Secondary Logo

Journal Logo

Institutional members access full text with Ovid®

Rotavirus and biliary atresia: can causation be proven?

Hertel, Paula M.a; Estes, Mary K.b

Current Opinion in Gastroenterology: January 2012 - Volume 28 - Issue 1 - p 10–17
doi: 10.1097/MOG.0b013e32834c7ae4

Purpose of review New knowledge on rotavirus infection in children and well established mouse models has renewed interest in whether rotavirus could cause biliary atresia, an idiopathic, obliterative infantile disease of bile ducts that is the primary indication for liver transplant in children.

Recent findings Studies in the rotavirus mouse model of biliary atresia indicate that infection of biliary epithelium is an inaugural event leading to biliary inflammation and obstruction, which is preceded by systemic spread of rotavirus, which also occurs during human rotavirus enteric infections. Viral factors, including rotavirus gene 4, are important for biliary infection and biliary atresia in mice. Specific host factors related to inflammatory processes (natural killer and T cells, interferon) are also critical, and a paucity of regulatory T cells in neonates may play a key role in pathogenesis in experimental biliary atresia. Rotavirus vaccination has substantially decreased rotavirus diarrheal disease worldwide and might enable demonstration of a cause–effect relationship between rotavirus infection and biliary atresia in humans.

Summary Rotavirus can be detected in the serum of mice and children and causes biliary atresia in neonatal mice. Approaches to re-examine whether rotavirus causes biliary atresia in children are discussed based on concepts from the mouse model of biliary atresia and rotavirus vaccination programs.

aDepartment of Pediatrics

bDepartments of Molecular Virology, Microbiology and Medicine, Baylor College of Medicine, Houston, Texas, USA

Correspondence to Paula M. Hertel, MD, Department of Pediatrics, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA. Tel: +1 832 824 2099; fax: +1 832 825 3633; e-mail:

© 2012 Lippincott Williams & Wilkins, Inc.