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• W2943462783 abstract "Varicella zoster virus (VZV) is an exclusively human, neurotropic, DNA alphaherpesvirus that produces varicella (chicken pox) and then becomes latent in neurons residing in the cranial nerve, dorsal root, and autonomic ganglia. As VZV-specific cell-mediated immunity wanes, virus can reactivate from 1 or more ganglia and travel peripherally to produce herpes zoster (HZ; shingles) in the corresponding dermatome(s). Risk factors for reactivation include aging, cancer, human immunodeficiency virus, and treatment with immunosuppressive therapy. The burden of VZV disease is substantial given that more than 90% of the world population harbors latent virus and approximately 50% will reactivate and develop HZ by 85 years of age. Herpes zoster can be complicated by stroke that has been clinically described as VZV vasculopathy, granulomatous angiitis, and HZ ophthalmicus with delayed contralateral hemiparesis when HZ occurs in the ophthalmic distribution of the trigeminal nerve followed by stroke involving the ipsilateral middle cerebral artery. Varicella zoster virus vasculopathy was first described in 18961Baudouin E. Lantuéjoul P. Les troublecas moteurs dans le zona.Gaz Hop. 1919; 92: 1293Google Scholar and included cases of varicella or zoster that were temporally associated with stroke presenting as hemiparesis. As more reports of VZV vasculopathy accrued, the wide spectrum of clinical presentations became evident with VZV vasculopathy presenting as ischemic or hemorrhagic stroke, affecting both large and small arteries. Importantly, one-third of VZV vasculopathy cases do not have an associated rash or cerebrospinal fluid pleocytosis; stroke presents an average of 4 months after rash; and the detection of VZV DNA in the cerebrospinal fluid is not as sensitive as the detection of anti-VZV antibodies—overall making diagnosis challenging.2Nagel M.A. Cohrs R.J. Mahalingam R. et al.The varicella zoster virus vasculopathies: clinical, CSF, imaging, and virologic features.Neurology. 2008; 70: 853-860Crossref PubMed Scopus (402) Google Scholar Given that stroke due to VZV is potentially treatable, it is essential to understand how often these events occur to guide clinicians in patient evaluation and treatment. Since 2009, several epidemiological studies have reported an increased risk of transient ischemic attack (TIA), stroke, myocardial infarction (MI), and acute coronary syndrome after HZ, particularly in individuals who develop zoster below 40 years of age.3Erskine N. Tran H. Levin L. et al.A systematic review and meta-analysis on herpes zoster and the risk of cardiac and cerebrovascular events.PLoS One. 2017; 12: e0181565Crossref PubMed Scopus (44) Google Scholar In this issue of Mayo Clinic Proceedings, Patterson et al4Patterson B.J. Rausch D.A. Irwin D.E. Liang M. Yan S. Yawn B.P. Analysis of vascular event risk following herpes zoster from 2007 to 2014 United States insurance claims data.Mayo Clin Proc. 2019; 94: 763-775Scopus (14) Google Scholar substantially add to this growing literature by conducting the largest retrospective study in the United States that investigates the association between HZ and the occurrence of TIA, stroke, and MI 4 weeks before to 52 weeks after the diagnosis of HZ. Using the MarketScan Commercial and Medicare claims data set linked with obesity and smoking status information, 23,339 patients with HZ and 46,378 matched controls were identified. Similar to other studies, the authors found a significant increase in the risk of TIA and stroke in patients with HZ compared with matched controls, which diminished within 1 year (P<.001 and P<.007, respectively; posthoc sensitivity analysis); in addition, they found that this risk is further elevated in younger adults (<50 years old), indicating the need for further research in younger adults, especially those with traditional risk factors (smoking, obesity, etc), to generate future treatment guidelines such as early vaccination. Specifically, during the aggregate period, patients with HZ of all ages or between 18 and 49 years of age were more likely to develop TIAs with adjusted incidence ratios of 1.56 (95% CI, 1.13-2.15) and 5.12 (95% CI, 1.37-19.10), respectively, as well as stroke with incidence ratios of 1.40 (95% CI, 0.93-2.11) and 8.12 (95% CI, 0.93-71.27), respectively. The authors acknowledged the limitations of their study, including data coding limitations and data entry error, the unavailability of race and socioeconomic status, and the inclusion of individuals with either commercial health coverage or supplemental insurance through Medicare that may not be representative of the US population. The likely mechanism for stroke produced by VZV is direct viral infection of cerebral arteries followed by inflammation and release of soluble factors that cause vascular damage. This assertion is supported by feline studies identifying afferent fibers from trigeminal and upper cervical ganglia to both intra- and extracranial blood vessels, providing an anatomical pathway for spread of virus to cerebral arteries after reactivation from ganglionic neurons.5Mayberg M.R. Zervas N.T. Moskowitz M.A. Trigeminal projections to supratentorial pial and dural blood vessels in cats demonstrated by horseradish peroxidase histochemistry.J Comp Neurol. 1984; 223: 46-56Crossref Scopus (266) Google Scholar Postmortem studies of affected cerebral arteries from patients with VZV vasculopathy report the presence of VZV DNA, antigen, and herpesvirus particles identified by electron microscopy6Gilden D.H. Kleinschmidt-DeMasters B.K. Wellish M. Hedley-Whyte E.T. Rentier B. Mahalingam R. Varicella zoster virus, a cause of waxing and waning vasculitis: the New England Journal of Medicine case 5-1995 revisited.Neurology. 1996; 47: 1441-1446Crossref PubMed Scopus (172) Google Scholar; histological changes include infiltrating immune cells, loss of medial smooth muscle cells predisposing to aneurysm and hemorrhage, and a thickened intima infiltrated by myofibroblasts, which may contribute to arterial occlusion and attendant ischemia as reviewed by Nagel and Bubak.7Nagel M.A. Bubak A.N. Varicella zoster virus vasculopathy.J Infect Dis. 2018; 218: S107-S112Crossref Scopus (38) Google Scholar Studies of VZV-infected primary human cerebrovascular adventitial fibroblasts reveal secretion of proinflammatory cytokines, increased active matrix metalloproteinases that can disrupt extracellular matrix, decreased programmed death ligand 1 that can contribute to persistent inflammation, and decreased major histocompatibility complex I that can prevent effective viral antigen presentation to immune cells reviewed in Nagel and Bubak.7Nagel M.A. Bubak A.N. Varicella zoster virus vasculopathy.J Infect Dis. 2018; 218: S107-S112Crossref Scopus (38) Google Scholar An interesting observation in epidemiological reports is the increased risk of cerebrovascular events even if zoster occurs in areas other than the ophthalmic distribution of the trigeminal nerve. This is explained by studies of simian varicella virus, the nonhuman primate equivalent of VZV, in which productive simian varicella virus infection during reactivation is detected in ganglia corresponding to the dermatomal distribution of zoster rash as well as in multiple other ganglia.8Mahalingam R. Traina-Dorge V. Wellish M. et al.Simian varicella virus reactivation in cynomolgus monkeys.Virology. 2007; 368: 50-59Crossref PubMed Scopus (47) Google Scholar In other words, virus has the capacity to reactivate from one ganglia and spread peripherally to the skin to produce zoster and from other ganglia in the same individual (such as the trigeminal ganglia) where virus can spread centrally to produce stroke. Finally, productive virus infection in patients with VZV vasculopathy is supported by the stabilization or improvement of stroke symptoms with acyclovir treatment2Nagel M.A. Cohrs R.J. Mahalingam R. et al.The varicella zoster virus vasculopathies: clinical, CSF, imaging, and virologic features.Neurology. 2008; 70: 853-860Crossref PubMed Scopus (402) Google Scholar and the decreased risk of stroke after antiviral treatment of HZ in epidemiological studies.9Langan S.M. Minassian C. Smeeth L. Thomas S.L. Risk of stroke following herpes zoster: a self-controlled case-series study.Clin Infect Dis. 2014; 58: 1497-1503Crossref PubMed Scopus (112) Google Scholar However, additional mechanisms may also be involved, including a virus-induced hypercoagulable state or vasospasm. Now that multiple studies in the United States, Europe, and Asia definitively report that zoster is a risk factor for TIA and stroke, the need for future studies are driven by several questions. A self-controlled case series study reported that treatment with antiviral drugs during acute zoster decreased the risk of stroke.9Langan S.M. Minassian C. Smeeth L. Thomas S.L. Risk of stroke following herpes zoster: a self-controlled case-series study.Clin Infect Dis. 2014; 58: 1497-1503Crossref PubMed Scopus (112) Google Scholar Can this risk be further reduced if patients with HZ are treated with antiviral drugs prophylactically during the following year when TIA and stroke risk are elevated, particularly if patients are younger than 50 years? Although zoster vaccination is unequivocally effective at preventing zoster and subsequent development of postherpetic neuralgia, it is unclear whether vaccination will be effective at reducing the risk of acute vascular events described in this study. One study suggests no reduction in stroke or MI risk in individuals vaccinated with the live attenuated zoster vaccine (Zostavax, Merck) compared with unvaccinated individuals; however, statistical power was limited because of a small sample size.10Minassian C. Thomas S.L. Smeeth L. Douglas I. Brauer R. Langan S.M. Acute cardiovascular events after herpes zoster: a self-controlled case series analysis in vaccinated and unvaccinated older residents of the United States.PLoS Med. 2015; 12: e1001919Crossref PubMed Scopus (63) Google Scholar For healthy adults 50 years and older, the Centers for Disease Control and Prevention are currently recommending the new 2-dose recombinant zoster vaccine (Shingrix, GlaxoSmithKline), which is a nonlive, subunit vaccine containing VZV glycoprotein E in combination with a novel adjuvant (AS01B). Studies of the ability of this new recombinant zoster vaccine to protect against VZV-associated stroke are imperative; caution on the use of this vaccine in patients with VZV vasculopathy is warranted until these studies are completed because the possibility exists that robust vaccine-mediated inflammation, if it occurs in a VZV-infected artery, may potentiate vasculitis. Analysis of Vascular Event Risk After Herpes Zoster From 2007 to 2014 US Insurance Claims DataMayo Clinic ProceedingsVol. 94Issue 5PreviewTo estimate the risk of transient ischemic attack (TIA), stroke, and myocardial infarction in periods covering 4 weeks before to 52 weeks after herpes zoster (HZ) diagnosis in US adults. Full-Text PDF Open AccessIn the Limelight: May 2019Mayo Clinic ProceedingsVol. 94Issue 5PreviewThis new monthly feature highlights four articles in the current print and online issue of Mayo Clinic Proceedings. These articles are also featured on the Mayo Clinic Proceedings' YouTube Channel ( https://mayocl.in/2U1xy5H ), and may be also discussed by an accompanying editorial. Full-Text PDF" @default.
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• W2943462783 title "Herpes Zoster, a Rash of Cerebrovascular Events" @default.
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