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Curr Opin Microbiol. 2007 Feb;10(1):47-51. Epub 2007 Jan 5.

Chlamydial interferon gamma immune evasion influences infection tropism.

Author information

1
Department of Medical Microbiology, University of Manitoba, Winnipeg, Manitoba, Canada.

Abstract

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.

PMID:
17208039
DOI:
10.1016/j.mib.2006.12.003
[Indexed for MEDLINE]

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