- Helicobacter pylori strain G1.1 is a clinical isolate obtained from a gastric cancer patient in Colombia, a country with one of the highest rates of H. pylori-associated gastric cancer in Latin America. This strain has gained attention for its relevance in understanding host-pathogen interactions in high-risk populations and for its contribution to insights on regional variation in H. pylori virulence factors.Â
- G1.1 belongs to the hpEurope population, which is somewhat unexpected given its Latin American origin, highlighting the complex phylogeographic mixing and ancestral recombination events in Colombian H. pylori populations—where strains often display European, African, and Amerindian genetic signatures due to centuries of human migration and admixture.
- Genomically, G1.1 carries a complete and functional cag pathogenicity island (cagPAI), enabling type IV secretion system (T4SS)-mediated translocation of the CagA oncoprotein into host epithelial cells. CagA from G1.1 is a Western-type variant, containing EPIYA-A, -B, and -C phosphorylation motifs, which allow it to undergo tyrosine phosphorylation inside host cells. Once translocated, CagA activates oncogenic signaling cascades, including SHP-2 and MAPK pathways, promotes cytoskeletal rearrangements, and contributes to pro-inflammatory responses such as IL-8 secretion. These activities are central to the gastric epithelial damage and inflammation that can eventually progress to malignancy.
- G1.1 also harbors a toxic vacA allele, specifically the s1/m1 genotype, which encodes a highly active Vacuolating cytotoxin A (VacA). This potent toxin induces intracellular vacuolation, mitochondrial dysfunction, and inhibition of T-cell proliferation, promoting bacterial persistence by modulating host immune responses. The combination of active CagA and VacA in G1.1 makes this strain highly virulent and potentially more capable of driving severe disease outcomes, consistent with its isolation from a cancer patient.
- In terms of outer membrane adhesins, G1.1 expresses BabA, which binds to Lewis b antigens on gastric epithelial cells and facilitates close adherence, which is crucial for efficient CagA delivery. It may also express other key adhesins like HopQ and SabA, which support persistent colonization and inflammatory signaling, although these features can be subject to phase variation and strain-specific regulation. Comparative studies have shown that Colombian strains like G1.1 exhibit unique combinations of virulence determinants, which are being explored to explain the discrepancy between infection prevalence and cancer incidence in different regions of the world.
- G1.1 has been used in cell culture and ex vivo gastric organoid studies to evaluate epithelial transformation, immune activation, and transcriptional changes upon infection. Additionally, its complete genome has been sequenced, making it a useful reference for comparative genomics, especially in studies investigating genetic diversity, population structure, and cancer risk stratification among H. pylori strains from Latin America.
- In summary, H. pylori strain G1.1 is a highly virulent clinical isolate with both active CagA and VacA, isolated from a gastric cancer patient in a high-risk population. It serves as an important model for studying strain-specific contributions to gastric carcinogenesis, especially in Latin America, where the burden of disease remains high. Its use in comparative and functional genomics helps illuminate how regional H. pylori diversity influences pathogenesis and cancer risk, making G1.1 a valuable strain in global gastric cancer research.
