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BiologyAs an obligate intracellular organism, Chlamydia trachomatis can only replicate inside eukaryotic host cells.
It has a unique developmental cycle, with metabolically inert, spore-like elementary bodies (EBs) that infect host cells and develop into metabolically active, replicative reticulate bodies (RBs) within a membrane-bound inclusion. The early stage of infection can present with a mucopurulent discharge but infections are often asymptomatic at this stage. In most infected women the infection resolves, but in those with persistent or repeated infections, the infection can spread upwards from the endocervix to the fallopian tubes.
In the eye, this leads to distortion of the eyelid margin, causing the lashes to turn inwards and rub against the cornea, a disease known as trachoma, which is a leading cause of preventable blindness. Similarly, genital chlamydial infections can cause scarring of the fallopian tubes, leading to infertility or ectopic pregnancy as a result of tubal occlusion by scar tissue. With the exception of the lymphogranuloma venereum (LGV) strains, which cause systemic illness and infect regional lymph nodes, C. The genome contains genes that are homologous with those encoding virulence factors in other bacteria, including a cytotoxin gene and genes encoding components of a type III secretion pathway94.

A conserved chlamydial protease, proteasome-like activity factor (Cpaf), is secreted into the host-cell cytoplasm, where it interferes with the assembly and surface expression of human leukocyte antigen molecules and inhibits apoptosis95. Some of the repeated genes revealed by genome sequencing almost certainly function as virulence determinants.
A family of polymorphic membrane proteins (Pmps) with structures similar to bacterial autotransporters contains members that are thought to function as adhesins96, 97.
There is also a large group of related proteins (Inc proteins) that have been shown to be located in the inclusion membrane and probably regulate traffic between the inclusion and chlamydial cells.The lack of a genetic system to investigate gene function in C.
The 'ocular' serovars (serovars A, B, Ba and C) have been shown to differ from the 'genital' serovars (serovars D–K) in that they do not have a functional tryptophan-synthase gene, rendering them more sensitive to the inhibitory activity of interferon- (IFN-)99. Surprisingly, the LGV strains, which cause considerably more acute pathology than the ocular and genital serovars, have only a truncated form of the cytotoxin gene, and the explanation for the different tissue tropism and pathogenesis of LGV strains remains obscure100.Immune responseThe rapidly declining age-specific prevalence of ocular C.
A study in The Gambia showed that the duration of untreated ocular infection is shorter in adults than in children101.
Several trachoma-vaccine trials were conducted in the 1960s using killed whole-organism vaccines, some of which provided a degree of protection.
At the same time, studies in primates indicated that vaccination could provoke more severe disease on subsequent challenge, suggesting that much of the damage caused by C.

A chlamydial heat-shock protein Hsp60, which is homologous to Escherichia coli GroEL, has been shown to elicit high antibody titres, which correlates with the severe sequelae of C. In vitro studies have shown that IFN- interferes with the chlamydial developmental cycle, leading to persistent infection with continuing release of Hsp60 (Ref. However, it remains uncertain whether the immune response to Hsp60 is itself the cause of immunopathological damage, or merely a marker of more severe or prolonged infection.Studies in trachoma-endemic communities indicate that, in humans, similar to mice, cell-mediated immune responses of the T-helper-1 type are important for the clearance of ocular C.
Current studies are exploring the role of regulatory T cells in limiting the degree of inflammation106, 107.
Studies of host-gene expression in the conjunctival epithelium are starting to identify the molecular pathways that are involved in fibrosis, and matrix metalloproteinase-9 seems to have an important role108. Case-control studies have identified polymorphisms in several immune-response genes, which are associated with the severe scarring sequelae of trachoma109, 110.

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