Author Correction: A dynamic COVID-19 immune signature includes associations with poor prognosis

Laing, Adam; Lorenc, Anna; Barrio, Irene del Molino del; Das, Abhishek; Fish, Matthew; Monin, Leticia; Muñoz-Ruiz, Miguel; McKenzie, Duncan R.; Hayday, Thomas; Francos-Quijorna, Isaac; Kamdar, Shraddha; Joseph, Magdalene; Davies, Daniel; Davis, Richard P.; Jennings, A.R.; Zlatareva, Iva; Vantourout, Pierre; Wu, Yin; Sofra, Vasiliki; Cano, Florencia; Greco, Maria; Theodoridis, Efstathios; Freedman, Joshua D.; Gee, Sarah; Chan, Joseph L.-K.; Ryan, Sarah; Bugallo-Blanco, Eva; Peterson, Pärt; Kisand, Kai; Haljasmägi, Liis; Chadli, Loubna; Moingeon, Philippe; Martinez, Lauren; Merrick, Blair; Bisnauthsing, Karen; Brooks, Kate; Ibrahim, Mohammad; Mason, Jeremy; Gómez, Federico López; Babalola, Kola; Abdul-Jawad, Sultan; Cason, John; Mant, Christine; Seow, Jeffrey; Graham, Carl; Doores, Katie J.; Rosa, Francesca Di; Edgeworth, Jonathan D; Shankar-Hari, Manu; Hayday, Adrian

doi:10.1038/s41591-020-01186-5

Cited by 67 publications

(43 citation statements)

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“…Finally, regarding COVID-19-induced “cytokine storm”, i.e., the uncontrolled systemic inflammatory response that relates to the release of high amounts of pro-inflammatory cytokines along with complement components, coagulation dysfunction and immunological “misfiring” [ 68 , 123 – 126 ]; the idea of adjunct immunotherapies which inhibit key pro-inflammatory pathways such as IL-6 signaling [ 127 , 128 ] is a reasonable approach. More specifically, studies in animal models and cell-based assays following SARS-CoV-2 infection, as well as serum and transcriptional profiling of COVID-19 patients, revealed an exaggerated abnormal inflammatory response being marked by reduced levels of type I and III IFNs, along with increased chemokines and IL-6 expression [ 129 ].…”

Section: Targeting the Adverse Effects Of Covid-19mentioning

confidence: 99%

Insights to SARS-CoV-2 life cycle, pathophysiology, and rationalized treatments that target COVID-19 clinical complications

et al. 2021

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Background Gaining further insights into SARS-CoV-2 routes of infection and the underlying pathobiology of COVID-19 will support the design of rational treatments targeting the life cycle of the virus and/or the adverse effects (e.g., multi-organ collapse) that are triggered by COVID-19-mediated adult respiratory distress syndrome (ARDS) and/or other pathologies. Main body COVID-19 is a two-phase disease being marked by (phase 1) increased virus transmission and infection rates due to the wide expression of the main infection-related ACE2, TMPRSS2 and CTSB/L human genes in tissues of the respiratory and gastrointestinal tract, as well as by (phase 2) host- and probably sex- and/or age-specific uncontrolled inflammatory immune responses which drive hyper-cytokinemia, aggressive inflammation and (due to broad organotropism of SARS-CoV-2) collateral tissue damage and systemic failure likely because of imbalanced ACE/ANGII/AT1R and ACE2/ANG(1–7)/MASR axes signaling. Conclusion Here we discuss SARS-CoV-2 life cycle and a number of approaches aiming to suppress viral infection rates or propagation; increase virus antigen presentation in order to activate a robust and durable adaptive immune response from the host, and/or mitigate the ARDS-related “cytokine storm” and collateral tissue damage that triggers the severe life-threatening complications of COVID-19.

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Section: Targeting the Adverse Effects Of Covid-19mentioning

confidence: 99%

Insights to SARS-CoV-2 life cycle, pathophysiology, and rationalized treatments that target COVID-19 clinical complications

et al. 2021

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“…Severe COVID-19 is associated with a number of distinct immunological signatures. For example, increased serum levels of proinflammatory cytokines such as IL-1β, IL-6, IP-10, and TNFα and the alarmins S100A8 and S100A9 are associated with worse outcomes (7)(8)(9)(10)(11)(12). Patients with less severe disease tend to have both lower levels of proinflammatory cytokines and higher levels of tissue repair factors (9).…”

Section: Introductionmentioning

confidence: 99%

Multi-omic profiling reveals widespread dysregulation of innate immunity and hematopoiesis in COVID-19

Wilk

Lee

Wei

et al. 2020

Preprint

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Our understanding of protective vs. pathologic immune responses to SARS-CoV-2, the virus that causes Coronavirus disease 2019 (COVID-19), is limited by inadequate profiling of patients at the extremes of the disease severity spectrum. Here, we performed multi-omic single-cell immune profiling of 64 COVID-19 patients across the full range of disease severity, from outpatients with mild disease to fatal cases. Our transcriptomic, epigenomic, and proteomic analyses reveal widespread dysfunction of peripheral innate immunity in severe and fatal COVID-19, with the most profound disturbances including a prominent neutrophil hyperactivation signature and monocytes with anti-inflammatory features. We further demonstrate that emergency myelopoiesis is a prominent feature of fatal COVID-19. Collectively, our results reveal disease severity-associated immune phenotypes in COVID-19 and identify pathogenesis-associated pathways that are potential targets for therapeutic intervention.One Sentence SummarySingle-cell profiling demonstrates multifarious dysregulation of innate immune phenotype associated with COVID-19 severity.

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“…Recent studies further confirmed IL-1, IL-10 and TNF-α in patients with severe COVID-19 were 2 to 100 times greater than normal levels, whereas IL-6 showed larger increases, even more than 1000 fold over the normal. Paralleled studies found markedly elevated IL-6 ranging from 100 to 10 000 pg/mL in severe patients [ [43] , [44] , [45] , [46] ]. While the emerging coronaviruses present similar clinical symptoms, the laboratory findings are characterized by distinct cytokine profiles ( Table 1 ).…”

Section: Cytokine Responses During Coronavirus Infectionmentioning

confidence: 66%

An enlightening role for cytokine storm in coronavirus infection

Zhao

Wei

Tao

2021

Clinical Immunology

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The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) outbreak in Wuhan, China has dispersed rapidly worldwide. Although most patients present with mild fever, cough with varying pulmonary shadows, a significant portion still develops severe respiratory dysfunction. And these severe cases are often associated with manifestations outside the respiratory tract. Currently, it is not difficult to find inflammatory cytokines upregulated in the blood of infected patients. However, some complications in addition to respiratory system with the coronavirus disease 2019 (COVID-19) are impossible to explain or cannot be attributed to virus itself. Thus excessive cytokines and their potentially fatal adverse effects are probably the answer to the multiple organ dysfunctions and growing mortality. This review provides a comprehensive overview of the mechanisms underlying cytokine storm, summarizes its pathophysiology and improves understanding of cytokine storm associated with coronavirus infections by comparing SARS-CoV-2 with severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV).

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Author Correction: A dynamic COVID-19 immune signature includes associations with poor prognosis

Cited by 67 publications

References 0 publications

Insights to SARS-CoV-2 life cycle, pathophysiology, and rationalized treatments that target COVID-19 clinical complications

Insights to SARS-CoV-2 life cycle, pathophysiology, and rationalized treatments that target COVID-19 clinical complications

Multi-omic profiling reveals widespread dysregulation of innate immunity and hematopoiesis in COVID-19

An enlightening role for cytokine storm in coronavirus infection

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