Late onset, symptomatic, demyelinating encephalomyelitis in mice infected with MHV-JHM in the presence of maternal antibody

S Perlman; R Schelper; E Bolger; D Ries

doi:10.1016/0882-4010(87)90020-9

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Late onset, symptomatic, demyelinating encephalomyelitis in mice infected with MHV-JHM in the presence of maternal antibody

Journal article

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Late onset, symptomatic, demyelinating encephalomyelitis in mice infected with MHV-JHM in the presence of maternal antibody

S Perlman, R Schelper, E Bolger and D Ries

Microbial Pathogenesis, Vol.2(3), pp.185-194

1987

DOI: 10.1016/0882-4010(87)90020-9

PMID: 2853274

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Abstract

The presence of maternal antibodies protected suckling C57BL/6 mice from the clinical manifestations of the acute encephalomyelitis caused by mouse hepatitis virus, strain JHM (MHV-JHM), a coronavirus, even though histological evidence of encephalomyelitis was found at early times after inoculation. 100% of infected suckling mice developed a fatal disease in the absence of maternal antibody. By 14 days after inoculation, the brains of all antibody-protected mice examined were nearly normal on histological examination. At 3–8 weeks post-inoculation, approximately 40% of the antibody-protected mice developed a neurological disease characterized by hindlimb paralysis and wasting. Evidence of inflammation and demyelination was apparent in the spinal cord and brainstem. The mice that remained asymptomatic at this time showed few signs of inflammation and none developed clinical disease over the following 9 months. Viral antigen could be detected in most of the mice examined at all times after inoculation, whether symptomatic or not, and was particularly evident in the animals with hindlimb paralysis. MHV-JHM could be consistently cultured from the mice with hindlimb paralysis. These results show that maternal immune factors can completely protect susceptible mice from the acute, fatal, clinical encephalomyelitis caused by MHV-JHM, but cannot prevent the establishment of a latent state and subsequent development of virus-induced, clinically evident, demyelinating disease. This model will be useful for studying the virus and host factors important for the development of MHV-JHM latency and subsequent virus-induced demyelination.

immunoperoxidase

maternal antibody

mouse hepatitis virus

demyelination

Details

Title: Subtitle: Late onset, symptomatic, demyelinating encephalomyelitis in mice infected with MHV-JHM in the presence of maternal antibody
Creators: S Perlman - Department of Pediatrics, University of Iowa School of Medicine, Iowa City, IA 52242, U.S.A
R Schelper - Department of Pathology, University of Iowa School of Medicine, Iowa City, IA 52242, U.S.A
E Bolger - Department of Pathology, University of Iowa School of Medicine, Iowa City, IA 52242, U.S.A
D Ries - Department of Pediatrics, University of Iowa School of Medicine, Iowa City, IA 52242, U.S.A
Resource Type: Journal article
Publication Details: Microbial Pathogenesis, Vol.2(3), pp.185-194
DOI: 10.1016/0882-4010(87)90020-9
PMID: 2853274
NLM abbreviation: Microb Pathog
ISSN: 0882-4010
eISSN: 1096-1208
Publisher: Elsevier India Pvt Ltd
Language: English
Date published: 1987
Academic Unit: Microbiology and Immunology; Stead Family Department of Pediatrics; Iowa Neuroscience Institute; Infectious Disease (Pediatrics)
Record Identifier: 9983777355802771

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