A. Laing, A. Lorenc, I. del Molino del Barrio, Abhishek Das, M. Fish, L. Monin, M. Muñoz-Ruiz, Duncan R. McKenzie, T. Hayday, Isaac Francos-Quijorna, S. Kamdar, Magdalene Joseph, Daniel Davies, Richard Davis, Aislinn Jennings, I. Zlatareva, P. Vantourout, Yin Wu, V. Sofra, Florencia Cano, M. Greco, E. Theodoridis, Joshua Freedman, S. Gee, Julie Nuo En Chan, Sarah Ryan, Eva Bugallo-Blanco, P. Peterson, K. Kisand, Liis Haljasmägi, Lauren Martinez, B. Merrick, K. Bisnauthsing, Kate Brooks, Mohammad Ibrahim, Jeremy Mason, F. L. Gomez, K. Babalola, Sultan Abdul- Jawad, J. Cason, C. Mant, K. Doores, J. Seow, C. Graham, F. Rosa, J. Edgeworth, M. Shankar-Hari, A. Hayday
medRxiv, 2020
Person-to-person transmission of SARS-CoV-2 virus has triggered a global emergency because of its potential to cause life-threatening Covid-19 disease. By comparison to pauci-symptomatic virus clearance by most individuals, Covid-19 has been proposed to reflect insufficient and/or pathologically exaggerated immune responses. Here we identify a consensus peripheral blood immune signature across 63 hospital-treated Covid-19 patients who were otherwise highly heterogeneous. The core signature conspicuously blended adaptive B cell responses typical of virus infection or vaccination with discrete traits hitherto associated with sepsis, including monocyte and dendritic cell dampening, and hyperactivation and depletion of discrete T cell subsets. This blending of immuno-protective and immuno-pathogenic potentials was exemplified by near-universal CXCL10/IP10 upregulation, as occurred in SARS1 and MERS. Moreover, specific parameters including CXCL10/IP10 over-expression, T cell proliferation, and basophil and plasmacytoid dendritic cell depletion correlated, often prognostically, with Covid-19 progression, collectively composing a resource to inform SARS-CoV-2 pathobiology and risk-based patient stratification.
Cited by 32 publications.
Field of study: Biology