Background: Pure red cell aplasia is characterized by anemia, reticulocytopenia and diminished bone marrow erythroid precursors. It has multifactorial etiology and consequently several therapeutic interventions.
Case: In August 2017, a young patient was diagnosed to have pure red cell aplasia. She was given immunosuppressive therapy for approximately two months but this treatment was stopped due to intolerance. Later on she developed herpes zoster infection that was treated with valacyclovir. Subsequently, it was noted that the patient became blood transfusion independent due to normalization of her hemoglobin and regeneration of the erythroid precursors in the bone marrow.
Discussion: Varicella zoster virus behaves differently from other members of the herpes group of viruses such as cytomegalovirus and Epstein-Barr virus. Two retrospective studies, performed in patients with malignant hematological disorders and bone marrow failure, have shown that infection with the virus may cause stimulation of the three cell lines in the bone marrow and superior overall survival.
Conclusion: The outcome of the patient presented confirms the findings of the two studies showing long-term beneficial effects of varicella zoster virus infections in immunocompromised individuals.
Varicella zoster virus (VZV), a double-stranded DNA virus, is a highly contagious human neurotropic virus that belongs to the alpha group of herpes viruses [1-4]. Primary VZV infection (chickenpox) occurs in childhood then the virus becomes latent in the nerve ganglia [1,5-7]. Reactivation of the virus may occur decades later and cause herpes zoster (HZ) which is manifested by a typical painful skin eruption that has characteristic dermatomal distribution [1,5]. Reactivation of VZV is usually predisposed to: old age; comorbid medical conditions such as diabetes mellitus, chronic obstructive airway disease, and end-stage renal disease; and immunosuppression due to malignancy, autoimmune disorders, immunosuppressive therapies, trauma, cytotoxic chemotherapy, hematopoietic stem cell transplantation (HSCT), and solid organ transplantation (SOT) [1,5-7].
Varicella zoster virus behaves differently from other herpes viruses as it differs from them in many aspects. Recently, there has been growing evidence on the beneficial effects of the virus in immune compromised hosts and these effects are translated into prolongation of survival. The reported beneficial effects of the virus include: (1) stimulation of bone marrow activity in patients with hematologic malignancies and bone marrow failure syndromes, (2) antitumor effects in various hematologic malignancies and solid tumors, and (3) association with graft versus host disease which has anticancer effects. Additionally, there are several reports on the safety of the live-attenuated even in severely immune suppressed individuals and on the emerging role of the virus in cancer immunotherapy. In this review, the following aspects of the virus will be thoroughly discussed: (1) new data on the genetic background, pathogenesis, vaccination, and new therapeutic modalities; (2) bone marrow microenvironment and hematopoiesis; (3) cells involved in the pathogenesis of the virus such as: mesenchymal stem cells, dendritic cells, natural killer cells, T-cells and mononuclear cells; (4) cellular proteins such as open reading frames, glycoproteins, promyelocytic leukemia protein, chaperons, and SUMOs; (5) extracellular vesicles, exosomes, and micro-RNAs; and (6) signaling pathways, cytokines, and interferons.
Introduction: Primary infection with varicella-zoster virus (VZV) results in chickenpox, characterized by viremia with a diffuse rash and seeding of multiple sensory ganglia, where the virus establishes lifelong latency. Herpes zoster is caused by reactivation of latent VZV in cranial-nerve or dorsal-root ganglia, with spread of the virus along the sensory nerve to the dermatome. Both entities have a benign clinical course in immunocompetent and young individuals. Although Herpes zoster virüs may result in Ramsey Hunt sendrom, it may rarely cause peripheral facial paralysis in the course of varicella.
Case report: A 4-year-old girl patient was admitted to the ear, nose, and throat clinic with a complaint of a rash over the body with vesicles and pustules a few days. She had left peripheral facial palsy about 2 days ago. In a general clinical examination, a few macular lesions, probably residues of vesicles, and fluid-filled blisters and pustules were observed on the back, chest, abdomen, upper, and lower limbs. She had remarkable left peripheral facial palsy. Her facial palsy was assessed as a grade II using the House-Brackmann Score. Otoscopic examination was normal and otalgia and auricular vesicle was absent. 1 mg/kg/day prednisone and 30 mg/kg/day acyclovir therapy were given to the patient due to the peripheral facial nerve palsy involvement of the VZV infection. Complete remission was achieved at 1 month after treatment.
Conclusion: Varicella-zoster virus (VZV) is one of eight herpes viruses known to cause human infection and is distributed worldwide. While the results of bell palsy are good, facial paralysis results during viral infections are severe. Cranial nerve involvement secondary to viral infection should be followed closely. The current standard of care for treatment is acyclovir and prednisone. Thus early treatment can be started in the face of developing complications and possible mortality and morbidity can be prevented.
Eucalyptus camaldulensis (Ec) is considered as a traditional medicinal plant with valuable therapeutic effects. Here we evaluated the antiviral activity of its ethanolic leave extract on different herpes viruses. Vero cells were infected with either of the tested viruses [herpes simplex virus -1 and 2 (HSV-1, HSV-2) and Varicella-Zoster Virus (VZV)] with or without treatment with Ec extract and viral infection development was evaluated by plaque assay. Our results showed significant antiviral activity of the examined extract against all tested viruses. The 80%-MeOH fraction of this extract offered the highest activity against these viruses with 50% inhibitory concentration (IC50) of 0.1±0.08, 0.3±0.02 and 1±0.03 μg/ml against HSV-1, HSV-2 and VZV respectively and 50% cytotoxicity (CC50) at 700 μg/ml. The highest antiviral effect of this fraction was obtained mainly when it was added during and post infection (p.i.) or when it was added only p.i. Also, this fraction significantly reduced the amount of infective endogenous viral particles in cells that were treated with the 80%-MeOH fraction only post viral entry into the host cells. A synergistic antiviral effect against all tested viruses was also observed when cells were treated with a combination of acyclovir (ACV) and 80%-MeOH fraction of Ec. Further study is required for the isolation and identification of the anti-virally active component/s of this fraction.
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