**1.1 Overview of Chlamydial persistence**

Persistence is the ability of bacteria to remain viable in the host for a prolonged period of time. Bacteria have evolved several strategies by which subpopulations can survive conditions that are lethal for most members of bacterial populations. Well-known examples are the formation of endospores in Bacillales and Clostridiales orders, the formation of exospores in Actinomycetales, the presence of "persister" cells occurring in most bacteria, and the formation of viable but nonculturable cells [1]. All the survival stages are characterized by partial or complete inhibition of metabolism and cell division. Common to all of these survival states is the ability of the "persister" cells to resume their developmental stage under favorable conditions [1].

In the context of *Chlamydia*, persistence or Chlamydial stress response is the reversible inhibition of cell division that interrupts the pathogen's developmental cycle in the presence of unfavorable growth conditions [2]. Chlamydial persistence *in vitro* is characterized by the presence of a "viable but non-cultivable growth stage resulting in a long-term relationship with the infected cell" [3]. Persistence is an important cause of recurrent Chlamydial disease characterized by chronic inflammation and tissue damage in epithelial cells. This chapter will discuss the recent developments in our understanding of *Chlamydia* persistence, focusing on past and current insights that have been obtained into the molecular and immunological basis of this stage of *Chlamydia* development.
