Chlamydial interferon gamma immune evasion influences infection tropism.
Chlamydia trachomatis is a human pathogen and Chlamydia muridarum is a mouse pathogen but paradoxically, they share near genomic synteny. The majority of strain-variable genes are located primarily in a hyper-variable region termed the plasticity zone. Tryptophan synthase and cytotoxin are plasticity zone genes unique to the human and murine strains, respectively. Tryptophan synthase is a virulence factor that differentiates C. trachomatis strains into genital and ocular disease pathotypes, whereas cytotoxin(s) is a virulence factor linked to murine infection tropism. Divergence in these loci is strongly correlated with host-specific interferon gamma effector activities, suggesting that these virulence genes have co-evolved with their respective hosts as a primary mechanism to evade innate immunity. These findings have important implications for chlamydial animal modeling studies.
McClarty
Grant
G
Department of Medical Microbiology, University of Manitoba, Winnipeg, Manitoba, Canada.
Caldwell
Harlan D
HD
Nelson
David E
DE
D000818:Animals; D001427:Bacterial Toxins / Q000235:genetics / Q000378:metabolism; D002689:Chlamydia / Q000235:genetics / Q000276:immunology* / Q000472:pathogenicity*; D002690:Chlamydia Infections / Q000276:immunology / Q000382:microbiology*; D006801:Humans; D007371:Interferon-gamma / Q000276:immunology*; D051379:Mice; D009876:Operon; D014367:Tryptophan Synthase / Q000235:genetics / Q000502:physiology; D014774:Virulence / Q000235:genetics
D001427:Bacterial Toxins; D007371:Interferon-gamma; D014367:Tryptophan Synthase