Pathogenesis of the B variant of encephalomyocarditis virus

Shafi, Raheel; Cerutis, D. Roselyn; Giron, David

doi:10.1002/jmv.1890400305

Cited by 13 publications

(3 citation statements)

References 21 publications

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“…In Alzheimer's disease and ischemic injury, the PyNs in CA1 (9) sustain damage. Picornaviruses, including Theiler's murine encephalomyelitis virus (TMEV) (14,21) and encephalomyocarditis virus (22,23), target CA1 neurons in a way similar to that adopted by kainic acid in the same area (24). BDV also induces CA1 lesions but only in interferon-g-deficient knockout mice (18).…”

Section: Discussionmentioning

confidence: 99%

Mutant Murine Hepatitis Virus-Induced Apoptosis in the Hippocampus

2014

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SUMMARY:The mutant virus Mu-3 was isolated from the soluble receptor-resistant mutant 7 virus (srr7), which is a neuropathogenic strain of the mouse hepatitis virus JHMV, and cloned as a soluble receptor-resistant mutant from the highly neuropathogenic JHMV strain cl-2 virus (cl-2). In order to identify specific characteristcs of Mu-3, the pathology of Mu-3-infected mice was compared with that of srr7-and cl-2-infected mice. The neuropathology after Mu-3 infection exhibited a mixed pattern comparable to that induced by srr7 and cl-2 infections. In addition, Mu-3 infection caused marked apoptotic lesions in the hippocampal region, particularly in the CA2 and CA3 subregions, in the brains of all infected mice. In contrast, in cl-2 infection, 10-20z of the infected mice exhibited apoptosis in the hippocampus, which was primarily observed in the CA1 subregion. Apoptosis also occurred in the pyramidal neurons and CD11b-bearing cells. The apoptotic cells, indicated by caspase 3-activation, were a mixed population of infected and a higher number of uninfected cells. These data indicated that apoptosis observed in Mu-3 infection could be induced by the indirect effects of infection in addition to direct effects of the infected cells occurring in a cell-autonomous manner.

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Section: Discussionmentioning

confidence: 99%

Mutant Murine Hepatitis Virus-Induced Apoptosis in the Hippocampus

2014

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“…Viral infection of the CNS is known to alter this tightly regulated equilibrium, leading to neuron death. 8 For example, acute CNS infection by members of the neurotropic picornavirus family, includ-ing Theiler's murine encephalomyelitis virus (TMEV), 17,18 the coxsackieviruses, 19 and encephalomyocarditis virus, 20,21 induces the death of hippocampal neurons in a range of hosts. 8 Case reports indicate that infection with neurovirulent picornaviruses results in extensive hippocampal lesions and cognitive impairment in humans.…”

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confidence: 99%

Apoptosis of Hippocampal Pyramidal Neurons Is Virus Independent in a Mouse Model of Acute Neurovirulent Picornavirus Infection

Buenz

Sauer

LaFrance‐Corey

et al. 2009

The American Journal of Pathology

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Many viruses, including picornaviruses, have the potential to infect the central nervous system (CNS) and stimulate a neuroinflammatory immune response, especially in infants and young children. Cognitive deficits associated with CNS picornavirus infection result from injury and death of neurons that may occur due to direct viral infection or during the immune responses to virus in the brain. Previous studies have concluded that apoptosis of hippocampal neurons during picornavirus infection is a cell-autonomous event triggered by direct neuronal infection. However, these studies assessed neuron death at time points late in infection and during infections that lead to either death of the host or persistent viral infection. In contrast, many neurovirulent picornavirus infections are acute and transient, with rapid clearance of virus from the host. We provide evidence of hippocampal pathology in mice acutely infected with the Theiler's murine encephalomyelitis picornavirus. We found that CA1 pyramidal neurons exhibited several hallmarks of apoptotic death, including caspase-3 activation, DNA fragmentation, and chromatin condensation within 72 hours of infection. Critically, we also found that many of the CA1 pyramidal neurons undergoing apoptosis were not infected with virus, indicating that neuronal cell death during acute picornavirus infection of the CNS occurs in a non-cell-autonomous manner. These observations suggest that therapeutic strategies other than antiviral interventions may be useful for neuroprotection during acute CNS picornavirus infection. Many viruses maintain neurovirulent potential, even when the vast majority of infections are silent or subclinical.

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“…Syrian hamsters showed viral replication in the brain and small focal areas of necrosis of neurons in the stratum pyramidal hippocampus and the stratum granulose cerebella following EMCV-D infection [18,19]. Introduction of EMCV-B virus by the intracerebral route in mice leads to replication of the virus in the CNS, indicating that cells in the CNS have receptor sites for EMCV-B [20]. …”

Section: Encephalomycarditis Virusmentioning

confidence: 99%

Role of Microglia in Oxidative Toxicity Associated with Encephalomycarditis Virus Infection in the Central Nervous System

Ano

Sakudo

Onodera

2012

IJMS

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The single-stranded RNA encephalomyocarditis virus (EMCV) can replicate in the central nervous system (CNS) and lead to prominent brain lesions in the stratum pyramidale hippocampus and the stratum granulosum cerebelli. Activated microglia cells infected by EMCV produce a massive burst of reactive oxygen species (ROS) via NADPH oxidase 2 (NOX2) activation, leading to neuronal death. Balancing this effect is mechanisms by which ROS are eliminated from the CNS. Cellular prion protein (PrPC) plays an important antioxidant role and contributes to cellular defense against EMCV infection. This review introduces recent knowledge on brain injury induced by EMCV infection via ROS generation as well as the involvement of various mediators and regulators in the pathogenesis.

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Pathogenesis of the B variant of encephalomyocarditis virus

Cited by 13 publications

References 21 publications

Mutant Murine Hepatitis Virus-Induced Apoptosis in the Hippocampus

Mutant Murine Hepatitis Virus-Induced Apoptosis in the Hippocampus

Apoptosis of Hippocampal Pyramidal Neurons Is Virus Independent in a Mouse Model of Acute Neurovirulent Picornavirus Infection

Role of Microglia in Oxidative Toxicity Associated with Encephalomycarditis Virus Infection in the Central Nervous System

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