title: Nectin-1-specific entry of herpes simplex virus 1 is sufficient for infection of the cornea and viral spread to the trigeminal ganglia.
abstract: OBJECTIVE
  Primary and recurrent infections of the cornea by herpes simplex virus 1 (HSV-1) are important causes of eye disease. Three unrelated classes of glycoprotein D receptors for HSV-1 entry into cells have been identified. This study was undertaken to uncover the relative significance of nectin-1 as an entry receptor in corneal infection and HSV-1 spread to the trigeminal ganglia (TG), a site important for HSV-1 latency and recurrent corneal infection.
  
  
  METHODS
  To assess the significance of nectin-1, a member of the immunoglobulin superfamily, in primary HSV-1 infection and spread to the TG, we used a murine model of corneal infection and a HSV-1 mutant, KOS(Rid1), which can only use nectin-1 for entry. Immunohistochemistry, real-time PCR, and plaque assays using HSV-1 infected tissues were performed.
  
  
  RESULTS
  We demonstrated that receptor usage by HSV-1 limited to nectin-1 does not significantly change the spread of HSV-1 in the corneal epithelium during primary infection. We also found that nectin-1-specific entry does not affect the capacity of the virus to spread to the TG from the cornea.
  
  
  CONCLUSIONS
  Our findings suggest that nectin-1 alone is sufficient for HSV-1 entry into the cornea and spread to the TG.
authors.affiliation: Department of Pathology, College of Medicine, University of Illinois at Chicago, Chicago, IL 60612, USA.
authors.forename: Navika D
authors.initials: ND
authors.lastname: Shukla
authors.forename: Vaibhav
authors.initials: V
authors.lastname: Tiwari
authors.forename: Tibor
authors.initials: T
authors.lastname: Valyi-Nagy
mesh_terms: D000818:Animals; D015815:Cell Adhesion Molecules / Q000235:genetics / Q000378:metabolism*; D004195:Disease Models, Animal; D019573:Epithelium, Corneal / Q000378:metabolism* / Q000473:pathology / Q000821:virology; D015870:Gene Expression; D006561:Herpes Simplex / Q000378:metabolism* / Q000473:pathology / Q000821:virology; D018259:Herpesvirus 1, Human / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D007150:Immunohistochemistry; D016849:Keratitis, Herpetic; D051379:Mice; D008807:Mice, Inbred BALB C; D009154:Mutation; D000075983:Nectins; D060888:Real-Time Polymerase Chain Reaction; D011991:Receptors, Virus / Q000235:genetics / Q000378:metabolism*; D012668:Trigeminal Ganglion / Q000378:metabolism* / Q000473:pathology / Q000821:virology; D010948:Viral Plaque Assay; D053586:Virus Internalization; D017735:Virus Latency; D014779:Virus Replication
chemical_list: D015815:Cell Adhesion Molecules; C000619010:NECTIN1 protein, human; C000619015:Nectin1 protein, mouse; D000075983:Nectins; D011991:Receptors, Virus