Pathogenesis of Experimental Encephalomyocarditis: A Histopathological, Immunohistochemical and Virological Study in Mice

Psalla, Dimitra; Psychas, V.; Spyrou, Vassiliki; Billinis, C.; Papaioannou, Nikolaos; Vlemmas, I.

doi:10.1016/j.jcpa.2006.04.003

Cited by 29 publications

(30 citation statements)

References 8 publications

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“…In sows, EMCV caused reproductive failure leading to abortion and fetal death [4]. In mice, EMCV can cause various diseases including acute neurological disorders, diabetes and myocarditis, while some strains, like EMC-B and G424/90, generated no visible symptoms following infection [5]. To date, the mechanisms involving virulence and pathogenesis of EMCV remain unknown.…”

mentioning

confidence: 99%

Alteration of encephalomyocarditis virus pathogenicity due to a mutation at position 100 of VP1

Zhu

Gong

et al. 2011

Sci. China Life Sci.

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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. encephalomyocarditis virus (EMCV), VP1, mutation, pathogenicity Citation:Zhu S, Ge X N, Gong X W, et al. Alteration of encephalomyocarditis virus pathogenicity due to a mutation at position 100 of VP1. Sci China Life Sci, 2011, 54: 535 -543,

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mentioning

confidence: 99%

Alteration of encephalomyocarditis virus pathogenicity due to a mutation at position 100 of VP1

Zhu

Gong

et al. 2011

Sci. China Life Sci.

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“…Moreover, EMCV increases the risks of xenotransplantation for human recipients [11]. In rodents, EMCV induces encephalitis, member paralysis, myocarditis and type 1 diabetes [12–14]. EMCV infection was also responsible for the deaths of various animals in zoos distributed in different countries [2, 15, 16].…”

Section: Backgroudmentioning

confidence: 99%

Transcriptional profiling of host cell responses to encephalomyocarditis virus (EMCV)

Wei

Zhang

et al. 2017

Virol J

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BackgroudEncephalomyocarditis virus (EMCV) has been discovered on pig farms worldwide and can cause myocarditis in piglets and reproductive failure in sows. However, little is known about the host transcriptional responses to infection and host-pathogen interactions.MethodsIn this study, transcription profiling was performed by Illumina RNA-Sequencing (RNA-seq) to identify EMCV induced differentially expressed genes in BHK-21 cells at serial time points (12, 24, and 30 h post infection (hpi)), using mock infected cells as control.ResultsWe identified 237, 241, and 207 differentially expressed genes (DEGs) respectively, majority of which were up-regulated. A large number of DEGs clustered into host defense, cellular signaling and metabolism categories. Moreover, short time series expression analysis revealed that 12 hpi was an important time point for expression change, indicating host virus resistance.ConclusionsThis RNA-seq analysis provides the first data for understanding the network of virus host interactions under EMCV infection in vitro, and for identifying host components which involved in the virus infection course.Electronic supplementary materialThe online version of this article (doi:10.1186/s12985-017-0718-4) contains supplementary material, which is available to authorized users.

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“…Previous studies showed that EMCV infection induces encephalitis, myocarditis, neurovirulence, paralysis and type I diabetes in mice (Cerutis et al, 1989;Psalla et al, 2006;Takeda et al, 1991;Yoon & Jun, 2006). In past decades, several EMCV virulence-related factors were determined and different strategies were adopted to obtain safe and effective live attenuated vaccines.…”

Section: Introductionmentioning

confidence: 99%

An attenuated EMCV-HB10 strain acts as a live viral vector delivering a foreign gene

Huang

Zhang

et al. 2016

Journal of General Virology

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We successfully constructed a full-length cDNA infectious clone of the encephalomyocarditis virus (EMCV) HB10 strain and obtained a partially attenuated rEMCV-C 9 virus with a shorter poly(C) tract. Our results showed that the length of the EMCV-HB10 poly(C) tract was related to the pathogenicity of the EMCV-HB10 strain in vivo. Using pEMCV-C 9 as the backbone, we constructed the novel viral vector pC 9 -MCS-D2A by inserting a cDNA fragment containing a 127 amino acid deletion in the 2A protein, a primary cleavage cassette, a FLAG tag and a multiple cloning site (MCS) at the junction of VP1 and D2A. Additionally, the enhanced green fluorescent protein (egfp) gene was cloned into the MCS of pC 9 -MCS-D2A to test its capacity to express foreign proteins. Insertion of the egfp gene did not affect viral replication, and a decrease in EGFP expression was observed within five serial passages. Furthermore, we found that rC 9 -EGFP-D2A was avirulent in vivo, induced neutralizing antibody production and conferred protective immune responses against lethal challenge with EMCV in mice. Taken together, our results demonstrated that we had constructed an attenuated live vector based on an EMCV-HB10 strain with two modified critical virulence factors (the poly(C) tract and 2A protein) that could be used as a candidate live vaccine and a potential live viral vector for foreign antigen delivery.

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Pathogenesis of Experimental Encephalomyocarditis: A Histopathological, Immunohistochemical and Virological Study in Mice

Cited by 29 publications

References 8 publications

Alteration of encephalomyocarditis virus pathogenicity due to a mutation at position 100 of VP1

Alteration of encephalomyocarditis virus pathogenicity due to a mutation at position 100 of VP1

Transcriptional profiling of host cell responses to encephalomyocarditis virus (EMCV)

An attenuated EMCV-HB10 strain acts as a live viral vector delivering a foreign gene

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