Susceptibility of primary culture neurons from rats of different ages to encephalomyocarditis (EMC) virus infection

Su, Weiping; Ikegami, Hiroki; Nakayama, Yasuya; Suzuki, Kazuhiko; Katayama, Kei‐ichi; Nakayama, Hiroyuki; Doi, Kunio

doi:10.1016/s0014-4800(03)00068-6

Cited by 7 publications

(3 citation statements)

References 26 publications

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“…To provide further information, the present study sought to determine the cause of 86 cases of non-suppurative meningoencephalitis in dogs and cats by the immunohistochemical examination of formalin-¢xed, para⁄n wax-embedded tissue. In addition to examination for known viral and bacterial pathogens and prion protein Sc ,West Nile virus (WNV), a recently emerging cause of disease, was included in the present study (Komar, 2000;Lichtensteiger et al, 2003;Austgen et al, 2004), together with encephalomyocarditis virus (EMCV), an agent so far demonstrated only in the CNS of pigs and rodents (Nowotny, 1996;Sue et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Non-suppurative Meningoencephalitis of Unknown Origin in Cats and Dogs: an Immunohistochemical Study

Schwab¹,

Herden²,

Seeliger³

et al. 2007

Journal of Comparative Pathology

104

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Non-suppurative meningoencephalitis of unknown cause is a frequent finding in dogs and cats. Fifty-three dogs and 33 cats with non-suppurative meningoencephalitis of unknown aetiology were examined immunohistochemically for 18 different infectious agents, including viruses, bacteria and prion protein(Sc). In 14 (26%) of the dogs and 13 (39%) of the cats a causative agent was identified in the central nervous system (CNS), two dogs and one cat giving positive results for two infectious agents simultaneously. The study revealed infections with known causative agents (porcine herpes virus 1, feline infectious peritonitis virus, Escherichia coli) and a new disease pattern of parvovirus infection in the CNS of dogs and cats. Infection of the CNS with feline leukaemia virus was found in a cat. Five dogs and four cats gave positive results for West Nile virus (WNV) antigen. In one dog, canine parainfluenza virus antigen was detected in the brain. Four dogs and four cats gave positive results for encephalomyocarditis virus (EMCV). The significance of the detection of WNV and EMCV antigen requires further study. The aetiology remained undetermined in 39 dogs (74%) and 20 cats (61%). Although it is possible that non-infectious causes play a more important role than previously thought, infections with hitherto unrecognized agents cannot be ruled out.

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Section: Introductionmentioning

confidence: 99%

Non-suppurative Meningoencephalitis of Unknown Origin in Cats and Dogs: an Immunohistochemical Study

Schwab¹,

Herden²,

Seeliger³

et al. 2007

Journal of Comparative Pathology

104

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“…Previous experiments have demonstrated that while EMCV replicates in numerous animal and human cells, a panel of rat cells were relatively resistant to EMCV infection (Kelly et al, 1983;Su et al, 2003). In an effort to gain understanding of the molecular mechanisms underlying resistance to EMCV infection and expansion of the host range, we examined the step(s) in the EMCV replication cycle that were blocked in buffalo rat liver-resistant cells.…”

Section: Encephalomyocarditis Virus (Emcv) Belongs To the Genusmentioning

confidence: 99%

Efficient infection of buffalo rat liver-resistant cells by encephalomyocarditis virus requires binding to cell surface sialic acids

Guy

Chilmonczyk

Crucière

et al. 2009

Journal of General Virology

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In contrast to the production of virus and cell lysis seen in baby hamster kidney cells infected with the strain 1086C of encephalomyocarditis virus (EMCV), in buffalo rat liver cells (BRL) neither virus replication nor cytopathic effects were observed. After 29 passages in BRL cells, each alternating with boosts of the recovered virus in BHK-21 cells, the virus acquired the ability to replicate effectively in BRL cells, attaining virus titres comparable to those in BHK-21 cells and producing complete cell destruction. The binding of virus on BRL cells was increased after adaptation and was similar to that observed on BHK-21 cells. Treatment of BRL cells with sialidase resulted in an 87 % reduction in virus binding and inhibition of infection. Sequence analyses revealed three mutations in the VP1 amino acid sequence of the adapted virus at positions 49 (LysAGlu), 142 (LeuAPhe) and 180 (IleAAla). The residue 49 is exposed at the surface of the capsid and is known to be part of a neutralization epitope. These results suggest that the adaptation of EMCV to BRL cells may have occurred through a mutation in a neutralizing site that confers to the virus a capacity to interact with cell surface sialic acid residues. Taken together, these data suggest a link between virus neutralization site, receptor binding and cell permissivity to infection.

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“…For hippocampal neurons, the hippocampus was dissected from postnatal day 1 mice in ice-cold L-15 medium (Sigma, St. Louis, MO). Hippocampal cells were isolated and cultured according to the method of Su et al (2003). Dissociated hippocampal cells were plated on glass coverslips precoated with poly-L-lysine (Sigma).…”

Section: Cell Culturementioning

confidence: 99%

Mice with GFAP‐targeted loss of neurofibromin demonstrate increased axonal MET expression with aging

Xing

Guha

et al. 2007

Glia

Self Cite

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Neurofibromatosis 1 (NF1) is a common genetic disease that predisposes patients to peripheral nerve tumors and central nervous system (CNS) abnormalities including low-grade astrocytomas and cognitive disabilities. Using mice with glial fibrillary acidic protein (GFAP)-targeted Nf1 loss (Nf1(GFAP)CKO mice), we found that Nf1(-/-) astrocytes proliferate faster and are more invasive than wild-type astrocytes. In light of our previous finding that aberrant expression of the MET receptor tyrosine kinase contributes to the invasiveness of human NF1-associated malignant peripheral nerve sheath tumors, we sought to determine whether MET expression is aberrant in the brains of Nf1 mutant mice. We found that Nf1(-/-) astrocytes express slightly more MET than wild-type cells in vitro, but do not express elevated MET in situ. However, fiber tracts containing myelinated axons in the hippocampus, midbrain, cerebral cortex, and cerebellum express higher than normal levels of MET in older (> or =6 months) Nf1(GFAP)CKO mice. Both Nf1(GFAP)CKO and wild-type astrocytes induced MET expression in neurites of wild-type hippocampal neurons in vitro, suggesting that astrocyte-derived signals may induce MET in Nf1 mutant mice. Because the Nf1 gene product functions as a RAS GTPase, we examined MET expression in the brains of mice with GFAP-targeted constitutively active forms of RAS. MET was elevated in axonal fiber tracts in mice with active K-RAS but not H-RAS. Collectively, these data suggest that loss of Nf1 in either astrocytes or GFAP(+) neural progenitor cells results in increased axonal MET expression, which may contribute to the CNS abnormalities in children and adults with NF1.

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Susceptibility of primary culture neurons from rats of different ages to encephalomyocarditis (EMC) virus infection

Cited by 7 publications

References 26 publications

Non-suppurative Meningoencephalitis of Unknown Origin in Cats and Dogs: an Immunohistochemical Study

Non-suppurative Meningoencephalitis of Unknown Origin in Cats and Dogs: an Immunohistochemical Study

Efficient infection of buffalo rat liver-resistant cells by encephalomyocarditis virus requires binding to cell surface sialic acids

Mice with GFAP‐targeted loss of neurofibromin demonstrate increased axonal MET expression with aging

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