Mumps virus Enders strain is sensitive to interferon (IFN) despite encoding a functional IFN antagonist

Area of Science:

• Virology
• Immunology
• Molecular Biology

Background:

• Mumps virus (MuV) encodes a V protein that antagonizes the interferon (IFN) response.
• MuV Enders strain exhibits poor growth in IFN-competent cells, suggesting host immunity impacts viral replication.

Purpose of the Study:

• To investigate the role of the host IFN system in controlling MuV Enders growth.
• To identify viral factors or adaptations that influence MuV sensitivity to IFN.

Main Methods:

• Multi-cycle growth assays in IFN-competent and IFN-compromised Hep2 cells.
• Selection and sequencing of rapidly growing MuV variants.
• Comparative growth rate analysis with parainfluenza virus type 5.

Main Results:

• MuV Enders grew poorly in naive Hep2 cells but well in compromised cells.
• Rapidly growing variants selected in compromised cells also grew well in naive cells.
• A mutation in the hemagglutinin-neuraminidase (HN) protein was identified in some fast-growing variants.

Conclusions:

• The host IFN system plays a critical role in controlling MuV replication, beyond viral IFN antagonists.
• Viral replication efficiency is influenced by a dynamic interplay between viral evasion and host detection.
• Factors beyond viral IFN antagonists significantly affect a virus's sensitivity to host antiviral responses.