HELICOBACTER PYLORI GENOTYPES AMONG BELARUS PATIENTS WITH GASTRODUODENAL DISORDERS AND THEIR ASSOCIATION WITH CLINICAL OUTCOME OLGA YANOVICH 1 *, MICHAIL DOROSHKO 2 and LEONID TITOV 1 1 Laboratory for Clinical and Experimental Microbiology, The Republican Scientific and Practical Center for Epidemiology and Microbiology, Minsk, Belarus 2 Diagnostic Department, Medical Center “Nordin”, Minsk, Belarus (Received: 6 March 2019; accepted: 10 April 2019) The aim of this study was to evaluate the prevalence of Helicobacter pylori genotypes (vacA and cagPAI) directly in gastric biopsy specimens in patients with gastric diseases in Belarus. Gastric biopsies were collected from 461 patients with different gastrointestinal disorders: superficial gastritis (287 subjects), atrophy gastritis (59 subjects), erosive gastritis (47 subjects), duodenal ulcer disease (54 subjects), and stomach ulcer (14 subjects). PCR-based genotyping was used to detect s1a, s1b, s2, m1a, m1b, m2, cagM, cagA, and cagT genes. Overall prevalence of vacA s1a allele was 60.5% followed by m2 (47.1%) and m1a (37.5%). The analysis of data showed that genotype s1a/m1a was significantly more prevalent in patients with duodenal ulcer (21.4% vs. 45.1%, OR = 3.0, 95% CI = 1.5–6.1). The cagA gene was found with a high incidence in most patients with inflammatory diseases of stomach and duodenum. There was a significant increase in the frequency of cagT in patients with duodenal ulcer as compared to superficial gastritis. A high cagM prevalence was found in patients with atrophy gastritis and duodenal ulcer disease. All three island genes of pathogenicity of cagPAI are more often detected in patients with duodenal ulcer, which increases the risk of developing duodenal ulcer by 4.5 times. Keywords: Helicobacter pylori genotypes, clinical outcome, cagPAI Introduction Helicobacter pylori (HP) is possibly the most widespread human pathogen that causes of gastritis, peptic ulceration, and gastric cancer. According to World Health Organization statistics, HP is reported as a class 1 carcinogen in gastric adenocarcinoma [1]. *Corresponding author; E-mail: oyanov74@mail.ru Acta Microbiologica et Immunologica Hungarica 66 (3), pp. 399–411 (2019) DOI: 10.1556/030.66.2019.016 First published online May 17, 2019 1217-8950/$20.00 © 2019 Akadémiai Kiad´ o, Budapest