LAUSR

Abstract Bacterial virulence factors are often located in their genomic islands (GIs). Helicobacter pylori, a highly diverse organism is reported to be associated with several gastrointestinal diseases like, gastritis, gastric cancer (GC), peptic ulcer, duodenal ulcer (DU) etc. A novel similarity score (Sm)-based comparative analysis with GIs of 50 H. pylori strains revealed clear idea of the various factors which promote disease progression. Two putative pathogenic GIs in some of the H. pylori strains were identified. One GI, having a putative labile enterotoxin and other dynamin-like proteins (DLPs), is predicted to increase the release of toxin by membrane vesicular formation. Another island contains a virulence-associated protein D (vapD) which is a component of a type-II toxin–antitoxin system (TAs), leads to enhance the severity of the H. pylori infection. Besides the well-known virulence factors like Cytotoxin-associated gene A (CagA) and vacA, several GIs have been identified which showed to have direct or indirect impact on H. pylori clinical outcomes. One such GI, containing lipopolysaccharide (LPS) biosynthesis genes was revealed to be directly connected with disease development by inhibiting the immune response. Another collagenase-containing GI worsens ulcers by slowing down the healing process. GI consisted of fliD operon was found to be connected to flagellar assembly and biofilm production. By residing in biofilms, bacteria can avoid antibiotic therapy, resulting in chronic infection. Along with well-studied CagA and vacuolating toxin A (vacA) virulent genes, it is equally important to study these identified virulence factors for better understanding H. pylori-induced disease prognosis.