Clinical and Molecular Aspects of Varicella Zoster Virus Infection

Gilden, Don; Nagel, Maria A.; Mahalingam, Ravi; Mueller, Niklaus H.; Brazeau, Elizabeth; Pugazhenthi, Subbiah; Cohrs, Randall J.

doi:10.2217/14796708.4.1.103

Cited by 38 publications

(27 citation statements)

References 154 publications

(136 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Biological plausibility is based on the ability of the varicella zoster virus to remain latent for decades after the primary infection in the cranial nerve, dorsal root, and autonomic ganglia along the entire neuroaxis (12). In addition, studies have revealed that reactivation of the latent virus is not necessarily accompanied by cutaneous outbreaks (13) and can occur at any period in life, most commonly in individuals older than 50 years and those with suppressed cellular immunity (14,15).…”

Section: Discussionmentioning

confidence: 99%

Risk Factors Associated With Vestibular Nerve Schwannomas

Corona¹,

Ferrite²,

Lopes³

et al. 2012

Otology &Amp; Neurotology

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 99%

Risk Factors Associated With Vestibular Nerve Schwannomas

Corona¹,

Ferrite²,

Lopes³

et al. 2012

Otology &Amp; Neurotology

View full text Add to dashboard Cite

show abstract

“…[1][2][3][4][5][6][7][8] 2. Clinical diagnosis of VZV neurologic disorders is confirmed by virologic analysis with the detection of VZV DNA or anti-VZV immunoglobulin G (IgG) antibody in the CSF.…”

Section: Cns Complications Of Varicella-zoster Virus (Vzv)mentioning

confidence: 99%

Pearls & Oy-sters: An unusual case of varicella-zoster virus cerebellitis and vasculopathy

Calabria¹,

Zappini²,

Vattemi³

et al. 2014

Neurology

View full text Add to dashboard Cite

Pearls & Oy-sters: An unusual case of varicella-zoster virus cerebellitis and vasculopathy PEARLS 1. CNS complications of varicella-zoster virus (VZV) occur mainly in immunocompromised or elderly patients and include meningitis, myelitis, acute encephalitis, vasculopathy, and, rarely, cerebellitis. CASE REPORT A 67-year-old woman presented with unsteadiness and dizziness of gradual onset. Two weeks before presentation, the patient had a painful vesicular rash at the left ear followed within 9 days by acute left peripheral facial palsy; a diagnosis of Ramsay Hunt syndrome (RHS) was made and oral valacyclovir was started. A few days after initiating valacyclovir, she developed gait instability, which gradually worsened. Her medical history disclosed well-controlled diabetes mellitus and hypertension, and therapy included metformin, ramipril, hydrochlorothiazide, and acetylsalicylic acid. On neurologic examination, the patient was unable to stand and walk unassisted; she had a wide-based gait, predominantly left-sided limb ataxia, and bilateral dysdiadochokinesia. On cranial nerve examination, the patient had a left lower motor neuron facial palsy and had pain in all 3 branches of the left trigeminal nerve. Deep tendon reflexes, strength, and sensation were normal. Head CT displayed hypodensity of the left medial pons, and, because of suspected CNS involvement by VZV, the patient was treated with IV acyclovir (10 mg/kg 3 times daily) for 10 days. Brain MRI, performed the second day of therapy, revealed one lesion in the left pons, one in the left midbrain, and one in the right periventricular area. All 3 lesions were hyperintense on T2 and diffusionweighted imaging sequences and hypointense on apparent diffusion coefficient, consistent with recent ischemic lesions ( figure). No other supratentorial or cerebellar lesions were seen. Magnetic resonance angiography (MRA) was normal. Absolute lymphocyte count was 550/mL (normal 0.95-4.40) with inversion of the CD41:CD81 T-cell ratio. CSF analysis showed 40 leukocytes/mL (mainly mononuclear cells), 40 erythrocytes/mL, protein 0.46 g/L (normal 0.15-0.45), and glucose 99 mg/dL (normal 45-80). CSF VZV PCR was positive and anti-VZV IgG antibody was detected in the CSF. PCR tests for other neurotropic viruses were negative. Common causes of stroke including atherosclerosis or dissection were excluded. After 2 days of treatment with IV acyclovir, the patient's symptoms improved and at discharge she had no difficulty in standing and walked with unilateral support. Facial pain was treated successfully with carbamazepine 400 mg/day. At the last follow-up 3 months later, the patient walked without support, retained a mild facial weakness, and denied facial pain after she gradually ceased carbamazepine.DISCUSSION We describe a healthy, immunocompetent adult patient who developed herpes zoster that progressed to cerebellar ataxia and trigeminal neuropathic pain. Brain MRI findings of focal ischemic lesions in the brainstem and right hemisphere are inconsistent with cerebellar invo...

show abstract

“…Subsequently, later in life, and as specific cell-mediated immunity to the virus declines with age or immunosuppression, VZV reactivates to cause shingles, often followed by postherpetic neuralgia, vasculopathy, myelopathy, retinal necrosis and cerebellitis. 3 The epidemiology of varicella exhibits significant differences in temperate and tropical regions. 4 In temperate locations, varicella primarily affects children 5 ; however, in tropical areas, varicella tends to occur at a later age, during adolescence and adulthood, with an increased risk of developing a more severe disease.…”

Section: Introductionmentioning

confidence: 99%