This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Benton, P. A. Articles by Lloyd, R. E. Search for Related Content PubMed PubMed Citation Articles by Benton, P. A. Articles by Lloyd, R. E.

 Previous Article  |  Next Article 

J. Virol., 08 1996, 5525-5532, Vol 70, No. 8
Copyright © 1996, American Society for Microbiology

The outcome of poliovirus infections in K562 cells is cytolytic rather than persistent after hemin-induced differentiation

PA Benton, DJ Barrett, RL Matts and RE Lloyd
Department of Microbiology and Immunology, University of Oklahoma Health Sciences Center, Oklahoma City 73190, USA.

K562-Mu erythroleukemia cells readily establish a long-term persistent poliovirus infection characterized by continuous virus production in the absence of complete p220 cleavage and host translation shutoff (R. E. Lloyd and M. Bovee, Virology 194:200-209, 1993). The mechanism of resistance appears to be modulated at the intracellular level and to be related to decreased virus-mediated cytopathic effects (P. A. Benton, J. W. Murphy, and R. E. Lloyd Virology 213:7-18, 1995). It is well documented that hemin induces the differentiation of K562 cells and alters the expression of several host proteins. We report here that growth of K562 cells in hemin prior to poliovirus infection results in a dose-dependent increase in virus-induced cell lysis and thereby alters the normally persistent outcome of infection to a more lytic phenotype. K562 cells infected after hemin treatment displayed increased host translation shutoff, p220 cleavage, viral protein synthesis, and viral RNA accumulation compared with nontreated cells. Since hemin treatment of K562 cells also induced the increased expression of several heat shock proteins (Hsp70, Hsc70, Hsp90, and cohort p60), we tested the hypothesis that their increased expression may play a role in altering poliovirus infection in hemin-treated K562 cells. However, neither heat stress nor oxidative stress, inducers of heat shock protein synthesis, altered the outcome (of virus infections. In addition, we report the novel finding that subunits of two translation initiation factors, p220 (eIF-4G) and eIF-2alpha, are cleaved as a result of hemin treatment of K562 cells. It is proposed that hemin alters the expression of specific host proteins in K562 cells, probably other than heat shock proteins, which changes the initial response to poliovirus infections from persistent to lytic.

This article has been cited by other articles:

• Zhang, J., Timoney, P. J., MacLachlan, N. J., McCollum, W. H., Balasuriya, U. B. R. (2008). Persistent Equine Arteritis Virus Infection in HeLa Cells. J. Virol. 82: 8456-8464 [Abstract] [Full Text]  
• Marissen, W. E., Guo, Y., Thomas, A. A. M., Matts, R. L., Lloyd, R. E. (2000). Identification of Caspase 3-mediated Cleavage and Functional Alteration of Eukaryotic Initiation Factor 2alpha in Apoptosis. J. Biol. Chem. 275: 9314-9323 [Abstract] [Full Text]  
• Marissen, W. E., Lloyd, R. E. (1998). Eukaryotic Translation Initiation Factor 4G Is Targeted for Proteolytic Cleavage by Caspase 3 during Inhibition of Translation in Apoptotic Cells. Mol. Cell. Biol. 18: 7565-7574 [Abstract] [Full Text]  
• Uma, S., Yun, B.-G., Matts, R. L. (2001). The Heme-regulated Eukaryotic Initiation Factor 2alpha Kinase. A POTENTIAL REGULATORY TARGET FOR CONTROL OF PROTEIN SYNTHESIS BY DIFFUSIBLE GASES. J. Biol. Chem. 276: 14875-14883 [Abstract] [Full Text]