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Research Article Free access | 10.1172/JCI117329

Selective reovirus infection of murine hepatocarcinoma cells during cell division. A model of viral liver infection.

J Taterka, M Sutcliffe, and D H Rubin

Department of Biology, University of Pennsylvania, Philadelphia 19104.

Find articles by Taterka, J. in: JCI | PubMed | Google Scholar

Department of Biology, University of Pennsylvania, Philadelphia 19104.

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

Department of Biology, University of Pennsylvania, Philadelphia 19104.

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

Published July 1, 1994 - More info

Published in Volume 94, Issue 1 on July 1, 1994
J Clin Invest. 1994;94(1):353–360. https://doi.org/10.1172/JCI117329.
© 1994 The American Society for Clinical Investigation
Published July 1, 1994 - Version history
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Abstract

Reovirus type 1, strain Lang (1/L), can infect hepatocytes in vivo only after hepatocellular damage is induced by hepatotoxins, surgical trauma, resection, or profound immunosuppression. To examine the role of cell cycle and cellular differentiation on liver cell susceptibility to reovirus infection, a murine hepatocarcinoma cell line, Hepa 1/A1, was infected with reovirus and assayed for the presence of infectious virus or reovirus antigen in cells. Despite a > 95% binding of reovirus to hepatocarcinoma cells as indicated by cytometric analysis; only 10% of hepatoma cells contained infectious virus by infectious center assay. In comparison, 100% of L cells were infected. Analysis of intracellular reovirus antigen revealed its presence in dividing but not in quiescent hepatocytes. This correlation of cellular division and cell capacity to support viral replication suggests that induction of hepatocyte proliferation may be a mechanism for liver susceptibility to reovirus infection.

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