Methods:

• Manipulating autophagy levels using chemical inhibitors (3-MA, bafilomycin A1, spautin-1, rapamycin) and siRNA knockdown of autophagy genes (ATG7, Beclin-1).
• Assessing BKPyV infection levels under altered autophagy conditions.
• Analyzing autophagosome formation and viral particle localization within cellular compartments using microscopy.

Main Results:

• Excess amino acids, which can influence autophagy, reduced BKPyV infection.
• Inhibitors of autophagy (3-MA, bafilomycin A1, spautin-1) decreased BKPyV infection.
• Rapamycin treatment, which enhances autophagy, increased BKPyV infection.
• Knockdown of ATG7 and Beclin-1 genes led to reduced BKPyV infection.
• BKPyV infection correlated with autophagosome formation and viral particles were found in autophagy-specific compartments.

Conclusions:

• Autophagy plays a novel, supportive role in promoting human BK polyomavirus (BKPyV) infection.
• Modulating autophagy can impact BKPyV viral load, suggesting potential therapeutic targets.