Alteration of encephalomyocarditis virus pathogenicity due to a mutation at position 100 of VP1Reportar como inadecuado




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Science China Life Sciences

, Volume 54, Issue 6, pp 535–543

First Online: 26 June 2011Received: 23 September 2010Accepted: 14 March 2011

Abstract

Encephalomyocarditis virus EMCV infection leads to many diseases including encephalitis, myocarditis and diabetes in its natural host, the mouse. In this study, we generated four cDNA clones with a point mutation at position 100 of VP1. The amino acids isoleucine, alanine, serine and proline were substituted with threonine in the four different clones of EMCV strain BJC3 by site-specific mutagenesis, and viable viruses were rescued. Although all mutants and wild-type viruses display different plaque morphologies, they replicate comparably in BHK-21 cells. The pathogenicity of the mutated viruses was systematically analyzed to investigate the importance of this amino acid in the viral pathogenicity and disease phenotype of EMCV infection in mice. The results showed that the isoleucine- T1100I and proline-mutated viruses T1100P exhibited a reduced mortality, lower cerebral virus loads and alleviated brain damage while the viruses with serine T1100S and alanine T1100A substitutions displayed similar properties as the wild-type virus. These findings indicate that the amino acid at position 100 of VP1 is important for EMCV in vivo infection, and its mutation alters the pathogenicity of viral infection in mice.

Keywordsencephalomyocarditis virus EMCV VP1 mutation pathogenicity This article is published with open access at Springerlink.com

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Autor: Shu Zhu - XinNa Ge - XiaoWen Gong - Xin Guo - YanHong Chen - HanChun Yang

Fuente: https://link.springer.com/article/10.1007/s11427-011-4172-z







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