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dc.contributor.authorLee, Sungseoken_US
dc.contributor.authorIves, Angela M.en_US
dc.contributor.authorBertke, Andrea S.en_US
dc.date.accessioned2017-02-28T23:32:50Z
dc.date.available2017-02-28T23:32:50Z
dc.date.issued2015-08-01en_US
dc.identifier.issn0022-538Xen_US
dc.identifier.urihttp://hdl.handle.net/10919/75201
dc.description.abstractHerpes simplex virus 1 (HSV-1) and HSV-2 establish latency in sensory and autonomic neurons after ocular or genital infection, but their recurrence patterns differ. HSV-1 reactivates from latency to cause recurrent orofacial disease, and while HSV-1 also causes genital lesions, HSV-2 recurs more efficiently in the genital region and rarely causes ocular disease. The mechanisms regulating these anatomical preferences are unclear. To determine whether differences in latent infection and reactivation in autonomic ganglia contribute to differences in HSV-1 and HSV-2 anatomical preferences for recurrent disease, we compared HSV-1 and HSV-2 clinical disease, acute and latent viral loads, and viral gene expression in sensory trigeminal and autonomic superior cervical and ciliary ganglia in a guinea pig ocular infection model. HSV-2 produced more severe acute disease, correlating with higher viral DNA loads in sensory and autonomic ganglia, as well as higher levels of thymidine kinase expression, a marker of productive infection, in autonomic ganglia. HSV-1 reactivated in ciliary ganglia, independently from trigeminal ganglia, to cause more frequent recurrent symptoms, while HSV-2 replicated simultaneously in autonomic and sensory ganglia to cause more persistent disease. While both HSV-1 and HSV-2 expressed the latency-associated transcript (LAT) in the trigeminal and superior cervical ganglia, only HSV-1 expressed LAT in ciliary ganglia, suggesting that HSV-2 is not reactivation competent or does not fully establish latency in ciliary ganglia. Thus, differences in replication and viral gene expression in autonomic ganglia may contribute to differences in HSV-1 and HSV-2 acute and recurrent clinical disease.en
dc.format.extent8383 - 8391 (9) page(s)en_US
dc.languageEnglishen_US
dc.publisherAmerican Society for Microbiologyen_US
dc.relation.urihttp://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000358278200024&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=930d57c9ac61a043676db62af60056c1en_US
dc.subjectVirologyen_US
dc.subjectEXPERIMENTAL GENITAL-INFECTIONen_US
dc.subjectTYPE-1en_US
dc.subjectLATENCYen_US
dc.subjectMODELen_US
dc.subjectPROTEINen_US
dc.subjectLOCALIZATIONen_US
dc.subjectPROPAGATIONen_US
dc.subjectEXPRESSIONen_US
dc.subjectNEURONSen_US
dc.subjectTARGETSen_US
dc.titleHerpes Simplex Virus 1 Reactivates from Autonomic Ciliary Ganglia Independently from Sensory Trigeminal Ganglia To Cause Recurrent Ocular Diseaseen_US
dc.typeArticle - Refereed
dc.description.versionPublished (Publication status)en_US
dc.title.serialJournal of Virologyen_US
dc.identifier.doihttps://doi.org/10.1128/JVI.00468-15
dc.identifier.volume89en_US
dc.identifier.issue16en_US
dc.identifier.orcidBertke, AS [0000-0002-8941-8010]en_US
pubs.organisational-group/Virginia Tech
pubs.organisational-group/Virginia Tech/All T&R Faculty
pubs.organisational-group/Virginia Tech/Faculty of Health Sciences
pubs.organisational-group/Virginia Tech/Veterinary Medicine
pubs.organisational-group/Virginia Tech/Veterinary Medicine/CVM T&R Faculty
pubs.organisational-group/Virginia Tech/Veterinary Medicine/Population Health Sciences


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