title: Interaction of herpes simplex virus type 2 (HSV-2) glycoprotein D with the host cell surface is sufficient to induce Chlamydia trachomatis persistence.
abstract: When presented with certain unfavourable environmental conditions, Chlamydia trachomatis reticulate bodies (RBs) enter into a viable, yet non-cultivable state called persistence. Previously, we established an in vitro C. trachomatis and herpes simplex virus type 2 (HSV-2) co-infection model. These data indicate that (i) viral co-infection stimulates chlamydial persistence, (ii) productive HSV replication is not required for persistence induction, and (iii) HSV-induced persistence is not mediated by any currently characterized anti-chlamydial pathway or persistence inducer. In this study we demonstrated that chlamydial infectivity, though initially suppressed, recovered within 44 h of co-infection with UV-inactivated HSV-2, demonstrating that HSV-induced persistence is reversible. Co-incubation of chemically fixed, HSV-2-infected inducer cells with viable, C. trachomatis-infected responder cells both suppressed production of infectious chlamydial progeny and stimulated formation of swollen, aberrantly shaped RBs. In addition, pre-incubation of viral particles with viral glycoprotein D (gD)-specific neutralizing antibody prevented co-infection-induced persistence. Finally, exposure of C. trachomatis-infected cells to a soluble, recombinant HSV-2 gD : Fc fusion protein decreased production of infectious EBs to a degree similar to that observed in co-infected cultures. Thus, we conclude that interaction of HSV gD with the host cell surface is sufficient to trigger a novel host anti-chlamydial response that restricts chlamydial development.
authors.affiliation: Department of Microbiology, East Tennessee State University, James H. Quillen College of Medicine, Johnson City, TN 37614, USA.
authors.forename: J
authors.initials: J
authors.lastname: Vanover
authors.affiliation: Department of Microbiology, East Tennessee State University, James H. Quillen College of Medicine, Johnson City, TN 37614, USA.
authors.forename: J
authors.initials: J
authors.lastname: Kintner
authors.affiliation: Department of Microbiology, East Tennessee State University, James H. Quillen College of Medicine, Johnson City, TN 37614, USA.
authors.forename: J
authors.initials: J
authors.lastname: Whittimore
authors.affiliation: Department of Microbiology, East Tennessee State University, James H. Quillen College of Medicine, Johnson City, TN 37614, USA.
authors.forename: R V
authors.initials: RV
authors.lastname: Schoborg
mesh_terms: D000914:Antibodies, Viral / Q000276:immunology; D002460:Cell Line; D002692:Chlamydia trachomatis / Q000254:growth & development / Q000472:pathogenicity / Q000502:physiology*; D006367:HeLa Cells; D018258:Herpesvirus 2, Human / Q000254:growth & development / Q000276:immunology / Q000502:physiology*; D006801:Humans; D011991:Receptors, Virus / Q000378:metabolism*; D014759:Viral Envelope Proteins / Q000502:physiology*
chemical_list: D000914:Antibodies, Viral; D011991:Receptors, Virus; D014759:Viral Envelope Proteins; C040570:glycoprotein D-herpes simplex virus type 2; C049545:simplexvirus receptor