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Updated: Jul 17, 2026

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
Published on: March 2, 2014
Chlamydial interferon gamma immune evasion influences infection tropism
Grant McClarty1, Harlan D Caldwell, David E Nelson
1Department 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.
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