Pathogenic human coronavirus infections: causes and consequences of cytokine storm and immunopathology
By Rudragouda Channappanavar, S. Perlman. Seminars in Immunopathology, 2017
2,337 citations recorded by the source corpus.
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.
Subfields: Infectious Diseases, Neurology
View Paper: https://www.semanticscholar.org/paper/3ccc7934a191f66aeef572f322381ca15512e450
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Citations in the corpus
- Molecular immune pathogenesis and diagnosis of COVID-19 (2020, neutral): “) by immune effector cells in SARS-CoV infection[15, 35-37].”
- Mechanisms of SARS-CoV-2 Transmission and Pathogenesis (2020, neutral): “Recent evidence suggests that systemic inflammation induces long-term sequela in heart tissues [66,79,80,82,84,87,90,95].”
- The use of anti-inflammatory drugs in the treatment of people with severe coronavirus disease 2019 (COVID-19): The Perspectives of clinical immunologists from China (2020, background): “In coronavirus pneumonia, such as severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS), accompanied by rapid virus replication, a large number of inflammatory cell infiltration and CS led to acute lung injury, acute respiratory distress syndrome (ARDS) and death [1, 2”
- Dysregulation of Immune Response in Patients With Coronavirus 2019 (COVID-19) in Wuhan, China (2020, background): “Virus-induced direct cytopathic effects and viral evasion of host immune responses are believed to play major roles in disease severity [15, 16].”
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- Anxiety and depression in COVID-19 survivors: Role of inflammatory and clinical predictors (2020, neutral): “Moreover, in COVID-19, unlike in SARS and MERS, elevated levels of T-helper-2 cell-secreted cytokines (such as IL-4 and IL-10) were found (Ye et al., 2020; Channappanavar and Perlman, 2017).”
- Longitudinal characteristics of lymphocyte responses and cytokine profiles in the peripheral blood of SARS-CoV-2 infected patients (2020, neutral): “The severity of pathological injury during SARS or MERS correlates with the extensive infiltration of neutrophils in the lung and increased neutrophil numbers in the peripheral blood [19].”
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- SARS-CoV-2 Receptor ACE2 Is an Interferon-Stimulated Gene in Human Airway Epithelial Cells and Is Detected in Specific Cell Subsets across Tissues (2020, neutral): “Whether type I IFNs are net protective or detrimental to the host might depend on the stage of infection; cell subsets in question; the SARS viral clade (Channappanavar et al., 2016; Channappanavar et al., 2019; Channappanavar and Perlman, 2017; Davidson et al., 2015); and other factors such as co-i”
- Evasion of Type I Interferon by SARS-CoV-2 (2020, background): “Coronaviruses use various approaches to evade the host immune response, including antagonizing IFN production, inhibiting IFN signaling, and enhancing IFN resistance (Channappanavar and Perlman, 2017; Kindler et al., 2016; Totura and Baric, 2012).”
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