%0 Journal Article %A Vanover, J. %A Kintner, J. %A Whittimore, J. %A Schoborg, R. V. %T Interaction of herpes simplex virus type 2 (HSV-2) glycoprotein D with the host cell surface is sufficient to induce Chlamydia trachomatis persistence %D 2010 %J Microbiology, %V 156 %N 5 %P 1294-1302 %@ 1465-2080 %R https://doi.org/10.1099/mic.0.036566-0 %K HSV-2UV, UV-inactivated HSV-2 %K α-Sal, anti-Salmonella common antigen antibody %K GAPDH, glyceraldehyde-3-phosphate dehydrogenase %K Blk , Fc, soluble Fc control protein %K HSV-1, -2, herpes simplex virus types 1, 2 %K IFN, interferon %K EB, elementary body %K RB, reticulate body %K NuAb, neutralizing monoclonal antibody %K HVEM, herpes viral entry mediator %K HPV, human papilloma virus %K gD , Fc, soluble gD fusion protein %K gD, -B, -C, -H/L, viral glycoproteins D, B, C, H/L %K TEM, transmission electron microscopy %K h.p.c.i., hours post co-incubation %K β-gal, β-galactosidase %K IFU, inclusion forming units %I Microbiology Society, %X 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. %U https://www.microbiologyresearch.org/content/journal/micro/10.1099/mic.0.036566-0