title: Varicella-zoster virus vasculopathy: immune characteristics of virus-infected arteries.
abstract: OBJECTIVE
  Pathologic changes in varicella-zoster virus (VZV)-infected arteries include inflammation, thickened intima, and paucity of smooth muscle cells. Since no criteria have been established for early vs late VZV vasculopathy, we examined inflammatory cells and their distribution in 6 normal arteries, and 2 VZV-infected arteries 3 days after onset of disease (early) and 10 months after protracted neurologic disease (late).
  
  
  METHODS
  VZV-infected temporal artery obtained 3 days after onset of ischemic optic neuropathy from an 80-year-old man, VZV-infected middle cerebral artery (MCA) obtained 10 months after protracted disease from a 73-year-old man, and 5 MCAs and 1 temporal artery from normal subjects, age 22-60 years, were examined histologically and immunohistochemically using antibodies against VZV and inflammatory cell subsets.
  
  
  RESULTS
  In both early and late VZV vasculopathy, T cells, activated macrophages, and rare B cells were found in adventitia and intima. In adventitia of early VZV vasculopathy, neutrophils and VZV antigen were abundant and a thickened intima was associated with inflammatory cells in vaso vasorum vessels. In media of late VZV vasculopathy, viral antigen, but not leukocytes, was found. VZV was not seen in inflammatory cells. Inflammatory cells were absent in control arteries.
  
  
  CONCLUSIONS
  Both VZV and neutrophils exclusively in adventitia in early VZV vasculopathy indicate that disease begins there. Late VZV vasculopathy is distinguished by viral antigen without inflammation in media, revealing a human virus in an immunoprivileged arterial media. Association of thickened intima and inflammation in vaso vasorum vessels in early VZV vasculopathy support the role of virus-induced inflammation in vessel wall remodeling.
authors.affiliation: Department of Neurology, University of Colorado School of Medicine, Aurora, CO, USA. maria.nagel@ucdenver.edu
authors.forename: Maria A
authors.initials: MA
authors.lastname: Nagel
authors.forename: Igor
authors.initials: I
authors.lastname: Traktinskiy
authors.forename: Kurt R
authors.initials: KR
authors.lastname: Stenmark
authors.forename: Maria G
authors.initials: MG
authors.lastname: Frid
authors.forename: Alexander
authors.initials: A
authors.lastname: Choe
authors.forename: Don
authors.initials: D
authors.lastname: Gilden
mesh_terms: D000328:Adult; D063194:Adventitia / Q000276:immunology; D000368:Aged; D000369:Aged, 80 and over; D001402:B-Lymphocytes / Q000276:immunology; D016022:Case-Control Studies; D005260:Female; D014645:Herpesvirus 3, Human / Q000276:immunology*; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000473:pathology / Q000821:virology; D008264:Macrophages / Q000276:immunology; D008297:Male; D008875:Middle Aged; D020768:Middle Cerebral Artery / Q000276:immunology* / Q000473:pathology / Q000821:virology; D009504:Neutrophils / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology; D013699:Temporal Arteries / Q000276:immunology* / Q000473:pathology / Q000821:virology; D017539:Tunica Intima / Q000276:immunology / Q000473:pathology; D014652:Vascular Diseases / Q000276:immunology* / Q000473:pathology / Q000821:virology; D014777:Virus Diseases / Q000276:immunology* / Q000473:pathology / Q000821:virology