Superinfection exclusion by vesicular stomatitis virus

Area of Science:

• Virology
• Cell Biology
• Molecular Biology

Background:

• Vesicular stomatitis virus (VSV) infection in baby hamster kidney (BHK21) cells leads to a phenomenon where cells resist superinfection.
• This resistance affects the ability of BHK21 cells to be infected by subsequent VSV virions or defective-interfering particles.

Purpose of the Study:

• To investigate the mechanism behind VSV-induced superinfection exclusion in BHK21 cells.
• To determine the role of viral gene expression and specific viral components in this exclusion phenomenon.

Main Methods:

• Infection of BHK21 cells with the Indiana strain of VSV.
• Assessing the susceptibility of infected cells to superinfection by VSV virions and defective-interfering particles.
• Evaluating the effect of other viruses (encephalomyocarditis, Newcastle disease, influenza A) on VSV superinfection.
• Investigating the requirement for viral gene expression and VSV glycoprotein G.

Main Results:

• VSV infection of BHK21 cells rapidly inhibits superinfection by VSV.
• This exclusion mechanism operates at the level of virus penetration.
• Viral gene expression and a functional VSV transmembrane glycoprotein G are essential for the exclusion.
• Infection with the New Jersey serotype of VSV also inhibits Indiana serotype VSV uptake.
• Infection with encephalomyocarditis, Newcastle disease, or influenza A viruses does not confer resistance to VSV superinfection.

Conclusions:

• VSV establishes a potent superinfection exclusion mechanism in BHK21 cells.
• The VSV glycoprotein G plays a critical role in mediating this exclusion, likely by interfering with virus entry.
• The exclusion is specific to VSV and not induced by other unrelated RNA or DNA viruses.