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Since the mutations known to enhance virulence to date account for only half of the severe invasive infections, additional mechanisms\/mutations need to be identified. Here, we conducted a genome-wide association study of\n                    <jats:italic>emm<\/jats:italic>\n                    89\n                    <jats:italic>S. pyogenes<\/jats:italic>\n                    strains to comprehensively identify pathology-related bacterial genetic factors (single-nucleotide polymorphisms [SNPs], indels, genes, or k-mers). Japanese (\n                    <jats:italic>n<\/jats:italic>\n                    = 311) and global (\n                    <jats:italic>n<\/jats:italic>\n                    = 666) cohort studies of strains isolated from invasive or non-invasive infections revealed 17 and 1075 SNPs\/indels and 2 and 169 genes, respectively, that displayed associations with invasiveness. We validated one of them, a non-invasiveness-related point mutation,\n                    <jats:italic>fhuB<\/jats:italic>\n                    T218C, by structure predictions and introducing it into a severe invasive strain and confirmed that the mutant showed slower growth in human blood. Thus, we report novel mechanisms that convert\n                    <jats:italic>emm<\/jats:italic>\n                    89\n                    <jats:italic>S. pyogenes<\/jats:italic>\n                    to an invasive phenotype and a platform for establishing novel treatments and prevention strategies.\n                  <\/jats:p>","DOI":"10.7554\/elife.101938","type":"journal-article","created":{"date-parts":[[2025,1,3]],"date-time":"2025-01-03T13:25:15Z","timestamp":1735910715000},"update-policy":"https:\/\/doi.org\/10.7554\/elife.101938","source":"Crossref","is-referenced-by-count":6,"title":["Identifying genetic variations in emm89 Streptococcus pyogenes associated with severe invasive 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