| Autor: |
Kafai NM; Department of Medicine, Washington University in St. Louis, St. Louis, Missouri, USA; email: natasha.kafai@wustl.edu, mdiamond@wustl.edu.; Department of Pathology and Immunology, Washington University in St. Louis, St. Louis, Missouri, USA., Diamond MS; Department of Medicine, Washington University in St. Louis, St. Louis, Missouri, USA; email: natasha.kafai@wustl.edu, mdiamond@wustl.edu.; Department of Pathology and Immunology, Washington University in St. Louis, St. Louis, Missouri, USA.; Department of Molecular Microbiology, Washington University in St. Louis, St. Louis, Missouri, USA.; Andrew M. and Jane M. Bursky Center for Human Immunology and Immunotherapy Programs, Washington University in St. Louis, St. Louis, Missouri, USA., Fox JM; Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA; email: julie.fox@nih.gov. |
| Abstrakt: |
Alphaviruses are emerging and reemerging viruses that cause disease syndromes ranging from incapacitating arthritis to potentially fatal encephalitis. While infection by arthritogenic and encephalitic alphaviruses results in distinct clinical manifestations, both virus groups induce robust innate and adaptive immune responses. However, differences in cellular tropism, type I interferon induction, immune cell recruitment, and B and T cell responses result in differential disease progression and outcome. In this review, we discuss aspects of immune responses that contribute to protective or pathogenic outcomes after alphavirus infection. |
