Therefore, strains may differ in their licA mutation rates depending on which LOS structure is modified with ChoP. To test this, we further stratified the number of licA gene PF-04929113 repeats between strains with different licD alleles for each species. Among NT H. influenzae, the range of repeats was

GSK3326595 mw similar among strains that possessed a licD I, licD III , or licD IV allele (6-45, 5-43, and 9-42 repeats, respectively) (Table 3). The average number of repeats was significantly different, however, for strains that possessed a licD III allele (34 repeats) than for strains that possessed a licD I or licD IV allele (25 and 26 repeats, respectively) (P = .015 and .032 using the student’s T test, respectively) (Table 3). Among H. haemolyticus, the range of licA repeats was more variable between strains with licD III and licD IV alleles (6-56 and 6-27 repeats, respectively), due mainly to three licD III -containing strains with licA genes that contained 39, 40, and 56 repeats (Table 3, Figure 3). In contrast to NT H. influenzae, however, the average number of repeats was not significantly different between H. haemolyticus strains possessing

licD III or licD IV alleles (16 and 13, respectively) (Table buy NVP-LDE225 3). These results suggest that NT H. influenzae strains that substitute ChoP on more proximal, exposed oligosaccharides chains may tend to have increased mutation rates within the repeat region of the licA gene. Discussion The strain population structure of NT H. influenzae is genetically very diverse and clones or clusters of NT H. influenzae strains that differentiate Endonuclease virulent from commensal

strains have not been identified [10, 41]. Given this diversity, together with the high prevalence of NT H. influenzae colonization in the healthy human population, it is reasonable to hypothesize that not all NT H. influenzae strains possess the same ability to cause disease, but rather, that a proportion of strains possess a range of variable genetic traits that allow for infection and disease under the right host conditions [42]. Thus, comparison of genetic trait prevalence between populations of NT H. influenzae and the closely related but strictly commensal species, H. haemolyticus, will highlight traits within the species’ gene pools that may offer clues to the virulence pathways of NT H. influenzae. For instance, ChoP expression in NT H. influenzae is strongly implicated as a virulence factor [43, 44] and is thought to enhance virulence though increased epithelial cell adherence, inhibition of bactericidal peptides, and modulation of the immune system during biofilm growth [20–22]. In this study, 58% of H. haemolyticus strains lacked a lic1 locus (and the ability to express ChoP) while only 8% of NT H.