Widespread arterial infection by varicella-zoster virus explains refractory giant cell arteritis

Virologic analysis of tissues from a patient with giant cell arteritis (GCA) who was treated with corticosteroids and died of extensive necrotizing granulomatous arteritis revealed widespread varicella-zoster virus (VZV) antigen in multiple large arteries. Long-term treatment with corticosteroids likely potentiated VZV infection. In 1997, a clinicopathologic case report described a 75-year-old woman with fatal aggressive steroidrefractory GCA that manifested as bilateral vision loss and myelopathy while on treatment with corticosteroids. The woman was not otherwise immunocompromised before becoming ill, and no cutaneous signs of herpesvirus infection developed during her 5-month illness. Bilateral temporal artery (TA) biopsies revealed GCA. Postmortem examination revealed spinal cord infarction secondary to extensive necrotizing granulomatous arteritis of spinal arteries. Based on detection of VZV in GCA-positive TAs and documented involvement of other large arteries in most patients with GCA, we revisited this case and searched for VZV in the archived TAs and in other large arteries, the spinal cord, and brain. Immunohistochemical examination detected VZV antigen (figure) in both TAs, in the aorta, in the left carotid artery, and in an unidentified artery from the Circle of Willis but not in renal or mesenteric arteries. Viral antigen was not seen in the brain or spinal cord. DNA extracted from every section of each VZV antigen–positive artery was analyzed by PCR with primers specific for VZV and herpes simplex virus (HSV)-1 as described and revealed VZV DNA, but not HSV-1 DNA, in the unidentified cerebral artery from the Circle of Willis despite formalin fixation.