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.
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