Abstract
An in vitro model of persistent infection of mouse fibroblasts (McCoy cells) with a trachoma strain (G17) of C. trachomatis was developed. Persistently infected cultures were established by infecting McCoy cells with high multiplicities of chlamydiae. After the 1st cycle of chlamydial replication, the host cells multiplied more rapidly than the parasites, so that the fraction of inclusion-bearing cells declined to < 1%. After 100 days, the proportion of inclusion-bearing cells rose dramatically and the cultures alternated between periods of massive host cell destruction by chlamydiae and periods of host cell proliferation. This cycle continued indefinitely as host cell and parasite reidentified as the original serotype. No changes in host cell susceptibility of chlamydial invasiveness were observed in hosts and parasites recovered from persistently infected populations. The parasite apparently maintained itself in McCoy cell populations by cell-to-cell transfer and an equilibrium between host and parasite multiplication was evidently achieved when the persistently infected cultures fluctuated periods of host cell destruction and proliferation.