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

¹ Department of Microbiology, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37614-0579, USA
² ViroMed Laboratories, Minnetonka, MN, USA
³ Department of Pharmacology, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN, USA

Correspondence
Robert V. Schoborg
schoborg{at}etsu.edu

Several inducers of chlamydial persistence have been described, including interferon- (IFN-), IFN-, IFN-β, and tumour necrosis factor- (TNF-) exposure, and iron, amino acid or glucose deprivation. 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. This study was designed to ascertain whether co-infection-induced persistence is mediated by a previously characterized mechanism. Luminex assays indicate that IFN-, IFN-, and TNF- are not released from co-infected cells. Semiquantitative RT-PCR studies demonstrate that IFN-β, IFN-, indoleamine 2,3-dioxygenase, lymphotoxin- and inducible nitric oxide synthase are not expressed during co-infection. These data indicate that viral-induced persistence is not stimulated by any persistence-associated cytokine. Supplementation of co-infected cells with excess amino acids, iron-saturated holotransferrin, glucose or a combination of amino acids and iron does not restore chlamydial infectivity, demonstrating that HSV-2-induced persistence is not mediated by depletion of these nutrients. Finally, inclusions within co-infected cells continue to enlarge and incorporate C₆-NBD-ceramide, indicating that HSV-2 co-infection does not inhibit vesicular transport to the developing inclusion. Collectively these data demonstrate that co-infection-induced persistence is not mediated by any currently characterized persistence inducer or anti-chlamydial pathway. Previous studies indicate that HSV-2 attachment and/or entry into the host cell is sufficient for stimulating chlamydial persistence, suggesting that viral attachment and/or entry may trigger a novel host pathway which restricts chlamydial development.

A supplementary table of primers and three supplementary figures are available with the online version of this paper.