Helicobacter pylori (H. pylori), a gram-negative spiral-shaped bacterium, specifically colonizes the human stomach. Once established in this harsh ecological niche, it stays there virtually for the entire life of the host. To date, numerous virulence
factors responsible for gastric colonization, survival, and tissue damage have been described for this bacterium. It is now well established that urease and flagella are virulence factors of H. pylori. Vacuolating cytotoxin (VacA), cytotoxin-associated
gene A (CagA), and cag pathogenicity island have also emerged as virulence factors, although the specific genes involved in virulence are still being determined. OipA (outer inflammatory proteins), H. pylori neutrophil-activating protein (HP-NAP), and
several adhesins, including BabA (blood group A antigen-binding adhesin) and IceA (induced by contact with epithelium), have been reported to be important virulence factors of H. pylori. In addition, CagE (picB) and lipopolysaccharide are considered as
other possible virulence factors. Since many researchers have defined virulence factors as those that contribute to inflammation and gastroduodenal diseases by H. pylori infection, it would be possible to define the role of specific factors in virulence
and to develop novel therapeutic drugs or vaccines to treat and prevent H. pylori infection more easily.
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