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Journal of Virology, March 2005, p. 3231-3242, Vol. 79, No. 6
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.6.3231-3242.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Dual Mechanisms of Pestiviral Superinfection Exclusion at Entry and RNA Replication

Young-Min Lee,1,2 Donna M. Tscherne,3 Sang-Im Yun,2 Ilya Frolov,1,{dagger} and Charles M. Rice1,3*

Department of Molecular Microbiology, Washington University School of Medicine, St. Louis, Missouri,1 Department of Microbiology, College of Medicine and Medical Research Institute, Chungbuk National University, Cheongju, Chungbuk, South Korea,2 Laboratory of Virology and Infectious Diseases, Center for the Study of Hepatitis C, The Rockefeller University, New York, New York3

Received 16 July 2004/ Accepted 1 November 2004

For many viruses, primary infection has been shown to prevent superinfection by a homologous second virus. In this study, we investigated superinfection exclusion of bovine viral diarrhea virus (BVDV), a positive-sense RNA pestivirus. Cells acutely infected with BVDV were protected from superinfection by homologous BVDV but not with heterologous vesicular stomatitis virus. Superinfection exclusion was established within 30 to 60 min but was lost upon passaging of persistently infected cells. Superinfecting BVDV failed to deliver a translatable genome into acutely infected cells, indicating a block in viral entry. Deletion of structural protein E2 from primary infecting BVDV abolished this exclusion. Bypassing the entry block by RNA transfection revealed a second block at the level of replication but not translation. This exclusion did not require structural protein expression and was inversely correlated with the level of primary BVDV RNA replication. These findings suggest dual mechanisms of pestivirus superinfection exclusion, one at the level of viral entry that requires viral glycoprotein E2 and a second at the level of viral RNA replication.

* Corresponding author. Mailing address: Laboratory of Virology and Infectious Diseases, Center for the Study of Hepatitis C, The Rockefeller University, 1230 York Avenue, New York, NY 10021. Phone: (212) 327-7046. Fax: (212) 327-7048. E-mail: ricec{at}mail.rockefeller.edu.

{dagger} Present address: Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, Tex.

Journal of Virology, March 2005, p. 3231-3242, Vol. 79, No. 6
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.6.3231-3242.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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