DIFFERENTIAL RECRUITMENT OF B-CELL AND T-CELL IN COXSACKIEVIRUS B4-INDUCED PANCREATITIS IS INFLUENCED BY A CAPSID PROTEIN

Two genetically similar variants of coxsackievirus B4, CB4-P and CB4-V , cause distinct disease syndromes in mice, A multidisciplinary approa ch was used to examine the events occurring in situ, The CB4-P variant induced acute pancreatitis, followed by repair of the exocrine tissue s, while the CB4-V variant induced chronic pancreatitis, characterized by extensive destruction of the exocrine tissues, Since CB4-V replica ted more efficiently than CB4-P in vivo, the more extensive tissue inj ury associated with CB4-V infection could be explained as the result o f a higher level of viral replication, However, the fact that CB4-V re plicated more efficiently in a mouse strain that survives infection th an in a strain that succumbs to infection suggests that immune-mediate d mechanisms as well as viral cytolysis may contribute to pancreatic t issue injury, To address the role of the immune system in virus-induce d pancreatitis, the cell types within the inflammatory infiltrate were analyzed by how 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 a nd T cells to the pancreatic tissues was influenced by viral strain, D ifferential recruitment of T and B cells may reflect altered antigenic sites between CB4-P and CB4-V. The viral sequence that affected T- an d B-cell recruitment was identified as a threonine residue at position 129 of the VP1 capsid protein.