title: Differential recruitment of B and T cells in coxsackievirus B4-induced pancreatitis is influenced by a capsid protein.
abstract: Two genetically similar variants of coxsackievirus B4, CB4-P and CB4-V, cause distinct disease syndromes in mice. A multidisciplinary approach was used to examine the events occurring in situ. The CB4-P variant induced acute pancreatitis, followed by repair of the exocrine tissues, while the CB4-V variant induced chronic pancreatitis, characterized by extensive destruction of the exocrine tissues. Since CB4-V replicated more efficiently than CB4-P in vivo, the more extensive tissue injury associated with CB4-V infection could be explained as the result of a higher level of viral replication. However, the fact that CB4-V replicated more efficiently in a mouse strain that survives infection than in a strain that succumbs to infection suggests that immune-mediated mechanisms as well as viral cytolysis may contribute to pancreatic tissue injury. To address the role of the immune system in virus-induced pancreatitis, the cell types within the inflammatory infiltrate were analyzed by flow cytometry. B cells (34 to 75%) were the most abundant, followed by T cells (10 to 30%), natural killer cells (4 to 8%), and macrophages (0 to 6%). Recruitment (and perhaps proliferation) of B and T cells to the pancreatic tissues was influenced by viral strain. Differential recruitment of T and B cells may reflect altered antigenic sites between CB4-P and CB4-V. The viral sequence that affected T- and B-cell recruitment was identified as a threonine residue at position 129 of the VP1 capsid protein.
authors.affiliation: Wadsworth Center for Laboratories and Research, New York State Department of Health, Albany 12201-2002, USA. arlene.ramsingh@wadsworth.org
authors.forename: A I
authors.initials: AI
authors.lastname: Ramsingh
authors.forename: W T
authors.initials: WT
authors.lastname: Lee
authors.forename: D N
authors.initials: DN
authors.lastname: Collins
authors.forename: L E
authors.initials: LE
authors.lastname: Armstrong
mesh_terms: D000818:Animals; D000956:Antigens, Viral / Q000276:immunology; D001402:B-Lymphocytes / Q000276:immunology*; D002213:Capsid / Q000276:immunology*; D002478:Cells, Cultured; D003384:Coxsackievirus Infections / Q000276:immunology*; D029822:Enterovirus B, Human / Q000276:immunology*; D005434:Flow Cytometry; D006367:HeLa Cells; D006321:Heart / Q000821:virology; D006801:Humans; D016130:Immunophenotyping; D007694:Killer Cells, Natural / Q000276:immunology; D008264:Macrophages / Q000276:immunology; D051379:Mice; D010195:Pancreatitis / Q000276:immunology / Q000821:virology*; D013154:Spleen / Q000276:immunology / Q000821:virology; D013601:T-Lymphocytes / Q000276:immunology*; D014779:Virus Replication
chemical_list: D000956:Antigens, Viral