Multiple infections by EBV, HCMV and Helicobacter pylori are highly frequent in patients with chronic gastritis and gastric cancer from Southwest Mexico: An observational study. Issue 3 (January 2019)

• Record Type: Journal Article
• Authors: Del Moral-Hernández, Oscar; Castañón-Sánchez, Carlos Alberto; Reyes-Navarrete, Salomón; Martínez-Carrillo, Dinorah N.; Betancourt-Linares, Reyes; Jiménez-Wences, Hilda; de la Peña, Sol; Román-Román, Adolfo; Hernández-Sotelo, Daniel; Fernández-Tilapa, Gloria
• Other Names: Feghaly. Rana El section editor.
• Is Part Of: Medicine. Volume 98:Issue 3(2019)
• Publication Date: 2019-01
• Subjects: chronic gastritis and gastric cancer -- epstein-barr virus -- Helicobacter pylori -- human cytomegalovirus; Medicine -- Periodicals; Medicine -- Periodicals; Médecine -- Périodiques; Geneeskunde; Medicine; Periodicals; Periodicals; 610.5
• DOI: 10.1097/MD.0000000000014124
• Languages: English
• ISSNs: 0025-7974

Abstract

Abstract : Abstract: The chronic inflammation and damage to the gastric epithelium induced by Helicobacter pylori ( H. pylori ) are the main risk factors for gastric cancer development. Epstein-Barr virus (EBV) and human cytomegalovirus (HCMV) induce chronic inflammation and have been found in gastric tumors. The objectives this observational study were to determine the frequency of multiple infections by Helicobacter pylori, Epstein-Barr virus (EBV) and human cytomegalovirus (HCMV) and to relate the infection by EBV and HCMV with H. pylori vacA/cagA genotypes in patients with chronic gastritis or gastric cancer. DNA from H. pylori, EBV and HCMV was detected by PCR in biopsies from 106 Mexican patients with chronic gastritis and 32 from gastric cancer. The cagA status and the vacA genotypes of H. pylori were determined by PCR. In chronic gastritis and gastric cancer EBV was found in 69.8% and 87.5%, HCMV in 52.8% and 53.1%, and H. pylori in 48.1% and 40.6%, respectively. In chronic gastritis, 53% of H. pylori + patients were EBV + and 33% were both EBV + /HCMV + ; in gastric cancer, 92.3% of H. pylori -infected individuals were EBV + and 46.1% were EVB + /HCMV + . All the intestinal- and mixed-type tumors and the 83.3% of diffuse-type tumors were EBV + . No significant differences were found between single infections or coinfections with the diagnosis or the cancer type. The H. pylori genotypes were not related to EBV or HCMV infection. The frequency of dual infections by H. pylori, EBV and HCMV is higher in patients from southwest Mexico than other populations. It is likely that these pathogens act synergistically to induce inflammation and gastric cancer.