Sequences specific for enterovirus detected in spinal cord from patients with motor neurone disease

Woodall, Chris; Riding, Miriam H.; Graham, D. I.; Clements, G. B.

doi:10.1136/bmj.308.6943.1541

Cited by 75 publications

(49 citation statements)

References 15 publications

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“…In mice, Theiler's virus causes persistent infection accompanied by primary demyelination (Cash et al, 1988) while in immunosuppressed patients, chronic meningoencephalitis and poliomyelitis may occur (Wilfert et al, 1977;Davis et al, 1977;Webster et al, 1993;McKinney et al, 1987). A role for enteroviruses has been postulated in the post-polio syndrome (Sharief et al, 1991) and in motor neurone disease (Martyn et al, 1988;Woodall et al, 1994) although, as discussed by Dalakas (1995) in the latest review, these findings have not been confirmed.…”

Section: Viral Genomic/templatementioning

confidence: 80%

“…(Woodruff, 1980;Kandolf and Hofschneider, 1989). In the last decade, there have been several reports suggesting that persistent enteroviruses may be the cause of various CNS and muscle disorders of unknown aetiology, including motor neurone disease (Martyn et al, 1988;Woodall et al, 1994), the post-polio syndrome (Sharief et al, 1991;Dalakas, 1995), the chronic fatigue syndrome (Archard et al, 1988;Behan and Behan, 1988;Gow et al, 1991) the autoimmune myopathies (Bowles et al, 1987;Behan and Behan, 1993) and the cardiomyopathies, especially dilated cardiomyopathy (DCM) (Bowles et al, 1986;Kandolf and Hofschneider, 1989;Tracy et al, 1990;Klingel et al, 1992). The evidence has been based on serological findings and the detection of enteroviral genomes in the affected tissues: in no case has infectious virus been isolated.…”

mentioning

confidence: 99%

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Genomic and template RNA transcription in a model of persistent enteroviral infection

Jw¹,

Wm²,

Cash³

et al. 1997

J Neurovirol

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Enteroviruses have been implicated in persistent infections of the nervous system and in certain paralytic motor neurone syndromes. Enteroviral persistence may depend on defective transcription, resulting in the abnormal production of equal amounts of genomic and template RNA strands rather than the normal ratio of 60 ± 100 : 1. An in vitro model of a persistent coxsackie virus in human skeletal muscle cells was investigated using in situ hybridisation and a semiquantitative parallel, complementary, reverse transcriptase polymerase chain reaction. The ratio of genomic to template RNA was found to be approximately 60 : 1. We conclude that enteroviral persistence in this in vitro model is not dependent on altered transcription. In vivo, other viral and host factors should be considered.

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Section: Viral Genomic/templatementioning

confidence: 80%

mentioning

confidence: 99%

Genomic and template RNA transcription in a model of persistent enteroviral infection

Jw¹,

Wm²,

Cash³

et al. 1997

J Neurovirol

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“…Severe demyelinating diseases may occur following infection, including acute disseminated encephalomyelitis (18) and acute transverse myelitis (27). Also, a number of delayed neuropathologies have been associated with previous coxsackievirus infection, including schizophrenia (47,52), encephalitis lethargica (16), and amyotrophic lateral sclerosis (62,63). If human neurotropic viruses persist, they could provide a chronic inflammatory stimulus, leading to regional cytokine induction and activation of autoreactive T cells through molecular mimicry and bystander activation (32,45).…”

mentioning

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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“…Firstly, the similarity of pathological lesions in the CNS of MND patients to those in poliomy elitis was noted many years ago. Recently Woodall et al [88] reported PCR detection of CVB-like RNA in post mortem CNS tissue from 11 of 15 patients with MND. but none of controls.…”

Section: The Possible Role O F Enteroviruses In Chronic Neuromuscularmentioning

confidence: 99%

Enterovirus Infections of the Central Nervous System

Muir

Loon

1997

Intervirology

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The genus Enterovirus is a large group of viruses belonging to the family Picornaviridae. They have a worldwide distribution, cause a wide spectrum of disease, and are a common cause of central nervous system disease. Included among the sixty-six enterovirus serotypes known to infect humans are the three poliovirus (PV) serotypes, the cause of paralytic poliomyelitis (PPM). PPM has been controlled in many parts of the world by vaccination. Molecular and functional comparison of PV vaccine strain and wild neurovirulent PV strains has provided an insight into mechanisms of neurovirulence. Enteroviruses are also the most commonly implicated viral agents of aseptic meningitis. Less commonly they cause a more serious encephalitis. Specific antiviral treatment for enterovirus infections is not currently available. Virological diagnosis is nonetheless important to distinguish between enterovirus-induced meningitis or encephalitis and other treatable causes of disease with a similar clinical picture.

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Sequences specific for enterovirus detected in spinal cord from patients with motor neurone disease

Cited by 75 publications

References 15 publications

Genomic and template RNA transcription in a model of persistent enteroviral infection

Genomic and template RNA transcription in a model of persistent enteroviral infection

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

Enterovirus Infections of the Central Nervous System

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