Article

Complications of Varicella Zoster Virus Reactivation

Department of Neurology, University of Colorado School of Medicine, Aurora, CO, USA, .
Current Treatment Options in Neurology (Impact Factor: 1.94). 06/2013; 15(4). DOI: 10.1007/s11940-013-0246-5
Source: PubMed

ABSTRACT

Purpose of review:
Varicella zoster virus (VZV) reactivation results in zoster, which may be complicated by postherpetic neuralgia, myelitis, meningoencephalitis, and VZV vasculopathy. This review highlights the clinical features, laboratory abnormalities, imaging changes, and optimal treatment of each of those conditions. Because all of these neurological disorders produced by VZV reactivation can occur in the absence of rash, the virological tests proving that VZV caused disease are discussed.

Recent findings:
After primary infection, VZV becomes latent in ganglionic neurons along the entire neuraxis. With a decline in VZV-specific cell-mediated immunity, VZV reactivates from ganglia and travels anterograde to the skin to cause zoster, which is often complicated by postherpetic neuralgia. VZV can also travel retrograde to produce meningoencephalitis, myelitis, and stroke. When these complications occur without rash, VZV-induced disease can be diagnosed by detection of VZV DNA or anti-VZV antibody in cerebrospinal fluid and treated with intravenous acyclovir.

Summary:
Awareness of the expanding spectrum of neurological complications caused by VZV reactivation with and without rash will improve diagnosis and treatment.

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    • "Varicella zoster virus (VZV), an exclusively human alphaherpesvirus , becomes latent in ganglionic neurons along the entire neuraxis after primary infection. Decades later, virus can reactivate to produce zoster and additional serious neurological and ocular complications (Gilden et al., 2011; Nagel and Gilden, 2013). VZV can infect neurons in vitro from multiple sources, including those derived from human embryonic stem cells [hESC; (Markus et al., 2011; Sloutskin et al., 2013)], human neural stem cells [hNSC; (Pugazhenthi et al., 2011)] and human induced pluripotent stem cells [iPSC; (Baird et al., 2014; Grose et al., 2013; Yu et al., 2013)]. "
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    ABSTRACT: Varicella zoster virus (VZV) is an exclusively human neurotropic alphaherpesvirus. It is unclear why human neurons infected in vitro with VZV at low multiplicity of infection do not exhibit a cytopathic effect (CPE) even though all VZV genes are transcribed, VZV proteins from all kinetic classes are translated and minimal infectious virus is produced. Here, we show that the lack of VZV-induced CPE correlates with the low abundance of viral DNA.
    Full-text · Article · Jun 2014 · Virology
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    • "Varicella zoster virus (VZV), an exclusively human alphaherpesvirus , becomes latent in ganglionic neurons along the entire neuraxis after primary infection. Decades later, virus can reactivate to produce zoster and additional serious neurological and ocular complications (Gilden et al., 2011; Nagel and Gilden, 2013). VZV can infect neurons in vitro from multiple sources, including those derived from human embryonic stem cells [hESC; (Markus et al., 2011; Sloutskin et al., 2013)], human neural stem cells [hNSC; (Pugazhenthi et al., 2011)] and human induced pluripotent stem cells [iPSC; (Baird et al., 2014; Grose et al., 2013; Yu et al., 2013)]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Varicella zoster virus (VZV) is an exclusively human neurotropic alphaherpesvirus. It is unclear why human neurons infected in vitro with VZV at low multiplicity of infection do not exhibit a cytopathic effect (CPE) even though all VZV genes are transcribed, VZV proteins from all kinetic classes are translated and minimal infectious virus is produced. Here, we show that the lack of VZV-induced CPE correlates with the low abundance of viral DNA.
    Full-text · Article · Jan 2014
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    • "After varicella, VZV remains latent in the sensory dorsal root ganglia and, when reactivated, replicates along the course of the nerve and appears as a vesicular skin rash [1,2,9]. In most cases, this is preceded by paresthesia, itching and pain or “pre-herpetic neuralgia” [2,9], and these sensory symptoms can be severe enough to suggest an alternative cause, such as coronary ischemia or an abdominal condition. "
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    ABSTRACT: The development of neurological complications due to varicella zoster virus (VZV) reactivation is relatively uncommon, particularly in the case of immunocompetent patients. Only a few cases have been described in the literature, most of which involved adult or elderly patients.Clinical presentation: Two days after his pediatrician had diagnosed herpes zoster and prescribed oral acyclovir 400 mg three times a day, a 14-year-old boy was admitted to our hospital because of mild fever, severe headache, slowness, drowsiness and vomiting. A cerebrospinal fluid examination was performed and showed an increased protein concentration (95 mg/dL), normal glucose level (48 mg/dL; blood glucose level, 76 mg/dL) and lymphocytic pleocytosis (1,400 lymphocytes/muL), and VZV DNA was detected by means of polymerase chain reaction (1,250 copies/mL). The results of immunological screening for HIV, lymphocyte subpopulation counts, serum immunoglobulin and complement (C3 and C4) levels, vaccine responsiveness and lymphocytes stimulation tests were unremarkable. Acyclovir was administered intravenously at a dose of 10 mg/kg three times a day and continued for 10 days. The therapy was highly effective and the patient's clinical condition rapidly improved: fever disappeared after two days, and all of the signs and symptoms of neurological involvement after four days. The skin lesions resolved in about one week, and no pain or dysesthesia was ever reported. Given the favourable evolution of the illness, the child was discharged without further therapy after the 10-day treatment. The findings of a magnetic resonance examination immediately after the discontinuation of the antiviral therapy were normal, and a control examination carried out about four weeks later did not find any sign or symptom of disease. VZV reactivation can also lead to various neurological complications in immunocompetent children. Prompt therapy with acyclovir and the integrity of the immune system are important in conditioning outcome, but other currently unknown factors probably also play a role.
    Full-text · Article · Nov 2013 · Italian Journal of Pediatrics
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