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Published on: November 8, 2015
Analysis of T cell responses against hepatitis C virus genotype 4 in Egypt
Mohamed Elrefaei1, Nabila El-sheikh, Karim Kamal
1California Department of Health Services, 850 Marina Bay Parkway, VRDL, Richmond, CA 94804, USA. melrefae@dhs.ca.gov
Insights
Hepatitis C virus (HCV) co-infection with Schistosoma mansoni (S. mansoni) in Egypt does not significantly impact the immune response to HCV genotype 4a. This suggests S. mansoni co-infection may not hinder HCV vaccine development.
Area of Science:
- Hepatology
- Immunology
- Infectious Diseases
Background:
- Hepatitis C virus (HCV) is a leading cause of chronic liver disease in Egypt.
- High prevalence of both HCV and Schistosoma mansoni (S. mansoni) in Egypt.
- Limited understanding of HCV/S. mansoni co-infection's impact on immune response to HCV genotype 4a.
Purpose of the Study:
- To investigate the effect of S. mansoni co-infection on cellular immune responses against HCV genotype 4a.
- To assess HCV 4a-specific T cell responses in Egyptians with chronic HCV and S. mansoni co-infection.
Main Methods:
- Evaluated HCV 4a-specific T cell responses against core and NS5B proteins.
- Studied 38 Egyptian volunteers with chronic HCV, with and without S. mansoni co-infection.
- Analyzed Th1 cytokine profiles and HCV-specific immune response rates.
Main Results:
- HCV 4a-specific responses detected in 53% (HCV alone) and 57% (co-infected) of individuals.
- Schistosomiasis altered Th1 cytokine profiles but did not affect overall HCV immune response rate (P=0.11).
- HCV-specific responses targeted conserved Core regions across different genotypes.
Conclusions:
- Egyptian patients with HCV genotype 4 mount effective HCV-specific T cell responses (CD4+ and CD8+).
- Concomitant S. mansoni infection does not appear to be a significant barrier to developing an HCV vaccine in this population.
- Findings support the potential for successful HCV vaccine strategies in Egypt.
Background/Aims:
Hepatitis C virus (HCV) remains the most common cause of chronic liver disease in Egypt. Despite the high prevalence of HCV and Schistosoma mansoni (S. mansoni) in Egypt, the effect of co-infection on the immune response against HCV genotype 4a has not been extensively examined.
Methods:
We evaluated the HCV 4a-specific responses against the core and non-structural 5B proteins in chronic HCV with or without S. mansoni co-infection in 38 volunteers from Egypt.
Results:
HCV 4a-specific responses were detected in 8/15 and 13/23 individuals with HCV alone or with concomitant schistosomiasis, respectively. Despite the alteration in the Th1 cytokine profile caused by schistosomiasis, the overall immune response rate against HCV was not affected (P=0.11). Seven individuals demonstrated HCV-specific responses against conserved regions of the Core that were previously identified for genotypes 1, 2 and 3 despite differences in HLA class I distribution.
Conclusions:
Egyptian patients infected with HCV genotype 4 can mount HCV-specific T cell responses, both CD4+ and CD8+ T cell-mediated, despite the prevalence of concomitant schistosomiasis. These findings suggest that S. mansoni co-infection may not represent a major obstacle to developing an HCV vaccine in this population.
