{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T12:06:22Z","timestamp":1791201982114,"version":"4.2.0"},"reference-count":75,"publisher":"Rockefeller University Press","issue":"1","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2010,1,18]]},"abstract":"<jats:p>Inflammatory lymphangiogenesis plays a crucial role in the development of inflammation and transplant rejection. The mechanisms of inflammatory lymphangiogenesis during bacterial infection, toll-like receptor ligand administration, and wound healing are well characterized and depend on ligands for the vascular endothelial grow factor receptor (VEGFR) 3 that are produced by infiltrating macrophages. But inflammatory lymphangiogenesis in nonlymphoid tissues during chronic viral infection is unstudied. Herpes simplex virus 1 (HSV-1) infection of the cornea is a leading cause of blindness and depends on aberrant host immune responses to antigen within the normally immunologically privileged cornea. We report that corneal HSV-1 infection drives lymphangiogenesis and that corneal lymphatics persist past the resolution of infection. The mechanism of HSV-1\u2013induced lymphangiogenesis was distinct from the described mechanisms of inflammatory lymphangiogenesis. HSV-1\u2013elicited lymphangiogenesis was strictly dependent on VEGF-A\/VEGFR-2 signaling but not on VEGFR-3 ligands. Macrophages played no role in the induction of lymphangiogenesis and were not a detectable source of VEGF-A. Rather, using VEGF-A reporter transgenic mice, we have identified infected epithelial cells as the primary source of VEGF-A during HSV-1 infection. Our results indicate that HSV-1 directly induces vascularization of the cornea through up-regulation of VEGF-A expression.<\/jats:p>","DOI":"10.1084\/jem.20091385","type":"journal-article","created":{"date-parts":[[2009,12,21]],"date-time":"2009-12-21T22:00:59Z","timestamp":1261432859000},"page":"101-115","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":152,"title":["VEGF-A expression by HSV-1\u2013infected cells drives corneal lymphangiogenesis"],"prefix":"10.1084","volume":"207","author":[{"given":"Todd R.","family":"Wuest","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology 1 and 2"},{"name":"Department of Ophthalmology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104 1 and 2"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel J.J.","family":"Carr","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology 1 and 2"},{"name":"Department of Ophthalmology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104 1 and 2"},{"name":"Department of Microbiology and Immunology 1 and 2"},{"name":"Department of Ophthalmology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104 1 and 2"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"291","published-online":{"date-parts":[[2009,12,21]]},"reference":[{"key":"2023072917451335700_bib1","doi-asserted-by":"publisher","first-page":"28759","DOI":"10.1074\/jbc.M103408200","article-title":"Activation of I\u03baB kinase by herpes simplex virus type 1. 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