Stroke After Varicella-zoster Infection

Ciccone, Sara; Faggioli, Raffaella; Calzolari, F.; Sartori, Stefano; Calderone, Milena; Borgna‐Pignatti, Caterina

doi:10.1097/inf.0b013e3181ddefb6

Cited by 47 publications

(13 citation statements)

References 47 publications

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“…The incidence of VZV vasculopathy is unknown. In children, up to one-third of ischaemic arteriopathies are associated with varicella 79 . In adults, the risk of stroke is increased by 30% within 1 year of zoster 80 and by 4.5-fold after zoster in the ophthalmic branch of the trigeminal nerve 81 .…”

Section: Mechanisms/pathophysiologymentioning

confidence: 99%

Varicella zoster virus infection

Gershon

Breuer

Cohen

et al. 2015

Nat Rev Dis Primers

562

531

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Infection with varicella zoster virus (VZV) causes varicella (chickenpox), which can be severe in immunocompromised individuals, infants and adults. Primary infection is followed by latency in ganglionic neurons. During this period, no virus particles are produced and no obvious neuronal damage occurs. Reactivation of the virus leads to virus replication, which causes zoster (shingles) in tissues innervated by the involved neurons, inflammation and cell death — a process that can lead to persistent radicular pain (postherpetic neuralgia). The pathogenesis of postherpetic neuralgia is unknown and it is difficult to treat. Furthermore, other zoster complications can develop, including myelitis, cranial nerve palsies, meningitis, stroke (vasculopathy), retinitis, and gastroenterological infections such as ulcers, pancreatitis and hepatitis. VZV is the only human herpesvirus for which highly effective vaccines are available. After varicella or vaccination, both wild-type and vaccine-type VZV establish latency, and long-term immunity to varicella develops. However, immunity does not protect against reactivation. Thus, two vaccines are used: one to prevent varicella and one to prevent zoster. In this Primer we discuss the pathogenesis, diagnosis, treatment, and prevention of VZV infections, with an emphasis on the molecular events that regulate these diseases. For an illustrated summary of this Primer, visit: http://go.nature.com/14×VI1

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Section: Mechanisms/pathophysiologymentioning

confidence: 99%

Varicella zoster virus infection

Gershon

Breuer

Cohen

et al. 2015

Nat Rev Dis Primers

562

531

View full text Add to dashboard Cite

show abstract

“…In children, post-varicella stroke is usually monophasic (Lanthier et al, 2005), typically presenting as an acute hemiparesis at, on average, 4 months after varicella (Ciccone et al, 2010; Miravet et al, 2007). Recently, the live attenuated varicella vaccine strain was shown to cause VZV vasculopathy in an immunodeficient child (Sabry et al, 2014), indicating the need for caution in vaccinating potentially immunocompromised children.…”

Section: Clinical Features Laboratory Abnormalities Diagnosis Anmentioning

confidence: 99%

Varicella zoster virus vasculopathy: The expanding clinical spectrum and pathogenesis

Nagel

Jones

Wyborny

2017

Journal of Neuroimmunology

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Varicella zoster virus (VZV) is a ubiquitous, human alphaherpesvirus that produces varicella on primary infection then becomes latent in ganglionic neurons along the entire neuraxis. In elderly and immunocompromised individuals, VZV reactivates and travels along nerve fibers peripherally resulting in zoster. However, VZV can also spread centrally and infect cerebral and extracranial arteries (VZV vasculopathy) to produce transient ischemic attacks, stroke, aneurysm, sinus thrombosis and giant cell arteritis, as well as granulomatous aortitis. The mechanisms of virus-induced pathological vascular remodeling are not fully elucidated; however, recent studies suggest that inflammation and dysregulation of programmed death ligand-1 play a significant role.

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“…16 The median time from clinical VZV infection to stroke was 18 weeks in a systematic review of the literature. 17 Existing data on the role of VZV in childhood AIS have, however, been limited by single-center design, recall bias in ascertainment of infections, absence of standardized assessment of herpes infections, or small numbers of cases, particularly for children. Data on other herpesviruses (HSV1, EBV) and childhood arteriopathy and AIS are limited to case reports.…”

Section: Introductionmentioning

confidence: 99%

Herpesvirus Infections and Childhood Arterial Ischemic Stroke

et al. 2016

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Background Epidemiological studies demonstrate that childhood infections, including varicella zoster virus (VZV), are associated with an increased risk of arterial ischemic stroke (AIS). Other herpesviruses have been linked to childhood AIS in case reports. We sought to determine whether herpesvirus infections, which are potentially treatable, increase risk of childhood AIS. Methods and Results We enrolled 326 centrally-confirmed cases of AIS and 115 stroke-free controls with trauma (ages 29 days-18 years) with acute blood samples (≤3 weeks after stroke/trauma); cases had convalescent samples (7-28 days later) when feasible. Samples were tested by commercial ELISA kits for IgM/IgG antibodies to herpes simplex virus (HSV) 1 and 2, cytomegalovirus (CMV), Epstein Barr virus (EBV), and varicella zoster virus (VZV). An algorithm developed a priori classified serologic evidence of past and acute herpesvirus infection as dichotomous variables. Median (quartiles) age was 7.7 (3.1-14.3) years for cases and 10.7 (6.9-13.2) for controls (p=0.03). Serologic evidence of past infection did not differ between cases and controls. However, serologic evidence of acute herpesvirus infection doubled the odds of childhood AIS, even after adjusting for age, race, and socio-economic status (OR 2.2; 95% confidence interval, 1.2-4.0; p=0.007). Among 187 cases with acute and convalescent blood samples, 85 (45%) showed evidence of acute herpesvirus infection, with HSV-1 found most often. Most infections were asymptomatic. Conclusions Herpesviruses may act as a trigger for childhood AIS, even if the infection is subclinical. Antivirals like acyclovir might have a role in the prevention of recurrent stroke if further studies confirm a causal relationship.

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Stroke After Varicella-zoster Infection

Cited by 47 publications

References 47 publications

Varicella zoster virus infection

Varicella zoster virus infection

Varicella zoster virus vasculopathy: The expanding clinical spectrum and pathogenesis

Herpesvirus Infections and Childhood Arterial Ischemic Stroke

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