期刊
SEMINARS IN IMMUNOPATHOLOGY
卷 39, 期 5, 页码 529-539出版社
SPRINGER HEIDELBERG
DOI: 10.1007/s00281-017-0629-x
关键词
SARS-CoV; MERS-CoV; Cytokine storm; Immunopathology; Interferon; Monocyte-macrophage
资金
- N.I.H. [PO1 AI060699, RO1 AI091322]
Human coronaviruses (hCoVs) can be divided into low pathogenic and highly pathogenic coronaviruses. The low pathogenic CoVs infect the upper respiratory tract and cause mild, cold-like respiratory illness. In contrast, highly pathogenic hCoVs such as severe acute respiratory syndrome CoV (SARS-CoV) and Middle East respiratory syndrome CoV (MERS-CoV) predominantly infect lower airways and cause fatal pneumonia. Severe pneumonia caused by pathogenic hCoVs is often associated with rapid virus replication, massive inflammatory cell infiltration and elevated proinflammatory cytokine/chemokine responses resulting in acute lung injury (ALI), and acute respiratory distress syndrome (ARDS). Recent studies in experimentally infected animal strongly suggest a crucial role for virus-induced immunopathological events in causing fatal pneumonia after hCoV infections. Here we review the current understanding of how a dysregulated immune response may cause lung immunopathology leading to deleterious clinical manifestations after pathogenic hCoV infections.
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