The role of highly toxigenic CagA and VacA strains of Helicobacter pylori in gastric carcinogenesis. Review

Abstract

Gastric cancer takes the 4th place as the main cause of death among oncological diseases in the world. The risk factors of gastric cancer include genetic predisposition, alcohol abuse, smoking, low socio‑economic level, nutritional characteristics, Epstein–Barr virus and Helicobacter pylori infection. Helicobacter pylori bacterium is the only statistically proven risk factor for stomach cancer. Gastric cancer develops in less than 3 % of ­H. pylori ‑infected patients, suggesting a unique interaction between the host immune response and H. pylori virulence factors. Expression of oncogenic cytotoxin‑associated protein gene A (CagA), vacuolating cytotoxin A (VacA), and outer membrane proteins is important for H. pylori in host pathogenesis. The paper gives consideration for the relationship between the virulence factors of H. pylori and the host, which is necessary for a better understanding of the pathogenesis and prevention of carcinogenesis. The strategy for the prevention of gastric cancer includes eradication therapy, but it is complicated by the growth of resistance to antimicrobial drugs. Only insignificant number of papers investigate effects of pathogenicity factors of H. pylori (CagA+ and VacA+) on the development of atrophy, intestinal metaplasia and dysplasia. In the literature, there is little data on the difference in antibiotic resistance between H. pylori highly toxigenic and non‑toxigenic strains. The aim of the article is to present current data on the impact of highly toxigenic CagA+VacA+ strains of H. pylori on the processes of gastric carcinogenesis and to determine their role in resistance to clarithromycin. Investigation of the relationship between highly toxigenic CagA and VacA strains with clinical and morphological manifestations of gastritis and antibiotic resistance will enable preventing the progression of precancerous changes and using effective treatment tactics.