Key result
TGEV infection evades type I interferon responses via IRE1α activation to boost viral replication.
Population
Models of Coronavirus Transmissible Gastroenteritis Virus (TGEV) infection
Design
Preclinical
Authors
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TGEV exploits IRE1α to suppress IFN-I via miR-30a-5p; leaves open whether this axis offers antiviral targets.
TGEV evades innate immunity by manipulating the IRE1α/miR-30a-5p/SOCS axis, highlighting IRE1α as a potential therapeutic target against coronavirus infection.
Ma et al. (2018) studied Transmissible gastroenteritis virus (TGEV) infection. TGEV infection vs. Mock infection was evaluated on miR-30a-5p levels and SOCS1/3 expression. TGEV infection evades the type I interferon antiviral response by activating IRE1α, which downregulates miR-30a-5p and subsequently increases SOCS1 and SOCS3 expression to facilitate viral replication.
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