| Criteria | H. pylori SS1 | H. pylori PMSS1 | Remarks |
| Origin | Mouse-adapted derivative of a human strain (Sydney Strain) | Mouse-adapted strain derived from clinical isolate 60190 | Both strains are adapted for mouse colonization but differ significantly in virulence factors |
| Mouse Colonization | Efficient colonizer in mice, used for chronic infection models | Strong colonizer in C57BL/6 mice; robust infection persistence | PMSS1 has superior colonization capacity in genetically resistant mouse strains |
| cag Pathogenicity Island (cagPAI) | Largely deleted or nonfunctional | Fully intact and functional | PMSS1 retains full CagA delivery capability; SS1 is cagA-negative or nonfunctional |
| CagA Status | Lacks functional CagA expression | Expresses functional CagA with EPIYA motifs | PMSS1 enables studies on CagA-related signaling; SS1 is unsuitable for CagA-focused research |
| VacA Genotype | Generally s2/m2 (non-toxic or low-toxic) | s1/m1 (cytotoxic) | PMSS1 exhibits stronger vacuolating activity; important in host cell damage models |
| Genetic Tractability | Poor transformation efficiency | Highly genetically tractable | PMSS1 supports advanced genetic manipulations; SS1 is less amenable |
| Use in Research | Chronic gastritis, immune response in murine models | Pathogenesis, CagA signaling, inflammation models | SS1 is standard for chronic colonization; PMSS1 for virulence and mechanistic studies |
| Genome Availability | Limited (partially characterized) | Fully sequenced and annotated | PMSS1 supports omics-based and gene-editing studies |
| Colonization Duration | Maintains infection long-term in mice | Maintains long-term infection with immune response modulation | Both suitable for chronic infection models, but PMSS1 allows mechanistic insights |
| Transformation Capability | Low | High | PMSS1 is ideal for molecular genetics and mutant construction |
