Varicella-Zoster Virus Reactivation Common After Stroke

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Varicella-Zoster Virus Reactivation Common After Stroke

Following AIS or TIA, a fifth of patients have varicella-zoster virus reactivation in cerebrospinal fluid.A fifth of patients have varicella-zoster virus (VZV) reactivation in cerebrospinal fluid (CSF) after acute ischemic stroke(AIS) or transient ischemic attack (TIA), according to results of a study published in the Journal of the American Heart Association. After infection with varicella, it becomes latent in the ganglia along the entire neuroaxis. Once reactivated, VZV causes herpes zoster (HZ) which presents as a painful vesicular rash and potentially cranial neuropathies and cerebritis. To better understand the relationship between VZV reactivation and stroke, investigators from University of Texas Southwestern Medical Center evaluated data from patients (N=177) who presented with AIS or TIA at their affiliated centers between 2014 and 2021 and received VZV reactivation testing in CSF and serum samples. The patients with (n=41) and without (n=136) VZV reactivation had mean ages of 58.4±15.2 and 57.3±14.5 years, 61% and 51% were men, 58% and 35% were Black, 20% and 18% had a history of 2 or more ischemic strokes, 34% and 13% were immunosuppressed (P =.0014), 32% and 16% had a history of HZ more than 4 months ago (P=.005), and 20% and 1.5% had a history of HZ in the past 4 months (P <.001), respectively. …we found that VZV reactivation in the CSF was present in 23.2% of patients with AIS or TIA who underwent VZV testing in CSF per treating team.

Reactivation of VZV was associated with elevated CSF white blood cell count of 5 or greater (41% vs 17% P=.001) and protein of greater than 42 mg/dL (78% vs 50%P.001) compared with no reactivation, respectively. The rate of VZV positivity by Stop Stroke Study-Trial of ORG 10172 in Acute Stroke Treatment (SSS-TOAST) etiology was highest for VZV (100%), followed by small vessel disease (33.3%), intracranial atherosclerotic disease (26.5%), undetermined (17.9%), and other determined (5.0%) whereas VZV positivity rates were 0% for extracranial atherosclerotic disease and cardioembolism. Among patients with VZV reactivation, all but 14 received treatment, with intravenous acyclovir for 2 weeks with or without oral valacyclovir for several months. A total of 10 patients received at least 1 follow-up VZV CSF test. A total of 7 patients had sustained VZV positivity at an average of 205 days and 5 patients had VZV resolution at 370 days. At an average follow-up of 1108 days after VZV positivity, 10 ischemic strokes, 1 subarachnoid hemorrhage, and 11 deaths occurred. The rate of recurrent stroke did not differ between patients who did (14.8%) and did not (21% P=.593) receive treatment for VZV. Recurrent stroke was more frequent among patients with HIV (42.8%) compared with those without HIV (5%; P=.015). The major limitation of this study was the reliance on provider ordering of VZV testing. As a result, the rate of VZV reactivation in this study does not represent the true prevalence of post-stroke reactivation. The study authors concluded, “…we found that VZV reactivation in the CSF was present in 23.2% of patients with AIS or TIA who underwent VZV testing in CSF per treating team.”

Disclosure: Some study authors declared affiliations with biotech, pharmaceutical, and/or device companies. Please see the original reference for a full list of authors’ disclosures.

This article originally appeared on The Cardiology Advisor

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