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      Herpes simplex virus encephalitis in human UNC-93B deficiency.

      Science (New York, N.Y.)
      Child, Preschool, Cytokines, biosynthesis, Encephalitis, Herpes Simplex, genetics, immunology, Female, Genetic Predisposition to Disease, Herpesvirus 1, Human, Humans, Infant, Interferon-alpha, Interferon-beta, Interferon-gamma, Interferons, Leukocytes, Mononuclear, Male, Membrane Transport Proteins, deficiency, physiology, Mutation, Pedigree, Signal Transduction, Toll-Like Receptor 3, agonists, Toll-Like Receptors

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          Abstract

          Herpes simplex virus-1 (HSV-1) encephalitis (HSE) is the most common form of sporadic viral encephalitis in western countries. Its pathogenesis remains unclear, as it affects otherwise healthy patients and only a small minority of HSV-1-infected individuals. Here, we elucidate a genetic etiology for HSE in two children with autosomal recessive deficiency in the intracellular protein UNC-93B, resulting in impaired cellular interferon-alpha/beta and -lambda antiviral responses. HSE can result from a single-gene immunodeficiency that does not compromise immunity to most pathogens, unlike most known primary immunodeficiencies. Other severe infectious diseases may also reflect monogenic disorders of immunity.

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