scholarly journals Varicella Zoster Virus Meningitis with Absence of Rash in an Immunocompetent Child

2021 ◽  
Vol 2021 ◽  
pp. 1-2
Author(s):  
Mariam Lagrine ◽  
Karima El fakiri ◽  
Noureddine Rada ◽  
Ghizlane Draiss ◽  
Nabila Soraa ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Varicella Zoster Virus ◽  
Clinical Condition ◽  
Neurological Complications ◽  
Varicella Zoster ◽  
Immunocompetent Child ◽  
Hiv Test ◽  
Rapid Hiv Test ◽  
Immunocompetent Patients ◽  
Csf Examination

Only a few cases in the literature have ever reported the reactivation of the varicella zoster virus (VZV) in children especially in the case of immunocompetent patients. It is an uncommon situation that may lead to several neurological complications. We report varicella zoster virus (VZV) meningitis in a 14-year-old healthy boy with no antecedent of rash. On his cerebrospinal fluid (CSF) examination, VZV DNA was detected. The rapid HIV test was negative. The treatment using acyclovir (20 mg/kg/8h) was effective, and the child’s clinical condition rapidly improved.

scholarly journals Molecular Aspects of Varicella-Zoster Virus Latency

2018 ◽  
Author(s):  
Daniel P. Depledge ◽  
Tomohiko Sadaoka ◽  
Werner J. D. Ouwendijk
Keyword(s):  
Varicella Zoster Virus ◽  
Molecular Mechanisms ◽  
Neurological Complications ◽  
In Vitro Models ◽  
New Era ◽  
Varicella Zoster ◽  
Virus Latency ◽  
Technological Advances ◽  
Molecular Aspects

Primary varicella-zoster virus (VZV) infection causes varicella (chickenpox) and the establishment of a lifelong latent infection in ganglionic neurons. VZV reactivates in about one-third of infected individuals to cause herpes zoster, often accompanied by neurological complications. The restricted host range of VZV and, until recently, the lack of suitable in vitro models to study VZV latency have seriously hampered molecular studies of viral latency. Nevertheless, recent technological advances facilitated a series of exciting studies that resulted in the discovery of a VZV latency-associated transcript (VLT) and have redefined our understanding of VZV latency and factors that initiate reactivation. Together, these findings pave the way for a new era of research that may finally unravel the precise molecular mechanisms that govern latency. In this review, we will summarize the implications of recent discoveries in the VZV latency field from both a virus and host perspective and provide a roadmap for future studies.

When infection mimics cauda equina syndrome: a cautionary tale

2021 ◽  
Vol 103 (6) ◽  
pp. e181-e183
Author(s):  
R Shah ◽  
N Jayakumar ◽  
S Athar ◽  
N Ashwood
Keyword(s):  
Magnetic Resonance Imaging ◽  
Cerebrospinal Fluid ◽  
Magnetic Resonance ◽  
Varicella Zoster Virus ◽  
Cauda Equina Syndrome ◽  
Cauda Equina ◽  
Lessons Learned ◽  
Resonance Imaging ◽  
Varicella Zoster ◽  
Elsberg Syndrome

A 63-year-old man presented to the emergency department with low back pain, perineal and genital numbness, together with bilateral lower limb paraesthesia and urinary retention. He was admitted under the orthopaedic service for investigation of suspected cauda equina syndrome. Magnetic resonance imaging of his spine did not reveal any evidence of cauda equina compression. Magnetic resonance imaging of his brain demonstrated nonspecific multiple hyperintensities in the right frontotemporal and left temporo-occipital regions. Computed tomography of his chest, abdomen, and pelvis did not identify any evidence of malignancy. Cerebrospinal fluid from a lumbar puncture showed a high leucocyte count (predominantly lymphocytes). Viral cerebrospinal fluid polymerase chain reaction was positive for varicella zoster virus. A diagnosis of varicella zoster virus myeloradiculitis (Elsberg syndrome) was established and the patient was treated with intravenous aciclovir. Unfortunately, the patient succumbed to a devastating intracerebral haemorrhage during his inpatient stay, probably due to vasculopathy from the underlying varicella zoster virus infection. This case describes a rare infectious mimic of cauda equina syndrome. Elsberg syndrome is an infectious syndrome characterised by bilateral lumbosacral myeloradiculitis, with varicella zoster virus being a well-recognised aetiological agent. We discuss the relevant literature in detail and identify the key, cautionary lessons learned from this case.

Aseptic meningitis caused by the Varicella-zoster virus after primary infection in an immunocompetent child: a case report

2018 ◽  
Vol 76 (2) ◽  
pp. 234-236
Author(s):  
Claudie Lamoureux ◽  
Charlotte Flatrès ◽  
Sophie Vallet ◽  
Adissa Tran - Minoui ◽  
Christopher Payan ◽  
...  
Keyword(s):  
Case Report ◽  
Varicella Zoster Virus ◽  
Aseptic Meningitis ◽  
Primary Infection ◽  
Varicella Zoster ◽  
Immunocompetent Child

scholarly journals Amylin, Aβ42, and Amyloid in Varicella Zoster Virus Vasculopathy Cerebrospinal Fluid and Infected Vascular Cells

2020 ◽  
Author(s):  
Andrew N Bubak ◽  
Cheryl Beseler ◽  
Christina N Como ◽  
Christina M Coughlan ◽  
Noah R Johnson ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Varicella Zoster Virus ◽  
Amyloid Fibrils ◽  
Central Nervous System Infection ◽  
Amyloid Deposition ◽  
Amyloid Formation ◽  
Varicella Zoster ◽  
Arterial Inflammation ◽  
Amyloidogenic Peptides ◽  
Interfering Rna

Abstract Background Varicella zoster virus (VZV) vasculopathy is characterized by persistent arterial inflammation leading to stroke. Studies show that VZV induces amyloid formation that may aggravate vasculitis. Thus, we determined if VZV central nervous system infection produces amyloid. Methods Aβ peptides, amylin, and amyloid were measured in cerebrospinal fluid (CSF) from 16 VZV vasculopathy subjects and 36 stroke controls. To determine if infection induced amyloid deposition, mock- and VZV-infected quiescent primary human perineurial cells (qHPNCs), present in vasculature, were analyzed for intracellular amyloidogenic transcripts/proteins and amyloid. Supernatants were assayed for amyloidogenic peptides and ability to induce amyloid formation. To determine amylin’s function during infection, amylin was knocked down with small interfering RNA and viral complementary DNA (cDNA) was quantitated. Results Compared to controls, VZV vasculopathy CSF had increased amyloid that positively correlated with amylin and anti-VZV antibody levels; Aβ40 was reduced and Aβ42 unchanged. Intracellular amylin, Aβ42, and amyloid were seen only in VZV-infected qHPNCs. VZV-infected supernatant formed amyloid fibrils following addition of amyloidogenic peptides. Amylin knockdown decreased viral cDNA. Conclusions VZV infection increased levels of amyloidogenic peptides and amyloid in CSF and qHPNCs, indicating that VZV-induced amyloid deposition may contribute to persistent arterial inflammation in VZV vasculopathy. In addition, we identified a novel proviral function of amylin.

scholarly journals Varicella Vaccine Meningitis as a Complication of Herpes Zoster in Twice-Immunized Immunocompetent Adolescents

2020 ◽  
Vol 35 (13) ◽  
pp. 889-895 ◽  
Author(s):  
Veena Ramachandran ◽  
Stephen C. Elliott ◽  
Kathie L. Rogers ◽  
Randall J. Cohrs ◽  
Miles Weinberger ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Herpes Zoster ◽  
Varicella Zoster Virus ◽  
Varicella Vaccine ◽  
The United States ◽  
Vaccine Virus ◽  
Virus Reactivation ◽  
Wild Type ◽  
Varicella Zoster ◽  
Intravenous Acyclovir

Varicella-zoster virus vaccination is recommended for virtually all young children in the United States, Canada, and several other countries. Varicella vaccine is a live attenuated virus that retains some of its neurotropic properties. Herpes zoster caused by vaccine virus still occurs in immunized children, although the rate is much lower than in children who had wild-type varicella. It was commonly thought that 2 varicella vaccinations would protect children against the most serious complication of meningitis following herpes zoster; however, 2 meningitis cases have already been published. We now report a third case of varicella vaccine meningitis and define risk factors shared by all 3 immunized adolescents. The diagnosis in cerebrospinal fluid in this third case was verified by amplifying and sequencing portions of the viral genome, to document fixed alleles found only in the vaccine strain. Viral antibody was also detected in the cerebrospinal fluid by confocal microscopy. When compared with the other 2 cases, remarkably all 3 were 14 years old when meningitis occurred. All 3 were treated with intravenous acyclovir, with complete recovery. The adolescent in our case report also had recurrent asthma, which was treated with both prednisone tablets and beclomethasone inhaler before onset of meningitis. When the 3 cases were considered together, they suggested that immunity to varicella-zoster virus may be waning sufficiently in some twice-immunized adolescents to make them vulnerable to varicella vaccine virus reactivation and subsequent meningitis. This complication rarely happens in children after wild-type varicella.

scholarly journals Reactivation of Varicella Zoster Virus after Vaccination for SARS-CoV-2

Vaccines ◽  
2021 ◽  
Vol 9 (6) ◽  
pp. 572
Author(s):  
Mina Psichogiou ◽  
Michael Samarkos ◽  
Nikolaos Mikos ◽  
Angelos Hatzakis
Keyword(s):  
Adverse Event ◽  
Herpes Zoster ◽  
T Cell ◽  
Varicella Zoster Virus ◽  
Time Window ◽  
Vaccine Safety ◽  
Cell Mediated Immunity ◽  
Varicella Zoster ◽  
Increased Risk ◽  
Immunocompetent Patients

Seven immunocompetent patients aged > 50 years old presented with herpes zoster (HZ) infection in a median of 9 days (range 7–20) after vaccination against SARS-CoV-2. The occurrence of HZ within the time window 1–21 days after vaccination defined for increased risk and the reported T cell-mediated immunity involvement suggest that COVID-19 vaccination is a probable cause of HZ. These cases support the importance of continuing assessment of vaccine safety during the ongoing massive vaccination for the COVID-19 pandemic and encourage reporting and communication of any vaccination-associated adverse event.

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