In a murine model, coxsackievirus B3 inoculation causes primary viral replication in the pancreas leading to acinar pancreatitis, which precedes the development of necrotizing myocarditis.
Does not alter clinical practice; hypothesis-generating for pancreatic tropism in human CVB3 myocarditis.
Balb/C weanling mice were inoculated intraperitoneally with a myocarditic variant of coxsackie-virus B3, with the aim of characterizing more fully the cell damage induced in the heart as well as in other organs. During the first week postinfection (pi), all animals developed acinar pancreatitis, followed by focal myocarditis. In accordance with the increasing infectivity titers, such progressive histopathological changes correlated with local viral replication. From day 4 pi, acinar degeneration accompanied by diffuse inflammatory exudate was observed in the pancreas, followed by fatty tissue replacement by day 8. In the heart, focal necrosis rather than inflammatory reaction first appeared at 4 days pi and became widespread by 6-8 days pi. Necrotic foci usually presented calcium deposits, with absence of myofibrils in the affected fibers. The fact that both periodic acid Schiff (PAS) and Best carmine staining remained positive even after diastase treatment ruled out basophilic necrosis. In summary, the pancreas appeared to be the site of primary viral replication leading to viremia.
No takes yet. Share an insight, caveat, or question.
Gómez et al. (1991) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: