CD59 association with infectious bronchitis virus particles protects against antibody-dependent complement-mediated...

Area of Science:

• Immunology
• Virology
• Molecular Biology

Background:

• CD59 protein regulates the complement system's terminal pathway by inhibiting C8/C9 factors.
• The role of CD59 in coronavirus infectious bronchitis virus (IBV) infection remains largely unexplored.

Purpose of the Study:

• To investigate the role of CD59 in IBV infection.
• To determine if CD59 influences viral particle release and immune evasion.

Main Methods:

• Analyzing CD59 expression levels in IBV-infected cells.
• Assessing the association of CD59 with IBV virions.
• Evaluating the impact of CD59 overexpression, knockdown, and cleavage on viral titers and viral components.

Main Results:

• CD59 expression was found to be downregulated in IBV-infected cells.
• CD59 was associated with IBV virions, protecting them from complement-mediated lysis.
• Overexpression of CD59 increased IBV titers, while knockdown/cleavage decreased them, suggesting a role in viral release.
• No significant changes in IBV N protein or viral RNA were observed in cell lysates, indicating CD59's role is in release, not replication.

Conclusions:

• CD59 plays a crucial role in facilitating IBV particle release.
• IBV has evolved a mechanism to exploit CD59 for protection against antibody-dependent complement-mediated lysis.
• CD59 downregulation is a key feature of IBV infection, aiding viral evasion and propagation.