Viral Hepatitis
Copyright ©2005 Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Nov 14, 2005; 11(42): 6624-6630
Published online Nov 14, 2005. doi: 10.3748/wjg.v11.i42.6624
Cytokine profile in Egyptian hepatitis C virus genotype-4 in relation to liver disease progression
Abdel-Rahman N Zekri, Mohammed S El-Din Ashour, Ahmed Hassan, Hanaa M Alam El-Din, Amal MR El-Shehaby, Maha A Abu-Shady
Abdel-Rahman N Zekri, Hanaa M Alam El-Din, Virology and Immunology Unit, Cancer Biology Department, National Cancer Institute, Cairo University, Egypt
Mohammed S El-Din Ashour, Maha A Abu-Shady, Microbiology Department, Faculty of Pharmacy, Azhar University, Egypt
Ahmed Hassan, Microbiology and Immunology Department, Sohag Faculty of Medicine, South Valley University, Egypt
Amal MR El-Shehaby, Biochemistry Department, El-Kaser El-Aini School of Medicine, Cairo University, Egypt
Author contributions: All authors contributed equally to the work.
Supported by the USA project BIO-8-002-009 and by the Grant office of National Cancer Institute, Cairo University
Correspondence to: Abdel-Rahman N Zekri, MSc, PhD, Virology and Immunology Unit, Cancer Biology Department, National Cancer Institute, Fom El-Khalig, Cairo 11796, Egypt. ncizakri@starnet.com.eg
Telephone: +20-10-1413-521 Fax: +20-2-3644-720
Received: May 25, 2004
Revised: July 16, 2004
Accepted: July 19, 2004
Published online: November 14, 2005
Abstract

AIM: To observe the imbalance between T helper cell Th1 and Th2 cytokines in several chronic hepatitis disease at different stages of disease progression.

METHODS: We measured the cytokine levels of Th1 (IL-2 and IL-2R), Th2 (IL-10) and the pro-inflammatory cytokines (IL-6 and IL-6R and TNF and TNF-RI and II) by the ELISA technique in the sera of 33 hepatocellular carcinoma (HCC) patients and 20 chronic liver disease (CLD) patients. In addition, 20 asymptomatic hepatitis C virus carriers and 20 healthy subjects negative for hepatitis C virus(HCV) markers served as controls.

RESULTS: Anti-HCV antibodies were found to be positive in 94% of HCC cases and 75% of CLD cases. On the other hand, HCV viremia was detected using RT-PCR in 67% of HCC cases and 65% of CLD cases. HBsAg was positive in 9% of HCC cases and 30% of CLD cases. Also bilharzial-Ab was positive in 55% of HCC cases, 65% of CLD cases and in 70% of asymptomatic carriers (ASC). HCC patients had significantly higher values of IL-2R, TNF-RII (P<0.001), and TNF-RI (P>0.05), but lower TNFα (P<0.001) and IL-6 (P = 0.032) in comparison to ASC. But, in comparison to non-cancer controls, HCC patients had higher values of IL-2R, IL-6R, TNF-RI and TNF-RII, but lower TNF-α (P<0.001). CLD patients had higher IL-2R, TNF-RI, and TNF-RII (P<0.001) than ASC. But, in comparison to non-cancer controls, CLD patients had higher values of IL-2R, TNF-RI and TNF-RII, but lower TNF-α (P<0.001). IL-10 was higher (though not significantly) in HCC and CLD patients than in symptomatic carriers and non-cancer controls.

CONCLUSION: Liver disease progression from CLD to HCC due to HCV genotype-4 infection is associated with an imbalance between Th1 and Th2 cytokines. IL-2R, TNF-RI, and TNF-RII could be used as potential markers.

Keywords: Cytokine; HCV; Genotype-4; Liver disease