Co-infection relationship with Epstein-Barr virus in gastroduodenal diseases with Helicobacter Pylori. Quantitative PCR and EBNA-1 gene-based approach
|Author(s)||S. Akkus 1, N. Gareayaghi 2, S. Saribas 1, S. Demiryas 3, D. Ozbey 1, N.. Kepil 4, M. Demirci 5, T. Ziver Sarp 6, H. Oyku Dinc 7, R. Akcin 1, O. Uysal 8, M. Tugberk Bakar 9, M. Talha Aygun 10, H. Bahar Tokman 1, B. Kocazeybek 1|
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(1) Istanbul University-Cerrahpasa, Cerrahpasa Medical Faculty, Department of Medical Microbiology, Istanbul, Turkey
(2) Istanbul Sisli Hamidiye Etfal Training and Research Hospital, Center for Blood, University of Health Sciences, Istanbul, Turkey
(3) Istanbul University-Cerrahpasa, Cerrahpasa Medical Faculty, Department of General Surgery, Istanbul, Turkey
(4) Istanbul University-Cerrahpasa, Cerrahpasa Medical Faculty, Department of Pathology, Istanbul, Turkey
(5) Kirklareli University Medical Faculty, Department of Medical Microbiology, Kirklareli, Turkey
(6) Eastern Mediterranean University, Faculty of Health Sciences, Department of Nutrition and Dietetic Famagusta, Cyprus, Mersin 10 Turkey
(7) Bezmialem Vakif University, Faculty of Pharmacy, Department of Pharmaceutical Microbiology, Istanbul, Turkey
(8) Bezmialem Vakif University, Medical Faculty, Department of Biostatistics, Istanbul, Turkey
(9) Istanbul University-Cerrahpasa, Cerrahpasa Medical Faculty,Department of Public Health, Istanbul, Turkey
(10) Istanbul University-Cerrahpasa, Cerrahpasa Medical Faculty student
Objective: Helicobacter pylori (Hp) and Epstein-Barr virus (EBV) are involved in gastric cancer (GC) etiology. EBV/Hp coinfection was thought synergistically increase gastroduodenal disease occurence. We aimed to determine the presence of EBV/Hp co-infection in gastroduodenal diseases.
Methods: The study group had 68 Hp (+) cases [25 GC, 13 IM (intestinal metaplasia), 30 PU (peptic ulcer)], and the control group had 40 NUD (non-ulcer dyspepsia) cases [20 Hp+, 20 Hp-]. EBV-DNA was detected by non-polymorphic EBNA-1 gene-based qPCR. EBV/EBNA-1 IgG levels were determined by quantitative and qualitative ELISA methods, respectively.
Results: EBV-DNA positivity was 32% (8/25), 6.6% (2/30) and 5% (1/20) in GC, PU and NUD Hp (+) cases, respectively. There was a significant difference (p = 0.001) between GC (32%) and NUD Hp (+) (5%) cases in terms of EBV-DNA positivity. Mean EBV-DNA copy numbers were 6568.54 ± 20351, 30.60 ± 159.88 and 13.85 ± 61.93 for GC, PU, and NUD, respectively. In terms of the mean EBV-DNA copy number, a significant difference was found between the groups (p = 0.005). In terms of EBV/EBNA-1 IgG antibody positivity, no significant difference was found between GC and NUD cases (p = 0.248). EBV DNA positivity was found to be significant (odds ration [OR] = 26.71 (p=0.009, %95CI 2.286- 312.041) in multivariate logistic regression.
Conclusion: Although we had a small number of GC cases, it can be suggested that the estimated risk created by the synergistic effect based on the addition of EBV increased 26 times in the presence of Hp in GC.
|Keywords: Helicobacter pylori, Epstein-Barr virus, Epstein-Barr nuclear antigen 1 (EBNA-1), gastric cancer, EBV/EBNA-1 IgG antibody, peptic ulcer.|
|The authors declare that they have no conflict of interest.|
© Acta Gastro-Enterologica Belgica.