Mouse hepatitis virus 3 pathogenicity expressed by a lytic viral infection in bone marrow 14.8+ mu+ B lymphocyte subpopulations.
Mouse hepatitis virus type 3 (MHV3) provides an excellent model for studying viral-B lymphocyte interaction in the immune system, which plays an important role in the outcome of an acute disease. Bone marrow B lymphocyte subpopulations, at various times postinfection, were studied in genetically C57BL/6 and resistant A/J mice, infected with pathogenic L2-MHV3 and its nonpathogenic variant, YAC-MHV3. B lineage cell subpopulations were identified by double immunofluorescence assays using mAb of terminal deoxynucleotidyl transferase, 14.8 and cytoplasmic (cu) or surface (su) Ig mu-chains. Results revealed diminished percentage and absolute number in the bone marrow 14.8+ mu+ B lymphocyte subpopulations, including pre-B (cu+ su-) and B (cu+ su+) cells of L2-MHV3-infected susceptible C57BL/6 mice; whereas, slight or no increase was evident in the cell subpopulations of L2-MHV3 infected resistant A/J mice or in YAC-MHV3 infected in both strains of mice. Abnormal large-sized forms of the 14.8+ mu+ cells occurred, at 48-h postinfection, in L2-MHV3-infected susceptible C57BL/6 mice only. In contrast, no change in the percentage and absolute number of precursor cells (terminal deoxynucleotidyl transferase positive) and pre pre-B cells (14.8+ mu-) were detected in all infected mice. In vitro L2-MHV3 infection of C57BL/6 bone marrow purified B lineage cell subpopulations showed that pre-B (cu+ su-) and B (cu+ su+) cells became abnormally large in size and depleted in number as a result of a productive and lytic viral replication. Low L2-MHV3 viral replication occurred in these cell subpopulations of A/J mice but no YAC-MHV3 virus was produced in the cells of both strains of mice. Pre pre-B (14.8+ mu-) cells in both strains were not permissive to L2-MHV3 or YAC-MHV3 viral replication. These results are discussed with regard to the role of humoral immunodeficiency in the pathogenic process.
Jolicoeur
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P
Département des Sciences Biologiques, Université du Québec, Montréal, Canada.
Lamontagne
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L
D000208:Acute Disease; D000818:Animals; D001402:B-Lymphocytes / Q000382:microbiology* / Q000473:pathology; D001853:Bone Marrow / Q000201:enzymology; D001855:Bone Marrow Diseases / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D004253:DNA Nucleotidylexotransferase; D006524:Hepatitis, Viral, Animal / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D007958:Leukocyte Count; D008212:Lymphocyte Depletion; D051379:Mice; D008805:Mice, Inbred A; D008810:Mice, Inbred C57BL; D006517:Murine hepatitis virus / Q000276:immunology / Q000472:pathogenicity*; D010641:Phenotype; D014779:Virus Replication
D004253:DNA Nucleotidylexotransferase