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	Identification of immune correlates of fatal outcomes in critically ill COVID-19 patients Jonathan Youngs , Nicholas M. Provine , Nicholas Lim , Hannah R. Sharpe , Ali Amini , Yi-Ling Chen , Jian Luo , Matthew D. Edmans , Panagiota Zacharopoulou , Wentao Chen , Oliver Sampson , Robert Paton , William J. Hurt , David A. Duncan , Anna L. Mcnaughton , Vincent N. Miao , Susannah Leaver , Duncan L. A. Wyncoll , Jonathan Ball , Philip Hopkins , Donal T. Skelly , Eleanor Barnes , Susanna Dunachie , Graham Ogg , Teresa Lambe , Ian Pavord , Alex K. Shalek , Craig P. Thompson , Luzheng Xue , Derek C. Macallan , Philip Goulder , Paul Klenerman , Tihana Bicanic Plos Pathogens 17 DOI: 10.1371/journal.ppat.1009804 Open Access Show Abstract ▼ Abstract: Prior studies have demonstrated that immunologic dysfunction underpins severe illness in COVID-19 patients, but have lacked an in-depth analysis of the immunologic drivers of death in the most critically ill patients. We performed immunophenotyping of viral antigen-specific and unconventional T cell responses, neutralizing antibodies, and serum proteins in critically ill patients with SARS-CoV-2 infection, using influenza infection, SARS-CoV-2-convalescent health care workers, and healthy adults as controls. We identify mucosal-associated invariant T (MAIT) cell activation as an independent and significant predictor of death in COVID-19 (HR = 5.92, 95% CI = 2.49–14.1). MAIT cell activation correlates with several other mortality-associated immunologic measures including broad activation of CD8+ T cells and non-Vδ2 γδT cells, and elevated levels of cytokines and chemokines, including GM-CSF, CXCL10, CCL2, and IL-6. MAIT cell activation is also a predictor of disease severity in influenza (ECMO/death HR = 4.43, 95% CI = 1.08–18.2). Single-cell RNA-sequencing reveals a shift from focused IFNα-driven signals in COVID-19 ICU patients who survive to broad pro-inflammatory responses in fatal COVID-19 –a feature not observed in severe influenza. We conclude that fatal COVID-19 infection is driven by uncoordinated inflammatory responses that drive a hierarchy of T cell activation, elements of which can serve as prognostic indicators and potential targets for immune intervention.	Sep 2021
	Pre-existing asthma as a comorbidity does not modify cytokine responses and severity of COVID-19 Jian Luo , Yi-Ling Chen , Wentao Chen , David A. Duncan , Alexander Mentzer , Julian C. Knight , Graham Ogg , Paul Klenerman , Ian D. Pavord , Luzheng Xue Allergy, Asthma & Clinical Immunology 17 DOI: 10.1186/s13223-021-00569-8 Open Access Show Abstract ▼ Abstract: Background: A significant portion of COVID-19 sufferers have asthma. The impacts of asthma on COVID-19 progression are still unclear but a modifying effect is plausible as respiratory viruses are acknowledged to be an important trigger for asthma exacerbations and a different, potentially type-2 biased, immune response might occur. In this study, we compared the blood circulating cytokine response to COVID-19 infection in patients with and without asthma. Methods: Plasma samples and clinical information were collected from 80 patients with mild (25), severe (36) or critical (19) COVID-19 and 29 healthy subjects at the John Radcliffe Hospital, Oxford, UK. The concentrations of 51 circulating proteins in the plasma samples were measured with Luminex and compared between groups. Results: Total 16 pre-existing asthma patients were found (3 in mild, 10 in severe, and 3 in critical COVID-19). The prevalence of asthma in COVID-19 severity groups did not suggest a clear correlation between asthma and COVID-19 severity. Within the same COVID-19 severity group, no differences were observed between patients with or without asthma on oxygen saturation, CRP, neutrophil counts, and length of hospital stay. The mortality in the COVID-19 patients with asthma (12.5%) was not higher than that in patients without asthma (17.2%). No significant difference was found between asthmatic and non-asthmatic in circulating cytokine response in different COVID-19 severity groups, including the cytokines strongly implicated in COVID-19 such as CXCL10, IL-6, CCL2, and IL-8. Conclusions: Pre-existing asthma was not associated with an enhanced cytokine response after COVID-19 infection, disease severity or mortality.	Jul 2021

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