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  • Meeting abstract
  • Open Access

Circulating apo 2L levels decreased in hepatitis C with the pegilated interferon-2 alpha treatment

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World Allergy Organization Journal20158:520

  • Published:


Chronic hepatitis C (HCV) infects approximately 170 million people and causes more than 350 000 deaths every year. Information regarding pathogenetic mechanism of acute hepatitis C infection is limited. Following innate immune activation, cellular immunity, including natural killer (NK) cell activation and antigen-specific CD8 cell proliferation occurs. CD8+ T lymphocytes directly kill infected cells via direct cell-cell contact, and release antiviral cytokines (e.g. IFN, TNF)


Eleven HCV-treatment naive HCV infected patients were treated with weight-based ribavirin daily in addition to either weekly pegIFN alfa-2b at 1.5 ug/kg, weekly pegIFN alfa-2a, or albinterferon alfa-2b at 900mcg every 2 weeks. All patients gave written informed consent approved by the Institutional Review Board prior to enrollment in the studies. Intensive serum monitoring was completed at study visits day 0 (pretreatment), weeks 4, 6 and 12.


In this present study, we aimed to investigate the relationship between IFN treatment response, HCV viral load and sApo 2L levels. Eleven HCV-treatment naive HCV infected patients were treated with pegIFN alfa-2a. Intensive serum circulating Apo 2L levels were monitered at study visits day 0 (pretreatment), weeks 4, 6 and 12.HCV-RNA and sApo 2L levels decreased gradually with PegIF-α 2 treatment and the differences were significant between day 0 and 4th week (p=0.001, p<0.005 and p=0.01, p<0.005 respectively); between day 0 and 12th week (p=0.001, p<0.005 and p=0.001, p<0.000 respectively); between 6th week and 12th week (p=0.01, p<0.05 and p=0.01, p<0.05 respectively).


We suggest that, decreased level of circulating Apo 2L may reflect its increased binding to its ligand expressed on hepatocyte or lymphocyte under the influence of PegIFN treatment.

Authors’ Affiliations

Department of Infectious Diseases and Clinical Microbiology, Akdeniz University, 07070 Antalya, Turkey
Internal Medicine, Allergy and Clinical Immunology, Genomics Research Center, Academia Sinica, 11529, Taipei, Taiwan
Department of Laboratory Medicine and Pathology, Mayo Clinic in Jacksonville, USA
Department of Infectious Diseases and Clinical Microbiology, Allergy and Clinical Immunology Unit, Tepecik Education and Research Hospital, Izmir, Turkey
Department of Gastroenterology, Antalya Training Hospital, Antalya, Turkey
Department of Infectious Diseases and Clinical Microbiology, Antalya Education and Research Hospital, Turkey
Department of Medical Biochemistry, Faculty of Medicine, Akdeniz University, 07070 Antalya, Turkey


© Yalcin et al; licensee BioMed Central Ltd. 2015

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver ( applies to the data made available in this article, unless otherwise stated.