Pathogenesis of Demyelination Induced by a Mouse Hepatitis

Weiner, Leslie P.

doi:10.1001/archneur.1973.00490230034003

Cited by 321 publications

(257 citation statements)

References 12 publications

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“…Mice that survive the acute stage of CNS MHV infection develop a demyelinating disease characterized by persistent viral RNA and antigen within white matter tracts accompanied by mononuclear cell infiltration and myelin destruction [9,14,[25][26][27][28]. Previous work demonstrating that chronic CXCL10 expression amplifies the severity of demyelination in MHV-infected mice led to the hypothesis that CXCR3 is similarly involved during chronic neurologic disease, allowing activated T cells to accumulate within the CNS in response to CXCL10 [19].…”

Section: Functional Significance Of Cxcr3 During Chronic Diseasementioning

confidence: 99%

Differential roles for CXCR3 in CD4⁺ and CD8⁺ T cell trafficking following viral infection of the CNS

et al. 2006

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Lymphocyte infiltration into the central nervous system (CNS) following viral infection represents an important component of host defense and is required for control of viral replication. However, the mechanisms governing inflammation in response to viral infection of the CNS are not well understood. Following intracranial (i.c.) infection of susceptible mice with mouse hepatitis virus (MHV), mice develop an acute encephalomyelitis followed by a chronic demyelinating disease. The CXC chemokine ligand 10 (CXCL10) is expressed following MHV infection and signals T cells to migrate into the CNS. The functional contribution of the CXCL10 receptor CXCR3 in host defense and disease in response to MHV infection was evaluated. The majority of CD4 + and CD8 + T cells infiltrating the CNS following MHV infection express CXCR3. Administration of anti-CXCR3 antibody reduced CD4 + T cell infiltration (p 0.05), while CD8 + T cell trafficking was not affected. Anti-CXCR3 treatment during chronic disease correlated with improved motor skills and reduced demyelination. The selective effect of anti-CXCR3 treatment on CD4 + T cells was not the result of either reduced proliferation or modulation in chemokine receptor gene expression. Therefore, CXCR3 signaling has a non-redundant role in T cell subset trafficking in response to viral infection.

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Section: Functional Significance Of Cxcr3 During Chronic Diseasementioning

confidence: 99%

Differential roles for CXCR3 in CD4⁺ and CD8⁺ T cell trafficking following viral infection of the CNS

et al. 2006

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“…Mouse hepatitis virus type 4 (MHV-4, JHM strain), a member of the coronavirus family, is attracting increasing interest as an agent of both virus-induced encephalomyelitis and virusinduced demyelination (Bailey et al, 1949;Waksman & Adams, 1962;Lampert et al, 1973 ;Weiner, 1973;ter Meulen et al, 1981 ;Knobler et al, 1981Knobler et al, , 1982. Resistance to MHV-4-induced fatal central nervous system disease is inherited as a single autosomal recessive trait, independent of the major histocompatibility complex, expressed at the level of the neuronal cell (Knobler et al, 1981).…”

Section: Introductionmentioning

confidence: 99%

Host Genetic Control of Mouse Hepatitis Virus Type 4 (JHM Strain) Replication. I. Restriction of Virus Amplification and Spread in Macrophages from Resistant Mice

Knobler

Tunison

Oldstone

1984

Journal of General Virology

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SUMMARYPeritoneal macrophages were used to analyse host genetic control of mouse hepatitis virus type 4 (MHV-4) infection. Both infectious centre and immunofluorescence assays indicated that only a subset of macrophages from either susceptible (BALB, C3H or C57BL/6J) or resistant (SJL/J) mice were initially infected with MHV-4 during the first cycle of infection. However, compared to macrophages from susceptible mice, three-to sixfold fewer SJL/J macrophages were infected, and there was no amplification of virus replication by involvement of adjacent cells during the second cycle of infection. Treatment of macrophages from susceptible mice with interferon beta could not duplicate the aborted second cycle of infection that occurred in macrophages from resistant mice.

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“…The original isolates of murine coronaviruses were recovered from different mouse strains and, so far, animal experiments to test the organ tropism of these viruses and to study the pathogenic mechanisms by which these strains induce diseases have mainly been carried out in mice (Lampert et al, 1973;Weiner, 1973). Recently, however, it has been shown in weanling rats that the murine coronavirus JHM induces different types of central nervous system (CNS) disease which can be accompanied by marked demyelination (Nagashima et al, 1978(Nagashima et al, a, b, 1979.…”

Section: Introductionmentioning

confidence: 99%

Genetic Variation of Neurotropic and Non-neurotropic Murine Coronaviruses

Stephenson

Koga

Wege

et al. 1981

Journal of General Virology

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SUMMARYThe murine coronavirus strains MHV JHM, MHV 1, MHV 2, MHV 3 and MHV A59 were tested for their neurovirulence in weanling rats. The strain JHM was found to be highly neurovirulent for weanling rats, whereas the other strains were not, or only slightly, neurovirulent. MHV 1 caused no lesions in weanling rats. The other strains (MHV 2, MHV 3 and MHV A59) induced predominantly subclinical infections in weanling rats as demonstrated by an increase of antibodies and inflammatory lesions in the liver. Analysis of these strains by cross-neutralization revealed variable degrees of antigenic relationship between these viruses which were not related to their neurovirutence. However, when these strains were compared by analysing the Tt-RNase-resistant oligonucleotides of virion RNA, the highly neurovirulent strain JHM was found to differ significantly in its nucleotide sequence from the other less-neurovirulent strains.

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Pathogenesis of Demyelination Induced by a Mouse Hepatitis

Cited by 321 publications

References 12 publications

Differential roles for CXCR3 in CD4⁺ and CD8⁺ T cell trafficking following viral infection of the CNS

Differential roles for CXCR3 in CD4⁺ and CD8⁺ T cell trafficking following viral infection of the CNS

Host Genetic Control of Mouse Hepatitis Virus Type 4 (JHM Strain) Replication. I. Restriction of Virus Amplification and Spread in Macrophages from Resistant Mice

Genetic Variation of Neurotropic and Non-neurotropic Murine Coronaviruses

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Pathogenesis of Demyelination Induced by a Mouse Hepatitis

Cited by 321 publications

References 12 publications

Differential roles for CXCR3 in CD4+ and CD8+ T cell trafficking following viral infection of the CNS

Differential roles for CXCR3 in CD4+ and CD8+ T cell trafficking following viral infection of the CNS

Host Genetic Control of Mouse Hepatitis Virus Type 4 (JHM Strain) Replication. I. Restriction of Virus Amplification and Spread in Macrophages from Resistant Mice

Genetic Variation of Neurotropic and Non-neurotropic Murine Coronaviruses

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Differential roles for CXCR3 in CD4⁺ and CD8⁺ T cell trafficking following viral infection of the CNS

Differential roles for CXCR3 in CD4⁺ and CD8⁺ T cell trafficking following viral infection of the CNS