Schistosomiasis has been incriminated in the significant increase in hepatitis C virus (HCV) infections, although the association has not been adequately explained. We hypothesized that the CCR5Δ32 mutation may be involved in the high prevalence of HCV with schistosomiasis. The aim was to explore the association between the CCR5Δ32 mutation in schistosomiasis patients and protection against HCV infection or progression. We compared 220 schistosomiasis patients (S group) and 190 patients with HCV and schistosomiasis (HCV/S group) for the presence of the CCR5Δ32 mutation. Clinical, biochemical, and radiological assessments were done. HCV infection was diagnosed with anti-HCV antibodies and a recombinant HCV antigen-based rapid immunochromatographic test, and confirmed by HCV reverse transcriptase PCR. HCV genotyping was done by reverse hybridization line probe assay. Schistosomiasis was diagnosed by FAST-ELISA and indirect hemagglutination for Schistosoma mansoni antibodies, and stool analysis for ova. Polymorphisms of the CCR5 receptor gene were assessed by PCR-based genotyping of the 32-bp deletion at the CCR5 locus in whole blood. Of HCV/S patients, 91.6 vs. 91.8 % of S patients had CCR5 WT/WT homozygosity (nonmutants). Heterozygous and homozygous CCR5Δ32 mutation patterns (CCR5Δ32/WT and CCR5Δ32/Δ32) were distributed similarly in the HCV/S and S groups (6.8 vs. 7.2 % and 0.53 vs. 0.90 %, respectively; p > 0.05, OR = 0.97). Genotype 4 was the predominant viral genotype (93 % of cases). No differences were observed in CCR5 gene patterns according to viral genotype, viral RNA count, or ALT level. However, CCR5Δ32 mutants (homozygous and heterozygous) had a lower rate of severe hepatic fibrosis vs. nonmutants (27 vs. 42 %, p = 0.101, OR = 0.51). Moreover, 53.4 % of CCR5Δ32/WT mutants showed spontaneous viral clearance vs. 26.2 % of nonmutants (p = 0.000, OR = 4.1). In conclusion, no association was detected between the CCR5Δ32 mutation and HCV disease susceptibility in schistosomiasis patients. However, patients with the CCR5Δ32 mutation and HCV infection were less prone to severe hepatic fibrosis and more likely to have spontaneous viral clearance than patients with the nonmutant genotype.

Conference Abstract| October 01 2000 Pancreatic fecal elastase in HCV associated liver disease E. M. Abdalla; E. M. Abdalla 1Clinical Pathology & Internal Medicine Departments, Faculty of Medicine, Suez Canal University: Ismailia, Egypt Search for other works by this author on: This Site PubMed Google Scholar A. S. Abd El-Hamid; A. S. Abd El-Hamid 1Clinical Pathology & Internal Medicine Departments, Faculty of Medicine, Suez Canal University: Ismailia, Egypt Search for other works by this author on: This Site PubMed Google Scholar F. Gobran; F. Gobran 1Clinical Pathology & Internal Medicine Departments, Faculty of Medicine, Suez Canal University: Ismailia, Egypt Search for other works by this author on: This Site PubMed Google Scholar Z. M. Nooman; Z. M. Nooman 1Clinical Pathology & Internal Medicine Departments, Faculty of Medicine, Suez Canal University: Ismailia, Egypt Search for other works by this author on: This Site PubMed Google Scholar A. M. Hassan A. M. Hassan 1Clinical Pathology & Internal Medicine Departments, Faculty of Medicine, Suez Canal University: Ismailia, Egypt Search for other works by this author on: This Site PubMed Google Scholar Biochem Soc Trans (2000) 28 (5): A153. https://doi.org/10.1042/bst028a153b Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Twitter LinkedIn Cite Icon Cite Get Permissions Citation E. M. Abdalla, A. S. Abd El-Hamid, F. Gobran, Z. M. Nooman, A. M. Hassan; Pancreatic fecal elastase in HCV associated liver disease. Biochem Soc Trans 1 October 2000; 28 (5): A153. doi: https://doi.org/10.1042/bst028a153b Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsBiochemical Society Transactions Search Advanced Search This content is only available as a PDF. © 2000 Biochemical Society2000 Article PDF first page preview Close Modal You do not currently have access to this content.

Conference Abstract| October 01 2000 Inhibin, a putative marker of spermatogenesis E. M. Abdalla; E. M. Abdalla 1Clinical Pathology & Dermatology Departments, Faculty of Medicine, Suez Canal University: Ismailia, Egypt Search for other works by this author on: This Site PubMed Google Scholar R. M. Wasfi; R. M. Wasfi 1Clinical Pathology & Dermatology Departments, Faculty of Medicine, Suez Canal University: Ismailia, Egypt Search for other works by this author on: This Site PubMed Google Scholar R. A. Abobakr; R. A. Abobakr 1Clinical Pathology & Dermatology Departments, Faculty of Medicine, Suez Canal University: Ismailia, Egypt Search for other works by this author on: This Site PubMed Google Scholar M. K. Eyada; M. K. Eyada 1Clinical Pathology & Dermatology Departments, Faculty of Medicine, Suez Canal University: Ismailia, Egypt Search for other works by this author on: This Site PubMed Google Scholar A. I. El-Akhras A. I. El-Akhras 1Clinical Pathology & Dermatology Departments, Faculty of Medicine, Suez Canal University: Ismailia, Egypt Search for other works by this author on: This Site PubMed Google Scholar Biochem Soc Trans (2000) 28 (5): A342. https://doi.org/10.1042/bst028a342a Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn MailTo Cite Icon Cite Get Permissions Citation E. M. Abdalla, R. M. Wasfi, R. A. Abobakr, M. K. Eyada, A. I. El-Akhras; Inhibin, a putative marker of spermatogenesis. Biochem Soc Trans 1 October 2000; 28 (5): A342. doi: https://doi.org/10.1042/bst028a342a Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsBiochemical Society Transactions Search Advanced Search This content is only available as a PDF. © 2000 Biochemical Society2000 Article PDF first page preview Close Modal You do not currently have access to this content.

Conference Abstract| October 01 2000 Soluble Intercellular Adhesion Molecule-1 and Soluble L-selectin Levels in Children With Bronchial Asthma E. M. Abdalla; E. M. Abdalla 1Clinical Pathology & Pediatric Department, Faculty of Medicine, Suez Canal University Search for other works by this author on: This Site PubMed Google Scholar O. Leheta; O. Leheta 1Clinical Pathology & Pediatric Department, Faculty of Medicine, Suez Canal University Search for other works by this author on: This Site PubMed Google Scholar A. Atef; A. Atef 1Clinical Pathology & Pediatric Department, Faculty of Medicine, Suez Canal University Search for other works by this author on: This Site PubMed Google Scholar S. Elsharkawy S. Elsharkawy 1Clinical Pathology & Pediatric Department, Faculty of Medicine, Suez Canal University Search for other works by this author on: This Site PubMed Google Scholar Biochem Soc Trans (2000) 28 (5): A153. https://doi.org/10.1042/bst028a153a Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Twitter LinkedIn Cite Icon Cite Get Permissions Citation E. M. Abdalla, O. Leheta, A. Atef, S. Elsharkawy; Soluble Intercellular Adhesion Molecule-1 and Soluble L-selectin Levels in Children With Bronchial Asthma. Biochem Soc Trans 1 October 2000; 28 (5): A153. doi: https://doi.org/10.1042/bst028a153a Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsBiochemical Society Transactions Search Advanced Search This content is only available as a PDF. © 2000 Biochemical Society2000 Article PDF first page preview Close Modal You do not currently have access to this content.