Role of viruses in etiology and pathogenesis of multiple sclerosis

Soldan, Samantha S.; Jacobson, Steven

doi:10.1016/s0065-3527(01)56037-6

Cited by 36 publications

(26 citation statements)

References 185 publications

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“…Various data point to a viral pathogenesis of MS: geographic association of disease susceptibility with evidence of MS clustering, abnormal response to a variety of viruses, increase of disease exacerbations with viral infection, and analogy with animal models and other human diseases in which viruses can cause demyelinating diseases. 46 Thus, given the central role of CD8 ϩ T cells in viral infections, our findings of an increase in the frequency of cells displaying the effector phenotype within the CD8 ϩ population and the display of an increased adhesive capacity in brain vessels by this cell subset further substantiate the hypothesis that viral infections or reactivations may trigger clinical exacerbations in RRMS.…”

Section: Discussionsupporting

confidence: 73%

CD8+ T cells from patients with acute multiple sclerosis display selective increase of adhesiveness in brain venules: a critical role for P-selectin glycoprotein ligand-1

Battistini¹

2003

Blood

157

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Section: Discussionsupporting

confidence: 73%

CD8+ T cells from patients with acute multiple sclerosis display selective increase of adhesiveness in brain venules: a critical role for P-selectin glycoprotein ligand-1

Battistini¹

2003

Blood

157

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“…This has become increasingly significant, as there is a greater appreciation for the role that these viruses play in neurological disease (11,33). An extensive study on a large cohort of children and adults documented a relative predominance of HHV-6A in cerebral spinal fluid from children.…”

Section: Discussionmentioning

confidence: 99%

“…Consistent evidence supporting the possible association of HHV-6 in multiple sclerosis (MS) would suggest that HHV-6 is also involved in this inflammatory disease of the CNS (33). Recent studies on autopsy brain samples from patients with MS have reported a higher frequency of HHV-6 DNA in MS plaques as opposed to normal-appearing white matter of the same patients and to unaffected brain specimens (7,17), and a recent investigation has documented significantly higher levels of HHV-6 gene transcripts in both lesional and normal-appearing white matter in autopsy brain samples from MS patients than in those from normal controls (27).…”

mentioning

confidence: 92%

Variant-Specific Tropism of Human Herpesvirus 6 in Human Astrocytes

Donati

Martinelli

Cassiani-Ingoni

et al. 2005

J Virol

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Though first described as a lymphotropic virus, human herpesvirus 6 (HHV-6) is highly neuropathogenic. Two viral variants are known: HHV-6A and HHV-6B. Both variants can infect glial cells and have been differentially associated with central nervous system diseases, suggesting an HHV-6 variant-specific tropism for glial cell subtypes. We have performed infections with both viral variants in human progenitor-derived astrocytes (HPDA) and monitored infected cell cultures for cytopathic effect (CPE), intra-and extracellular viral DNA load, the presence of viral particles by electronic microscopy, mRNA transcription, and viral protein expression. HHV-6A established a productive infection with CPE, visible intracellular virions, and high virus DNA loads. HHV-6B-infected HPDA showed no morphological changes, intracellular viral particles, and decreasing intra-and extracellular viral DNA over time. After long-term passage, HHV-6B-infected HPDA had stable but low levels of intracellular viral DNA load with no detectable viral mRNA. Our results demonstrate that HHV-6A and HHV-6B have differential tropisms and patterns of infection for HPDA in vitro, where HHV-6A results in a productive lytic infection. In contrast, HHV-6B was associated with a nonproductive infection. These findings suggest that HHV-6 variants might be responsible for specific infection patterns in glial cells in vivo. Astrocytes may be an important reservoir for this virus in which differential tropism of HHV-6A and HHV-6B may be associated with different disease outcomes.

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“…A large variety of DNA viruses, especially human herpes virus 6, and RNA viruses from many different families, for example, human T-cell leukaemia virus 1 and human endogenous retroviruses, have been studied for their association with MS. None has received more attention than MV [122,123]. Increased levels of antibodies to a number of viruses including measles have been observed in serum and CSF samples [124,125].…”

Section: Multiple Sclerosismentioning

confidence: 99%

Morbilliviruses and human disease

Rima

Duprex

2005

The Journal of Pathology

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Morbilliviruses are a group of viruses that belong to the family Paramyxoviridae. The most instantly recognizable member is measles virus (MV) and individuals acutely infected with the virus exhibit a wide range of clinical symptoms ranging from a characteristic mild selflimiting infection to death. Canine distemper virus (CDV) and rinderpest virus (RPV) cause a similar but distinctive pathology in dogs and cattle, respectively, and these, alongside experimental MV infection of primates, have been useful models for MV pathogenesis. Traditionally, viruses were identified because a distinctive disease was observed in man or animals; an infectious agent was subsequently isolated, cultured, and this could be used to recapitulate the disease in an experimentally infected host. Thus, satisfying Koch's postulates has been the norm. More recently, particularly due to the advent of exceedingly sensitive molecular biological assays, many researchers have looked for infectious agents in disease conditions for which a viral aetiology has not been previously established. For these cases, the modified Koch's postulates of Bradford Hill have been developed as criteria to link a virus to a specific disease. Only in a few cases have these conditions been fulfilled. Therefore, many viruses have over the years been definitely and tentatively linked to human diseases and in this respect the morbilliviruses are no different. In this review, human diseases associated with morbillivirus infection have been grouped into three broad categories: (1) those which are definitely caused by the infection; (2) those which may be exacerbated or facilitated by an infection; and (3) those which currently have limited, weak, unsubstantiated or no credible scientific evidence to support any link to a morbillivirus. Thus, an attempt has been made to clarify the published data and separate human diseases actually linked to morbilliviruses from those that are merely anecdotally associated.

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Role of viruses in etiology and pathogenesis of multiple sclerosis

Cited by 36 publications

References 185 publications

CD8+ T cells from patients with acute multiple sclerosis display selective increase of adhesiveness in brain venules: a critical role for P-selectin glycoprotein ligand-1

CD8+ T cells from patients with acute multiple sclerosis display selective increase of adhesiveness in brain venules: a critical role for P-selectin glycoprotein ligand-1

Variant-Specific Tropism of Human Herpesvirus 6 in Human Astrocytes

Morbilliviruses and human disease

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