Varicella-zoster virus-related neurological complications: From infection to immunomodulatory therapies.

The Varicella-zoster virus (VZV), classified as a neurotropic member of the Herpesviridae family, exhibits a characteristic pathogenicity, predominantly inducing varicella, commonly known as chickenpox, during the initial infectious phase, and triggering the reactivation of herpes zoster, more commonly recognized as shingles, following its emergence from a latent state. The pathogenesis of VZV-associated neuroinflammation involves a complex interplay between viral replication within sensory ganglia and immune-mediated responses that contribute to tissue damage and dysfunction. Upon primary infection, VZV gains access to sensory ganglia, establishing latent infection within neurons. During reactivation, the virus can spread along sensory nerves, triggering a cascade of inflammatory mediators, chemokines, and immune cell infiltration in the affected neural tissues. The role of both adaptive and innate immune reactions, including the contributions of T and B cells, macrophages, and dendritic cells, in orchestrating the immune-mediated damage in the central nervous system is elucidated. Furthermore, the aberrant activation of the natural defence mechanism, characterised by the dysregulated production of immunomodulatory proteins and chemokines, has been implicated in the pathogenesis of VZV-induced neurological disorders, such as encephalitis, myelitis, and vasculopathy. The intricate balance between protective and detrimental immune responses in the context of VZV infection emphasises the necessity for an exhaustive comprehension of the immunopathogenic mechanisms propelling neuroinflammatory processes. Despite the availability of vaccines and antiviral therapies, VZV-related neurological complications remain a significant concern, particularly in immunocompromised individuals and the elderly. Elucidating these mechanisms might facilitate the emergence of innovative immunomodulatory strategies and targeted therapies aimed at mitigating VZV-induced neuroinflammatory damage and improving clinical outcomes. This comprehensive understanding enhances our grasp of viral pathogenesis and holds promise for pioneering therapeutic strategies designed to mitigate the neurological ramifications of VZV infections.

Serious neurological adverse events in immunocompetent children and adolescents caused by viral reactivation in the years following varicella vaccination.

Serious adverse events following vaccination include medical complications that require hospitalisation. The live varicella vaccine that was approved by the Food and Drug Administration in the United States in 1995 has an excellent safety record. Since the vaccine is a live virus, adverse events are more common in immunocompromised children who are vaccinated inadvertently. This review includes only serious adverse events in children considered to be immunocompetent. The serious adverse event called varicella vaccine meningitis was first reported in a hospitalised immunocompetent child in 2008. When we carried out a literature search, we found 15 cases of immunocompetent children and adolescents with varicella vaccine meningitis; the median age was 11 years. Eight of the children had received two varicella vaccinations. Most of the children also had a concomitant herpes zoster rash, although three did not. The children lived in the United States, Greece, Germany, Switzerland, and Japan. During our literature search, we found five additional cases of serious neurological events in immunocompetent children; these included 4 cases of progressive herpes zoster and one case of acute retinitis. Pulses of enteral corticosteroids as well as a lack of herpes simplex virus antibody may be risk factors for reactivation in immunocompetent children. All 20 children with adverse events were treated with acyclovir and recovered; 19 were hospitalised and one child was managed as an outpatient. Even though the number of neurological adverse events remains exceedingly low following varicella vaccination, we recommend documentation of those caused by the vaccine virus.

An adult with hemorrhagic varicella co-infects with cytomegalovirus: a case report.

BACKGROUND: Hemorrhagic varicella (HV) is a particular form of chicken pox.,with high mortality in adults. This form of the disease is rare, to date, approximately 4 cases have been reported. Occasional cases of HV have been documented in adults with hematologic disorders or other diseases. While there is one reported case of simultaneous reactivation of cytomegalovirus in an adult with chickenpox, there is a lack of information regarding changes in liver function indicators for such patients. This is unfortunate, as CMV reactivation can further exacerbate liver failure and increase mortality. In this report, we present a case of hemorrhagic varicella reactivation with cytomegalovirus and provide some relevant discussions. CASE PRESENTATION: We present the case of a 25-year-old male with HV, who had a history of nephrotic syndrome generally controlled with orally administered prednisone at a dosage of 50 mg per day for two months. The patient arrived at the emergency room with complaints of abdominal pain and the presence of hemorrhagic vesicles on his body for the past 3 days. Despite medical evaluation, a clear diagnosis was not immediately determined. Upon admission, the leukocyte count was recorded as 20.96 × 109/L on the first day, leading to the initiation of broad-spectrum antibiotic treatment. Despite the general interpretation that a positive IgG and a negative IgM indicate a previous infection, the patient's extraordinarily elevated IgG levels, coupled with a markedly increased CMV DNA quantification, prompted us to suspect a reactivation of the CMV virus. In light of these findings, we opted for the intravenous administration of ganciclovir as part of the treatment strategy. Unfortunately,,the patient succumbed to rapidly worsening symptoms and passed away. Within one week of the patient's demise, chickenpox gradually developed in the medical staff who had been in contact with him. In such instances, we speculate that the patient's diagnosis should be classified as a rare case of hemorrhagic varicella. CONCLUSION: Swift identification and timely administration of suitable treatment for adult HV are imperative to enhance prognosis.

Recurrent Infection by varicella-zoster virus with facial scarring / Infecção recorrente pelo vírus varicela-zoster com sequelas cicatriciais na face

Primary contact with the varicella-zoster virus occurs through varicella (chickenpox) and culminates with this virus entering the sensory nerves and remaining latent in the dorsal root ganglion. Transmission occurs by dissemination of infectious particles of the varicella-zoster virus by the aerosol released from nasopharyngeal secretions or skin lesions, or by direct contact with lesions. Herpes zoster occurs after clinically evident reactivation of the virus, affecting the whole distribution of the infected sensory nerve. When compared with primary infection, herpes zoster has a more severe character, requiring the use of pharmaceutical drugs. The cause of reactivation is unknown and may be associated with predisposing factors, such as age, stress or impaired immune system. This study reports a case of a patient who presented clinical manifestations compatible with varicella zoster infection exacerbated by the use of homemade remedies, resulting in a secondary infection and facial scarring.

O contato primário com o vírus varicela-zoster ocorre na varicela (catapora), culminando com a transposição desse vírus para os nervos sensitivos, onde estabelece sua latência no gânglio espinhal dorsal. A transmissão ocorre por disseminação das partículas infecciosas do vírus varicela-zoster através de aerossóis liberados a partir de secreções do nasofaringe ou lesões cutâneas ou, ainda, pelo contato direto com lesões. O herpes-zoster clinicamente evidente ocorre após a reativação do vírus, com o envolvimento da distribuição do nervo sensitivo afetado. Quando comparado com a infecção primária, o herpes-zoster desenvolve um caráter de maior severidade, sendo sempre necessária a administração de uma terapêutica medicamentosa eficaz. A causa dessa reativação é desconhecida, podendo estar relacionada a fatores predisponentes como a faixa etária, estresse ou imunodeficiências. Neste trabalho relata-se um caso clínico em que a paciente apresentou manifestações clínicas condizentes com um quadro característico de infecção por varicela-zoster, complicado por uso de medicação caseira, resultando em infecção secundária e cicatrizes faciais.

Differentiation of wild-type varicella-zoster strains from India and the Oka vaccine strain using a VZV open reading frame - 62 based PCR-RFLP technique

Since the introduction of varicella vaccination in India, surveillance of circulating VZV strains has gained significance. Differentiating wild-type VZV strains from the Oka vaccine strain can be achieved only by molecular genotyping methods. The development of PCR methods for VZV strain differentiation has been hampered by the fact that the VZV genome is highly conserved. We used VZV ORF 62 PCR-RFLP analysis to identify and differentiate wild-type VZV strains in India from the Oka vaccine strain. Digestion of VZV ORF 62 amplicons with SmaI, enabled accurate strain differentiation; the Oka strain was positive for three SmaI sites, compared to two SmaI sites in the wild-type VZV strains that we tested.

Varicella pneumonia in immunocompetent adults: report of two cases, with emphasis on high-resolution computed tomography findings

We report two cases of varicella pneumonia in immunocompetent patients, with emphasis on high-resolution computer tomography manifestations. The predominant findings consisted of multiple bilateral nodules, ranging from 1-10 mm in diameter, with or without a surrounding halo of ground-glass attenuation. Other findings include ground-glass opacities, focal areas of consolidation and small pleural effusions.

Vitrectomia em necrose progressiva da retina (P.O.R.N. syndrome) em Aids / Vitrectomy in progressive outer retinal necrosis (P.O.R.N. syndrome) in Aids

Apresenta-se um paciente com AIDS e retinite por varicella-zoster vírus (P.O.R.N. syndrome), com descolamento total de retina em olho esquerdo e pequena área de necrose retiniana periférica em olho direito. Foi realizado vitrectomia, endofotocoagulação e injeção de óleo de silicone na cavidade vítrea precocemente no olho direito e aciclovir EV (30 mg/dia) como tentativa de prevenir o descolamento de retina e a progressão da síndrome neste olho. No pós operatório imediato a visão do paciente era de 20/20. No entanto, em 21 dias a visão era de vultos nos dois olhos e 45 dias após o paciente retornava amaurótico.