OBJECTIVE: We describe 3 Japanese patients with peculiar renal and/or coronary arterial stenosis and/or multiple aneurysms after herpes virus infection, following ischemic symptoms. We investigated for viral antigens and viral DNA in situ, and for shared abnormalities of cellular immunity. METHODS: Panarteriography was performed diagnostically, and patients were grouped as follows: 3 patients with peculiar renal and/or coronary artery narrowing and/or multiple aneurysms; another 3 patients with renal fibromuscular dysplasia; and other young adults with effort angina, with no history of herpes virus infection, as controls. Detection of viral antigens and viral DNA in situ was done by polymerase chain reaction method and immunohistochemical staining. Cellular immunity was examined at the time of ischemic symptoms. RESULTS: Viral antigens and DNA were scarcely detected, except in herpes zoster skin lesion with leukocytoclastic vasculitis. However, shared abnormalities of cellular immunity, such as a decreased CD4+ T cell number and reduced natural killer cell activity, were more prominent in the 3 patients with unique vasculopathy after herpes virus infection. CONCLUSION: Unique vasculopathy following herpes virus infection might be a more severe and extensive disease. We speculate that sustained viral infection, repetitive activation of virus related antigens, and suppressed immune state might contribute to formation of peculiar vascular alterations.
OBJECTIVE: We describe 3 Japanese patients with peculiar renal and/or coronary arterial stenosis and/or multiple aneurysms after herpes virus infection, following ischemic symptoms. We investigated for viral antigens and viral DNA in situ, and for shared abnormalities of cellular immunity. METHODS: Panarteriography was performed diagnostically, and patients were grouped as follows: 3 patients with peculiar renal and/or coronary artery narrowing and/or multiple aneurysms; another 3 patients with renal fibromuscular dysplasia; and other young adults with effort angina, with no history of herpes virus infection, as controls. Detection of viral antigens and viral DNA in situ was done by polymerase chain reaction method and immunohistochemical staining. Cellular immunity was examined at the time of ischemic symptoms. RESULTS: Viral antigens and DNA were scarcely detected, except in herpes zoster skin lesion with leukocytoclastic vasculitis. However, shared abnormalities of cellular immunity, such as a decreased CD4+ T cell number and reduced natural killer cell activity, were more prominent in the 3 patients with unique vasculopathy after herpes virus infection. CONCLUSION: Unique vasculopathy following herpes virus infection might be a more severe and extensive disease. We speculate that sustained viral infection, repetitive activation of virus related antigens, and suppressed immune state might contribute to formation of peculiar vascular alterations.