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Research Article Free access | 10.1172/JCI115776

Molecular basis of age-dependent gastric inactivation of rhesus rotavirus in the mouse.

D M Bass, M Baylor, R Broome, and H B Greenberg

Department of Pediatrics, Stanford University, California 94305.

Find articles by Bass, D. in: PubMed | Google Scholar

Department of Pediatrics, Stanford University, California 94305.

Find articles by Baylor, M. in: PubMed | Google Scholar

Department of Pediatrics, Stanford University, California 94305.

Find articles by Broome, R. in: PubMed | Google Scholar

Department of Pediatrics, Stanford University, California 94305.

Find articles by Greenberg, H. in: PubMed | Google Scholar

Published June 1, 1992 - More info

Published in Volume 89, Issue 6 on June 1, 1992
J Clin Invest. 1992;89(6):1741–1745. https://doi.org/10.1172/JCI115776.
© 1992 The American Society for Clinical Investigation
Published June 1, 1992 - Version history
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Abstract

Rotavirus requires specific proteolytic activation by trypsin for efficient replication in tissue culture. To observe the nature of intestinal proteolytic activation of rotavirus in vivo, metabolically labeled rhesus rotavirus (RRV) grown in the presence of trypsin inhibitors was administered to adult and 10-d-old suckling mice by gavage. In the adult stomach, vp4 was cleaved in a manner distinct from in vitro trypsin cleavage. In the suckling stomach, RRV vp4 remains largely uncleaved. The alternative cleavage in the adult stomach was associated with a profound decrease in viral infectivity. vp4 from RRV recovered from the suckling small intestinal lumen was cleaved in a pattern similar or identical to in vitro trypsin-activated virus with bands comigrating with vp5* and vp8*. In contrast, vp4 was not observed in any recognizable form in RRV recovered from adult intestines. Comparison of infectivity of virus recovered from suckling and adult intestines revealed a 10,000-fold decrease in titer in the virus recovered from the adult intestine. In vitro digestions of RRV revealed that pepsin digestion can cleave RRV vp4 and markedly enhance acid-induced loss of rotavirus infectivity. Subsequent digestion with chymotrypsin removes most of the pepsin cleavage products of vp4. Virus injected directly into jejunal loops of adult mice and virus administered orally to adult mice pretreated with antiacid drugs retained infectivity. These studies indicate the development of gastric acid and pepsin secretion may be an important host defense factor in rotavirus gastroenteritis.

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