Primary and Acquired Immunodeficiencies Associated With Severe Varicella-Zoster Virus Infections
| Autor: | Rahila Ansari, Robert A. Bonomo, Andrea Lisco, Steven M. Holland, Christa S. Zerbe, Donald H. Gilden, Jeffrey I. Cohen, Lindsey B. Rosen |
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| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Microbiology (medical) Herpesvirus 3 Human viruses medicine.disease_cause Herpes Zoster Virus 03 medical and health sciences 0302 clinical medicine Immune system Chickenpox Interferon medicine Humans Online only Articles Immunodeficiency biology integumentary system business.industry Autoantibody Varicella zoster virus virus diseases Interferon-alpha medicine.disease 030104 developmental biology Infectious Diseases 030220 oncology & carcinogenesis Immunology biology.protein Leukocytes Mononuclear Antibody business medicine.drug |
| Zdroj: | Clin Infect Dis |
| ISSN: | 1537-6591 |
| Popis: | BackgroundAlthough most cases of varicella or zoster are self-limited, patients with certain immune deficiencies may develop severe or life-threatening disease.MethodsWe studied a patient with varicella-zoster virus (VZV) central nervous system (CNS) vasculopathy and as part of the evaluation, tested his plasma for antibodies to cytokines. We reviewed the literature for cases of varicella or zoster associated with primary and acquired immunodeficiencies.ResultsWe found that a patient with VZV CNS vasculopathy had antibody that neutralized interferon (IFN)-α but not IFN-γ. The patient’s plasma blocked phosphorylation in response to stimulation with IFN-α in healthy control peripheral blood mononuclear cells. In addition to acquired immunodeficiencies like human immunodeficiency virus (HIV) or autoantibodies to IFN, variants in specific genes have been associated with severe varicella and/or zoster. Although these genes encode proteins with very different activities, many affect IFN signaling pathways, either those that sense double-stranded RNA or cytoplasmic DNA that trigger IFN production, or those involved in activation of IFN stimulated genes in response to binding of IFN with its receptor.ConclusionsImmune deficiencies highlight the critical role of IFN in control of VZV infections and suggest new approaches for treatment of VZV infection in patients with certain immune deficiencies. |
| Databáze: | OpenAIRE |
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