Abstract
Cardioviruses are members of the Picornaviridae family and infect a variety of mammals, from mice to humans. Replication of cardioviruses produces double stranded RNA that is detected by helicases in the RIG-I-like receptor family and leads to a signaling cascade to produce type I interferon. Like other viruses within Picornaviridae, however, cardioviruses have evolved several mechanisms to inhibit interferon production. In this review, we summarize recent findings that have uncovered several proteins enabling efficient detection of cardiovirus dsRNA and discuss which cell types may be most important for interferon production in vivo. Additionally, we describe how cardiovirus proteins L, 3C and L∗ disrupt interferon production and antagonize the antiviral activity of interferon effector molecules.
Highlights
Picornaviridae is an important family of single-stranded, positive-polarity RNA viruses that includes >30 genera with over 75 species (Zell et al, 2017)
L∗ is only expressed by Theiler’s murine encephalomyelitis virus (TMEV) and is important for infection of macrophages, persistence of the virus in mice and inhibiting RNase L, 2B∗ results from a frameshifting mechanism conserved in cardioviruses that regulates the ratio of structural and non-structural proteins translated over time
Double-stranded RNA is a necessary product of picornavirus replication, as positive-stranded genome is copied to produce a negative-stranded, full-length template, which is in turn used to produce additional genomes. dsRNA is recognized by several sensor proteins within the cell and triggers a signal transduction pathway that results in transcription of the type I IFN (IFN-α/β) genes, as well as IFN-λ
Summary
Picornaviridae is an important family of single-stranded, positive-polarity RNA viruses that includes >30 genera with over 75 species (Zell et al, 2017). Within Picornaviridae, the genus Cardiovirus includes encephalomyocarditis virus (EMCV), Theiler’s murine encephalomyelitis virus (TMEV) and Saffold viruses (SAFV). EMCV has been found to infect over 30 host species and contains one serotype, Mengo virus, which was isolated in 1948 in the Mengo district of Uganda (Dick et al, 1948). L∗ is only expressed by TMEV and is important for infection of macrophages, persistence of the virus in mice and inhibiting RNase L (van Eyll and Michiels, 2000; Sorgeloos et al, 2013), 2B∗ results from a frameshifting mechanism conserved in cardioviruses that regulates the ratio of structural and non-structural proteins translated over time. Protein 2B∗ itself is only thought to be important for replication of EMCV, as mutants that abolish its expression had a small plaque phenotype. 2B∗ in TMEV and SAFV is unlikely to act as a protein as it is predicted to encode a peptide of 14 amino acids (Loughran et al, 2011)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
