Insights into the pathogenesis of herpes simplex encephalitis from mouse models
Autor: | Silvia M. Vidal, Mathieu Mancini |
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Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
Central Nervous System viruses Central nervous system Disease Biology Virus Article Pathogenesis 03 medical and health sciences Mice 0302 clinical medicine Immunity Immunopathology Genetics medicine Autophagy Animals Humans Simplexvirus Genetic Predisposition to Disease Myeloid Cells Lymphocytes Immunity Cellular Cell Death medicine.disease Virology Immunity Innate 3. Good health Disease Models Animal 030104 developmental biology medicine.anatomical_structure Viral replication Gene Expression Regulation Host-Pathogen Interactions Interferon Type I Disease Susceptibility Encephalitis Herpes Simplex 030217 neurology & neurosurgery Encephalitis Biomarkers Signal Transduction |
Zdroj: | Mammalian Genome |
ISSN: | 1432-1777 |
Popis: | A majority of the world population is infected with herpes simplex viruses (HSV; human herpesvirus types 1 and 2). These viruses, perhaps best known for their manifestation in the genital or oral mucosa, can also cause herpes simplex encephalitis, a severe and often fatal disease of the central nervous system. Antiviral therapies for HSV are only partially effective since the virus can establish latent infections in neurons, and severe pathological sequelae in the brain are common. A better understanding of disease pathogenesis is required to develop new strategies against herpes simplex encephalitis, including the precise viral and host genetic determinants that promote virus invasion into the central nervous system and its associated immunopathology. Here we review the current understanding of herpes simplex encephalitis from the host genome perspective, which has been illuminated by groundbreaking work on rare herpes simplex encephalitis patients together with mechanistic insight from single-gene mouse models of disease. A complex picture has emerged, whereby innate type I interferon-mediated antiviral signaling is a central pathway to control viral replication, and the regulation of immunopathology and the balance between apoptosis and autophagy are critical to disease severity in the central nervous system. The lessons learned from mouse studies inform us on fundamental defense mechanisms at the interface of host-pathogen interactions within the central nervous system, as well as possible rationales for intervention against infections from severe neuropathogenic viruses. |
Databáze: | OpenAIRE |
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