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Journal of Virology, July 2004, p. 7775-7783, Vol. 78, No. 14
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.14.7775-7783.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Parvovirus B19-Induced Apoptosis of Hepatocytes

Brian D. Poole,1,2 Yuory V. Karetnyi,3,{dagger} and Stanley J. Naides2*

Integrated Biosciences Graduate Program,1 Division of Rheumatology, Department of Medicine, Pennsylvania State University College of Medicine, Hershey, Pennsylvania,2 Division of Rheumatology, Department of Internal Medicine, The University of Iowa, Iowa City, Iowa3

Received 5 November 2003/ Accepted 8 March 2004

Parvovirus B19 (B19 virus) can persist in multiple tissues and has been implicated in a variety of diseases, including acute fulminant liver failure. The mechanism by which B19 virus induces liver failure remains unknown. Hepatocytes are nonpermissive for B19 virus replication. We previously reported that acute fulminant liver failure associated with B19 virus infection was characterized by hepatocellular dropout. We inoculated both primary hepatocytes and the hepatocellular carcinoma cell line Hep G2 with B19 virus and assayed for apoptosis by using annexin V staining. Reverse transcriptase PCR analysis and immunofluorescence demonstrated that B19 virus was able to infect the cells and produce its nonstructural protein but little or no structural capsid protein. Infection with B19 virus induced means of 28% of Hep G2 cells and 10% of primary hepatocytes to undergo apoptosis, which were four- and threefold increases, respectively, over background levels. Analysis of caspase involvement showed that B19 virus-inoculated cultures had a significant increase in the number of cells with active caspase 3. Inhibition studies demonstrated that caspases 3 and 9, but not caspase 8, are required for B19 virus-induced apoptosis.

* Corresponding author. Mailing address: Division of Rheumatology, Department of Medicine, Pennsylvania State University College of Medicine, Milton S. Hershey Medical Center, 500 University Dr., Hershey, PA 17033. Phone: (717) 531-5384. Fax: (717) 531-8274. E-mail: snaides{at}psu.edu.

{dagger} Present address: Beckman Coulter, Inc., Chaska, MN 55318.

Journal of Virology, July 2004, p. 7775-7783, Vol. 78, No. 14
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.14.7775-7783.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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