In vivo evolution of a Klebsiella pneumoniae capsule defect with wcaJ mutation promotes complement-mediated opsono-phagocytosis during recurrent infection.
William G BainBrian AhnHernán F PeñalozaChristi L McElhenyNathanial TolmanRick van der GeestShekina Gonzalez-FerrerNathalie ChenXiaojing AnRia HosuruMohammadreza TabaryErin PapkeNaina KohliNauman FarooqWilliam BachmanTolani F OlonisakinZeyu XiongMarissa P GriffithMara SullivanJonathan FranksMustapha M MustaphaAlina IovlevaTomeka SuberRobert M Q ShanksViviana P FerreiraDonna Beer StolzDaria Van TyneYohei DoiJanet S LeePublished in: The Journal of infectious diseases (2024)
Loss of function in wcaJ led to increased complement resistance, complement binding, and opsono-phagocytosis, which may promote KPC-Kp persistence by enabling co-existence of increased bloodstream fitness and reduced tissue virulence.