Abstract
This paper considers current views on the classical determinants of Helicobacter pylori virulence, pathogenetic effects of phosphorylation, and the process of CagA translocation into gastric mucosa (GM) cells and characterizes surface membrane receptors of VacA binding to epithelial cells of the gastric mucosa. The necessity of genetic typing of Helicobacter pylori to determine the potential virulence of a microorganism in order to predict the course of H. pylori-associated diseases and to select targeted therapy is substantiated.
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