Mutation of a major histocompatibility class I locus, H-2D, leads to an increased virus burden and disease susceptibility in Theiler's virus-induced demyelinating disease
| Autor: | Stephen D. Miller, Roger D. Melvold, M. C. Dal Canto, Howard L. Lipton |
|---|---|
| Rok vydání: | 1995 |
| Předmět: |
Male
Picornavirus viruses Mutant Locus (genetics) CD8-Positive T-Lymphocytes Kidney Virus Cell Line Mice Cellular and Molecular Neuroscience Virus antigen Theilovirus Cricetinae Virology MHC class I Demyelinating disease medicine Animals biology Histocompatibility Antigens Class I Viral Load medicine.disease biology.organism_classification Mice Mutant Strains Mice Inbred C57BL Spinal Cord Neurology Viral replication Mice Inbred DBA Mutation Immunology biology.protein Female Neurology (clinical) Demyelinating Diseases Poliomyelitis |
| Zdroj: | Journal of Neurovirology. 1:138-144 |
| ISSN: | 1538-2443 1355-0284 |
| DOI: | 10.3109/13550289509113960 |
| Popis: | Genetic studies have demonstrated that susceptibility to Theiler's murine encephalomyelitis virus (TMEV)-induced demyelinating disease is multigenic with linkage to the MHC class I locus, H-2D. We have analyzed the effect of mutations (H-2bm13 and H-2bm14) in the H-2Db gene on central nervous system (CNS) virus replication, virus-specific delayed type hypersensitivity (DTH) and disease induction in mutant [bm 14D2F1 and bm13D2F1] and parental B6D2F1 hybrids. The results indicate that substitutions of only a single residue (bm14D2F1) or three residues (bm13D2F1) in H-2D in the mutant leads to a sequence of events culminating in disease susceptibility. Mutation of the H-2D gene is associated with reduced or delayed virus clearance following the acute phase of exponential CNS virus growth and an increased level of virus persistence. Concomittant with the greater virus antigen burden, mutant mice respond with higher levels of virus-specific DTH and develop inflammatory demyelinating lesions. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|