Abstract
An in vitro model of persistent infection of mouse fibroblasts (McCoy cells) with a trachoma strain (G17) of Chlamydia trachomatis has been developed. Persistently infected cultures were established by infecting McCoy cells with high multiplicities of chlamydiae. After the first cycle of chlamydial replication, the host cells multiplied more rapidly than the parasites, so that the fraction of inclusion-bearing cells declined to less than 1%. However, 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 densities fluctuated periodically. The chlamydiae in the cycling populations were reidentified as the original serotype. No changes in either host cell susceptibility or chlamydial invasiveness were observed in hosts and parasites recovered from persistently infected populations. All evidence suggests that the parasite maintained itself in McCoy cell populations by cell-to-cell transfer and that an equilibrium between host and parasite multiplication was achieved when the persistently infected cultures fluctuated between periods of host cell destruction and proliferation.