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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.
Microbiology (Reading). 2008 Mar;154(Pt 3):971-978. doi: 10.1099/mic.0.2007/012161-0.
Microbiology (Reading). 2008.
PMID: 18310043
Free article.
Interaction of herpes simplex virus type 2 (HSV-2) glycoprotein D with the host cell surface is sufficient to induce Chlamydia trachomatis persistence.
Vanover J, Kintner J, Whittimore J, Schoborg RV.
Vanover J, et al.
Microbiology (Reading). 2010 May;156(Pt 5):1294-1302. doi: 10.1099/mic.0.036566-0. Epub 2010 Jan 28.
Microbiology (Reading). 2010.
PMID: 20110302
Free PMC article.
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An early event in the herpes simplex virus type-2 replication cycle is sufficient to induce Chlamydia trachomatis persistence.
Deka S, Vanover J, Sun J, Kintner J, Whittimore J, Schoborg RV.
Deka S, et al.
Cell Microbiol. 2007 Mar;9(3):725-37. doi: 10.1111/j.1462-5822.2006.00823.x. Epub 2006 Nov 28.
Cell Microbiol. 2007.
PMID: 17140408
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Chlamydia trachomatis enters a viable but non-cultivable (persistent) state within herpes simplex virus type 2 (HSV-2) co-infected host cells.
Deka S, Vanover J, Dessus-Babus S, Whittimore J, Howett MK, Wyrick PB, Schoborg RV.
Deka S, et al.
Cell Microbiol. 2006 Jan;8(1):149-62. doi: 10.1111/j.1462-5822.2005.00608.x.
Cell Microbiol. 2006.
PMID: 16367874
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