Coxsackievirus B1–induced chronic inflammatory myopathy: differences in induction of autoantibodies to muscle and nuclear antigens by cloned myopathic and amyopathic viruses

Tam, Patricia E.; Fontana, Donna R.; Messner, Ronald P.

doi:10.1016/s0022-2143(03)00108-2

Cited by 13 publications

(12 citation statements)

References 30 publications

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“…Evidence in a clinical setting suggests that type B coxsackieviruses (CVB) can cause acute demyelinating diseases, such as acute disseminated myelitis and acute transverse myelitis (18,27). Intriguingly, persistent CVB infections have been associated with myocarditis (29,61), diabetes (32), chronic inflammatory myopathy (53), and, most recently, Sjogren's disease (55). Viral RNA persistence is thought to correlate with chronic disease, which suggests that the long-term presence of viral materials may be a potential mechanism for disease induction.…”

Section: Discussionmentioning

confidence: 99%

Viral Persistence and Chronic Immunopathology in the Adult Central Nervous System following Coxsackievirus Infection during the Neonatal Period

Feuer

Ruller

et al. 2009

J Virol

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Coxsackieviruses are significant human pathogens, and the neonatal central nervous system (CNS) is a major target for infection. Despite the extreme susceptibility of newborn infants to coxsackievirus infection and viral tropism for the CNS, few studies have been aimed at determining the long-term consequences of infection on the developing CNS. We previously described a neonatal mouse model of coxsackievirus B3 (CVB3) infection and determined that proliferating stem cells in the CNS were preferentially targeted. Here, we describe later stages of infection, the ensuing inflammatory response, and subsequent lesions which remain in the adult CNS of surviving animals. High levels of type I interferons and chemokines (in particular MCP-5, IP10, and RANTES) were upregulated following infection and remained at high levels up to day 10 postinfection (p.i). Chronic inflammation and lesions were observed in the hippocampus and cortex of surviving mice for up to 9 months p.i. CVB3 RNA was detected in the CNS up to 3 months p.i at high abundance (ϳ10 6 genomes/mouse brain), and viral genomic material remained detectable in culture after two rounds of in vitro passage. These data suggest that CVB3 may persist in the CNS as a low-level, noncytolytic infection, causing ongoing inflammatory lesions. Thus, the effects of a relatively common infection during the neonatal period may be long lasting, and the prognosis for newborn infants recovering from acute infection should be reexplored.

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Section: Discussionmentioning

confidence: 99%

Viral Persistence and Chronic Immunopathology in the Adult Central Nervous System following Coxsackievirus Infection during the Neonatal Period

Feuer

Ruller

et al. 2009

J Virol

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“…This finding indicates that differences in the immunogenicities of viral determinants are linked to the pathogenic phenotype of the virus, resulting in either a qualitative or quantitative difference in the immune response to infection. This difference is also apparent in the production of autoantibodies to muscle and nuclear antigens, which are found in mice infected with myopathic, but not amyopathic, virus (23).…”

Section: Vol 77 2003 Notes 11851mentioning

confidence: 93%

Multiple Viral Determinants Mediate Myopathogenicity in Coxsackievirus B1-Induced Chronic Inflammatory Myopathy

Tam

Weber-Sanders

Messner

2003

J Virol

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Mice infected with myopathic coxsackievirus B1 Tucson (CVB1 T ) develop chronic inflammatory myopathy (CIM) consisting of hind limb weakness and inflammation. Amyopathic virus variants are infectious but attenuated for CIM. In this report, viral clones, chimeras, and sequencing were used to identify viral determinants of CIM. Chimeras identified several regions involved in CIM and localized a weakness determinant to nucleotides 2493 to 3200 of VP1. Sequencing of multiple clones and viruses identified five candidate determinants that were strictly conserved in myopathic viruses with one located in the 5 untranslated region (UTR), three in the VP1 capsid, and one in the 3C protease. Taken together, these studies implicate Tyr-87 and/or Val-136 as candidate determinants of weakness. They also indicate that there are at least two determinants of inflammation and one additional determinant of weakness encoded by myopathic CVB1 T .

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“…One possible explanation of these data was molecular mimicry; perhaps CVB infection induced antiviral antibodies that cross-reacted with myosin, but this was shown not to be the case (98). In studies of chronic myositis, both CVB-specific antibodies and autoantibodies were found, but there was no statistically significant association with the extent of myopathy; rather, the autoantibodies appeared to be an independent reflection of the damage done by the virus infection (132). Taken together, these data indicate that CVB myocarditis favors the induction of autoantibodies, but these may be the consequence of disease rather than its cause.…”

Section: What Mechanisms Might Underlie Cvb Myocarditis?mentioning

confidence: 98%

Molecular Mimicry, Bystander Activation, or Viral Persistence: Infections and Autoimmune Disease

et al. 2006

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SUMMARY Virus infections and autoimmune disease have long been linked. These infections often precede the occurrence of inflammation in the target organ. Several mechanisms often used to explain the association of autoimmunity and virus infection are molecular mimicry, bystander activation (with or without epitope spreading), and viral persistance. These mechanisms have been used separately or in various combinations to account for the immunopathology observed at the site of infection and/or sites of autoimmune disease, such as the brain, heart, and pancreas. These mechanisms are discussed in the context of multiple sclerosis, myocarditis, and diabetes, three immune-medicated diseases often linked with virus infections.

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Coxsackievirus B1–induced chronic inflammatory myopathy: differences in induction of autoantibodies to muscle and nuclear antigens by cloned myopathic and amyopathic viruses

Cited by 13 publications

References 30 publications

Viral Persistence and Chronic Immunopathology in the Adult Central Nervous System following Coxsackievirus Infection during the Neonatal Period

Viral Persistence and Chronic Immunopathology in the Adult Central Nervous System following Coxsackievirus Infection during the Neonatal Period

Multiple Viral Determinants Mediate Myopathogenicity in Coxsackievirus B1-Induced Chronic Inflammatory Myopathy

Molecular Mimicry, Bystander Activation, or Viral Persistence: Infections and Autoimmune Disease

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