November 30, 2025Journal of VirologyOpen Access

The viral proteins of influenza A virus competitively bind to TRIM31 with MAVS to fine-tune the antiviral innate immunity

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Discussion

Analysis reveals influenza A virus exploits TRIM31 to balance antiviral response in host cells, impacting viral proteins and immunity.

Viral proteins of influenza A virus finely balance antiviral and proviral effects via TRIM31, enhancing immune interactions.
Type-I interferon signaling is modulated by TRIM31, an E3 ubiquitin ligase involved in viral replication dynamics.
E3 ubiquitin ligase TRIM31 enhances stability of viral proteins despite not affecting overall influenza A virus replication directly.
Findings indicate a nuanced strategy of influenza A virus adaptation to host immune responses through TRIM31.

Huang et al. (2025) studied this question.

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