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Semin Immunopathol. 2017 Jul;39(5):529-539. doi: 10.1007/s00281-017-0629-x. Epub 2017 May 2.

Pathogenic human coronavirus infections: causes and consequences of cytokine storm and immunopathology.

Author information

1
Department of Microbiology, University of Iowa, BSB 3-712, Iowa City, IA, 52242, USA.
2
Department of Microbiology, University of Iowa, BSB 3-712, Iowa City, IA, 52242, USA. Stanley-perlman@uiowa.edu.

Abstract

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 pro-inflammatory 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.

KEYWORDS:

Cytokine storm; Immunopathology; Interferon; MERS-CoV; Monocyte-macrophage; SARS-CoV

PMID:
28466096
PMCID:
PMC7079893
DOI:
10.1007/s00281-017-0629-x
[Indexed for MEDLINE]
Free PMC Article

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