Zoological transmission of encephalomyocarditis virus in the United States: Virus evolution, host ecology, and capsid antigenicity derived from an outbreak
Zoological transmission of encephalomyocarditis virus in the United States: Virus evolution, host ecology, and capsid antigenicity derived from an outbreak is drawing significant interest across the industry.
Author summary Much has been learned about the molecular biology and pathogenesis of encephalomyocarditis virus (EMCV) over the last several decades, as it has been used as an important model system on many fronts, including deducing mechanisms of myocardial pathogenesis and viral-induced diabetes, antiviral immunity, polyprotein processing, as well as a prototype for protein expression via an internal ribosome entry site (IRES), ribosomal skipping, and ribosomal frameshifting. Despite this wealth of information, very little is known about the ecology and evolution of the virus in nature, in particular in the United States. To zoological institutions, EMCV is a major concern, as it can cause devastating outbreaks resulting in fatal myocarditis and/or encephalitis in numerous wildlife species. Herein, we investigated an outbreak that was precipitated by the death of an African elephant, in hopes to begin to shed light on the transmission dynamics and genetic and antigenic diversity of EMCV that exists in North America.
Experts suggest this could influence future trends and innovation in the sector.
More updates are expected as the story develops.
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