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. 2005 Jun 3;8:15–28. doi: 10.1016/S0165-5728(85)80044-8

Host genetic regulation of acute MHV-4 viral encephalomyelitis and acute experimental autoimmune encephalomyelitis in (BALB/cKe × SJL/J) recombinant-inbred mice*

RL Knobler 1,*, DS Linthicum 2, M Cohn 3
PMCID: PMC7119749  PMID: 2579095

Abstract

In the present report we provide the strain distribution patterns of susceptibility to acute mouse hepatitis virus type-4 (MHV-4) encephalomyelitis, acute experimental allergic encephalomyelitis (EAE) and vasoactive amine sensitivity (VAAS) for 9 (CXJ) recombinant-inbred strains between BALB/cKe (C) and SJL/J (J) mice. We confirm that susceptibility to MHV-4 is not linked to the H-2 complex, and that all strains susceptible to acute EAE have both a responder H-2 haplotype (H-2s or H-2d) and induced (B. pertussis) VAAS. In addition, we provide evidence that susceptibility to acute EAE induction is controlled by an additional presently unmapped locus and that an EAE-like histopathological disease does not usually follow MHV-4 infection intracerebrally in animals susceptible to MHV-4, acute EAE and induced VAAS.

Key words: Acute experimental allergic encephalomyelitis (EAE), Genetic regulation of host, MHV-4 viral encephalomyelitis, Recombinant inbred mice, Vasoactive amine sensitivity (VAAS)

Footnotes

*

This is Publication No. 3081-IMM from the Department of Immunology, Scripps Clinic and Research Foundation.

This work was supported in part by USPHS Grants NS-12428, AI 1 P40 RR01 641-01 and National Multiple Sclerosis Society Grant 1256-B-3. RLK was the Ralph I. Straus Fellow of the National Multiple Sclerosis Society, and currently is recipient of Teacher Investigator Development Award NS08003 from the NINCDS. DSL is a ‘Scholar’ of the Leukemia Society of America, Inc.

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