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Originally published online as doi:10.1189/jlb.0507335 on August 21, 2007

Published online before print August 21, 2007
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(Journal of Leukocyte Biology. 2007;82:1301-1310.)
© 2007 by Society for Leukocyte Biology

Hepatitis C virus core protein up-regulates anergy-related genes and a new set of genes, which affects T cell homeostasis

M. Domínguez-Villar, A. Muñoz-Suano, B. Anaya-Baz, S. Aguilar, J. P. Novalbos, J. A. Giron, M. Rodríguez-Iglesias and F. Garcia-Cozar1

Puerto Real University Hospital Research Unit, School of Medicine, Department of Biochemistry (Microbiology and Immunology), University of Cadiz, Cadiz, Spain

1 Correspondence: Hospital Universitario de Puerto Real, Unidad de Investigacion, Carretera NIV, Km665, 11510 Puerto Real, Cadiz, Spain. E-mail: curro.garcia{at}uca.es

Hepatitis C virus (HCV) infection is the main cause for chronic hepatitis, leading to cirrhosis and hepatic carcinoma. Virally induced immune dysfunction has been called as the cause for viral persistence. Previous results demonstrate that CD4 Jurkat cells stably expressing the HCV core protein show an increased activation of NFAT transcription factor and an impaired IL-2 promoter activity, affecting intracellular signaling pathways in a manner that mimics clonal anergy. We had shown previously that NFAT activates a transcriptional program, ensuing in immunological tolerance. In the present work, we have engineered lentiviral vectors expressing the HCV core to analyze the events, which unfold in the initial phase of HCV core-induced anergy. We show that genes initially described to be up-regulated by ionomycin-induced anergy in mice are also up-regulated in humans, not only by ionomycin but also by HCV core expression. We also show that HCV core is sufficient to cause NFAT nuclear translocation and a slow-down in cell-cycle progression, and using whole genome microarrays, we identify novel genes up-regulated in Jurkat cells expressing HCV core. The relevance of our results is highlighted by the presence of HCV in CD4 T cells from HCV chronically infected patients.

Key Words: immune evasion • HCV • gene expression • CD4 T cells • anergy • tolerance




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