Coxsackievirus B 3Cpro Protease Cleaves MAVS and TRIF to Attenuate Host Type I Interferon and Apoptotic Signaling
Author Information
Author(s): Amitava Mukherjee, Stefanie A. Morosky, Elizabeth Delorme-Axford, Naomi Dybdahl-Sissoko, M. Steven Oberste, Tianyi Wang, Carolyn B. Coyne
Primary Institution: University of Pittsburgh
Hypothesis
Coxsackievirus B3 (CVB3) uses its 3Cpro protease to cleave MAVS and TRIF, thereby suppressing host immune responses.
Conclusion
CVB3's 3Cpro protease cleaves MAVS and TRIF, which inhibits type I interferon and apoptotic signaling, allowing the virus to evade host immunity.
Supporting Evidence
- CVB3 infection cleaves MAVS and TRIF, inhibiting type I IFN signaling.
- 3Cpro is necessary for the cleavage of MAVS and TRIF.
- Cleavage of MAVS and TRIF occurs at specific sites that disrupt their signaling functions.
- 3Cpro localizes to TRIF signalosomes and interacts with TRIF.
Takeaway
Coxsackievirus B3 has a special tool that cuts important parts of our immune system, helping it hide from our body's defenses.
Methodology
The study involved infecting cells with CVB3 and analyzing the cleavage of MAVS and TRIF using immunoblotting and luciferase assays.
Limitations
The study primarily focused on in vitro experiments, and the in vivo relevance of the findings needs further investigation.
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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