Trachoma and LGV biovars of Chlamydia trachomatis share the same glycosaminoglycan-dependent mechanism for infection of eukaryotic cells.

A sulphated glycosaminoglycan-dependent mechanism of microbial infection for mammalian cells was characterized for the Chlamydia trachomatis trachoma and lymphogranuloma venereum (LGV) biovars. We demonstrated that the trachoma and LGV biovars compete for the same receptor(s) on host cells and that their infectivity was inhibited by heparin or heparan sulphate. Using a specific heparan sulphate lyase (heparitinase) to treat organisms, the infectivity of both biovars was abolished. Furthermore, exogenous heparan sulphate rescued chlamydial infectivity following treatment with heparitinase and the restored infectivity was neutralized by an anti-heparan sulphate monoclonal antibody. These data suggest that heparan sulphate-like-mediated interactions between C. trachomatis and eukaryotic cells are essential for infectivity.