Antigenic Assessment of Coronaviruses Isolated From Patients With Multiple Sclerosis

Fleming, John O.; Zaatari, Fouad A. K. El; Gilmore, Wendy; Berne, John D.; Burks, Jack S.; Stohlman, Stephen A.; Tourtellotte, Wallace W.; Weiner, Leslie P.

doi:10.1001/archneur.1988.00520300047017

Cited by 22 publications

(14 citation statements)

References 37 publications

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“…One of the viruses used in this study, coronavirus SD, and another isolate, SK, were reportedly recovered from brain tissue obtained from MS patients at autopsy (Burks et al, 1980) . These two virus isolates have serologic cross-reactivity to both murine coronaviruses and HCV OC43 (Gerdes et al, 1981) but others have demonstrated that they are antigenically and genetically more closely related to murine coronaviruses than to prototypic human coronaviruses (Fleming et al, 1988 ;Weiss, 1983) . Our unpublished data show a 97% se-quence identity in the 3' end of the genome between SD and MHV JHM in agreement with these earlier reports .…”

Section: Discussionmentioning

confidence: 99%

“…Frozen sections were fixed in -20° methanol for 10 min then washed three times with PBS . Sections were incubated with monoclonal antibody (Mab)1 .3 .1 (Fleming et al, 1988) at 37° for 20 min then washed with PBS . Immunoperoxidase detection was done with Mab 1 .3 .1 utilizing the Peroxidase Anti-Peroxidase kit from BioGenex Laboratories .…”

Section: Animals and Experimental Designmentioning

confidence: 99%

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Coronavirus infects and causes demyelination in primate central nervous system

et al. 1992

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Two species of primates, Owl and African green monkeys, were inoculated intracerebrally with either the neurotropic mouse hepatitis virus JHM or the putative multiple sclerosis brain coronavirus isolate SD. These viruses caused an acute to subacute panencephalitis and/or demyelination in the infected animals. The course of pathogenesis and sites of detected viral RNA and antigen was dependent both on animal species and virus strain but the results clearly showed that these viruses replicated and disseminated in the central nervous system (CNS) of these primates. This study suggests that human CNS may be susceptible to coronavirus infection.

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Section: Discussionmentioning

confidence: 99%

Section: Animals and Experimental Designmentioning

confidence: 99%

Coronavirus infects and causes demyelination in primate central nervous system

et al. 1992

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“…Clinical recovery and myelin repair occur in the following 2-8 weeks (Kristensson et al, 1986;Lavi et al, 1984a,b;Woyciechowska et al, 1984). Although the viral-induced demyelinating lesions closely resemble those seen in multiple sclerosis, no specific association between multiple sclerosis and coronaviruses has been demonstrated so far (Fleming et al, 1988). We have chosen the MHV-A59 model for our studies since the virus caused demyelination in the spinal cord of a high proportion of the animals; subsequently, myelin repair can be followed closely in these spinal cord regions.…”

Section: Introductionmentioning

confidence: 99%

Expression of viral and myelin gene transcripts in a murine CNS demyelinating disease caused by a coronavirus

Jordan

Friedrich

Godfraind

et al. 1989

Glia

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C57BI/6N mice develop a CNS demyelinating disease when inoculated intracranially at 4 weeks of age with the A59 strain of mouse hepatitis virus (MHV-A59). In order to explore the virus-host interactions, the histological features of the demyelinating disease were correlated with the spatial and temporal distribution of viral transcripts and the expression of oligodendrocyte-specific genes (myelin basic protein, proteolipid protein, myelin-associated glycoprotein, and 2',3' cyclic nucleotide 3'-phosphohydrolase) in the spinal cord of diseased mice. Three distinct phases in the disease were identified. In the first phase, 1 week postinfection (1 WPI), virus replication was widespread in both gray and white matter but was preferentially occurring in glial cells. In the ventral and dorsal root zones where viral transcripts were most abundant, all myelin gene transcripts were decreased before demyelination was seen. During the second phase of the disease (2-3 WPI), viral transcripts decreased in abundance and became restricted to the white matter. Numerous demyelinating lesions were observed and were characterized by inflammatory cells, paucity of oligodendrocytes, and a profound decrease of all myelin gene transcripts. In the third phase of the disease (4-6 WPI) no viral transcripts were detected, and remyelination began. In the lesions and the tissue surrounding them, transcripts of all myelin genes increased to levels above normal. The increased expression of myelin gene transcripts occurred in a synchronized manner and with a cellular distribution reminiscent of that seen in developmental myelination. These molecular events correlated with efficient remyelination and clinical recovery in this murine demyelinating disease.

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“…In humans, CoV have been associated with community-acquired upper respiratory tract infections (4). Human CoV (HCoV) have also been implicated in outbreaks of diarrhea as well as in demyelinating disorders of the central nervous system, though these data are controversial (5,6). The study and identification of HCoV have been hampered by the difficulty in propagating these viruses in vitro.…”

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confidence: 99%