Hepatic damage caused by Coxsackievirus B3 is dependent on age‐related tissue tropisms associated with the Coxsackievirus‐adenovirus receptor

This study was designed to explore the role of coxsackievirus‐adenovirus receptor (CAR) in pathogenesis of CVB3 infected hepatocyte via in vitro and mice study. CVB3 (CVB3/2630) was isolated from liver tissue of a neonate with fulminant hepatitis. Cell lines A549, HeLa, HEp2 and Huh‐7 were maintained in Dulbecco's modified Eagle's medium. One‐day‐old or seven‐day‐old mice progeny were used in the experiments. Viraemia was noted in seven‐day‐old ICR mice 2 hours of an intraperitoneal injection. Thereafter the highest viral titers were detected in blood, liver and spleen. Histopathological studies of the liver demonstrated polymorphonuclear cells infiltration, massive hepatic cells necrosis and apoptosis. CAR was more expressed in liver than other tissues. Expression of CAR decreased with mice age. Anti‐CAR monoclonal antibody prevented infection of Huh‐7 cells from CVB3. Furthermore, anti‐CAR monoclonal antibody pretreatment can reduce mortality and decrease level of liver enzymes in CVB3‐infected mice. These findings indicate that CAR plays an important role in the initiation of CVB infections and is closely associated with hepatotropism and age‐specific susceptibility. This article is protected by copyright. All rights reserved.
Source: FEMS Immunology and Medical Microbiology - Category: Microbiology Authors: Tags: Research paper Source Type: research