Encephalomyocarditis virus employs intricate strategies to escape the host innate immune machinery and interacts with certain host proteins to dampen the infection process.
This review highlights the mechanisms by which encephalomyocarditis virus evades host innate immunity, contributing to its virulence in causing myocarditis.
A variety of animals can be infected by encephalomyocarditis virus (EMCV). EMCV is the established causative agent of myocarditis and encephalitis in some animals. EMCV causes high fatality in suckling and weaning piglets, making pigs the most susceptible domestic animal species. Importantly, EMCV has zoonotic potential to infect the human population. The ability of the pathogen to avoid and undermine the initial defence mechanism of the host contributes to its virulence and pathogenicity. A large body of literature highlights the intricate strategies employed by EMCV to escape the innate immune machinery to suit its "pathogenic needs." Here, we also provide examples on how EMCV interacts with certain host proteins to dampen the infection process. Hence, this concise review aims to summarize these findings in a compendium of decades of research on this exciting yet underappreciated topic.
Xie et al. (Sat,) conducted a review in Encephalomyocarditis virus (EMCV) infection. Encephalomyocarditis virus employs intricate strategies to escape the host innate immune machinery and interacts with certain host proteins to dampen the infection process.
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