Mengovirus, also known as Columbia SK virus, mouse Elberfield virus, and Encephalomyocarditis virus (EMCV), belongs to the genus Cardiovirus which is a member of the Picornaviridae.[1] Its genome is a single stranded positive-sense RNA molecule, making the Mengoviruses a class IV virus under the Baltimore classification system. The genome is approximately 8400nt in length, and has 5’ VG protein (Virus genome protein) and a 3’ polyadenine tail. Mengovirus was isolated by George W. A. Dick in 1948, in the Mengo district of Entebbe in Uganda, from a captive rhesus monkey that had developed hind limb paralysis.[2][3]
| Mengovirus | |
|---|---|
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| Surface depiction of Mengovirus (2MEV) coloured by radial height to illuminate surface features | |
Virus classification 
| |
| (unranked): | Virus |
| Realm: | Riboviria |
| Kingdom: | Orthornavirae |
| Phylum: | Pisuviricota |
| Class: | Pisoniviricetes |
| Order: | Picornavirales |
| Family: | Picornaviridae |
| Genus: | Cardiovirus |
| Species: | |
| Virus: | Mengovirus
|
Structure
editMengovirus is a non-enveloped virus which has a nucleocapsid made up of 12 subunits. The virion is 30 nm in diameter and displays icosahedral symmetry.[citation needed]
Gene expression and genome replication
editOnce inside a host cell, the Mengovirus genome acts as a piece of mRNA and is directly translated by the host ribosomes in the cytoplasm. There is a large un-translated region at the 5’ end of the RNA that has a ribosome binding site, removing the need of a cap. A single polypeptide is made and is cleaved into individual proteins by viral proteases. The genome is divided into three parts: P1, P2, and P3. P1 encodes the virus capsid proteins, P2 and P3 encode genes required for genome replication to occur. For replication to occur an intermediate double-stranded RNA molecule is made to be used as a template for the production of positive sense genomes.[citation needed]
Infection
editMengovirus is infectious to vertebrate animals, and has been isolated from mice and other rodents. It can also cause acute fever in humans. There is no specific treatment for a Mengovirus infection; although dipyridamole has been shown to inhibit its replication.[4] The illness is not severe enough to require vaccination. The Mengovirus is able to suppress the host's immune response by reducing the expression of Nuclear Factor kappa B using the 5’ un-translated region.[citation needed]
References
edit- ^ Carocci, M; Bakkali-Kassimi, L (2012). "The encephalomyocarditis virus". Virulence. 3 (4): 351–67. doi:10.4161/viru.20573. PMC 3478238. PMID 22722247.
- ^ Dick, G. W.; Smithburn, K. C.; Haddow, A. J. (948). "Mengo Encephalomyelitis Virus. Isolation and Immunological Properties". Br J Exp Pathol. 29 (6): 547–558. PMC 2073198.
- ^ Dick, G.W.A.; Haddow, A.J.; Best, A.M.; Smithburn, K.C. (1948). "Mengo Encephalomyelitis". The Lancet. 252 (6521): 286–289. doi:10.1016/S0140-6736(48)90652-7.
- ^ Fata-Hartley, Cori L.; Palmenberg, Ann C. (2005). "Dipyridamole Reversibly Inhibits Mengovirus RNA Replication". Journal of Virology. 79 (17): 11062–11070. doi:10.1128/jvi.79.17.11062-11070.2005. PMC 1193570. PMID 16103157.
Further reading
edit- Rueckert RR (1990) Picornavirus and their multiplication. In: Fields BN, Knipe DM (eds) Virology, 2nd edn. Raven Press, New York, pp 507–548.
- Encephalomyocarditisvirus ICTVdB Index of Viruses, Version 28, June, 2002. Retrieved on 2007-07-15.
- Zoll; et al. (2002). "The Mengovirus Leader Protein Suppresses Alpha/Beta Interferon Production by Inhibition of the Iron/Ferritin-Mediated Activation of NF- B". Journal of Virology. 76 (19): 9664–9672. doi:10.1128/JVI.76.19.9664-9672.2002. PMC 136484. PMID 12208945.
- Fata-Hartley, Cori L.; Palmenberg, Ann C. (2005). "Dipyridamole Reversibly Inhibits Mengovirus RNA Replication". Journal of Virology. 79 (17): 11062–11070. doi:10.1128/jvi.79.17.11062-11070.2005. PMC 1193570. PMID 16103157.