Journal
JOURNAL OF VIROLOGY
Volume 74, Issue 19, Pages 9206-9213Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.74.19.9206-9213.2000
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Funding
- NINDS NIH HHS [NS30606, P01 NS030606] Funding Source: Medline
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Demyelination is the pathologic hallmark of the human immune-mediated neurologic disease multiple sclerosis, which may be triggered or exacerbated by viral infections. Several experimental animal models have been developed to study the mechanism of virus-induced demyelination, including coronavirus mouse hepatitis virus (MHV) infection in mice. The envelope spike (S) glycoprotein of MHV contains determinants of properties essential for virus-host interactions. However, the molecular determinants of MHV-induced demyelination are still unknown. To investigate the mechanism of MHV-induced demyelination, we examined whether the S gene of MHV contains determinants of demyelination and whether demyelination is linked to viral persistence. Using targeted RNA recombination, we replaced the S gene of a demyelinating virus (MHV-A59) with the S gene of a closely related, nondemyelinating virus (MHV-2). Recombinant viruses containing an S gene derived from MHV-2 in an MHV-A59 background (Penn98-1 and Penn98-2) exhibited a persistence-positive, demyelination-negative phenotype. Thus, determinants of demyelination map to the S gene of MHV, Furthermore, viral persistence is insufficient to induce demyelination, although it may be a prerequisite for the development of demyelination.
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