Herpes simplex virus co-infection-induced Chlamydia trachomatis persistence is not mediated by any known persistence inducer or anti-chlamydial pathway.

The article discusses a study which showed that herpes simplex virus co-infection-induced Chlamydia trachomatis persistence is not mediated by any known persistence inducer or anti-chlamydial pathway. A tissue-culture model of Chlamydia trachomatis/herpes simplex virus type-2 (HSV-2) co-infection indicates that viral co-infection stimulates the formation of persistent chlamydiae. Luminex assays indicate that interferon (IFN)-gamma, interferon-alpha and tumor necrosis factor (TNF)-alpha are not released from co-infected cells while semiquantitative reverse transcriptase polymerase chain reaction (RT-PCR) studies show that IFN-beta, IFN-gamma, indoleamine 2,3-dioxygenase, lymphotoxin-alpha and inducible persistence is not stimulated by any persistence-associated cytokine.