Severe immunosuppression and not a cytokine storm characteri
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COVID-19-associated morbidity and mortality have been attributed to a pathologic host response. Two divergent hypotheses have been proposed: a hyper-inflammatory ‘cytokine-storm’-mediated injury versus failure of host protective immunity resulting in unrestrained viral dissemination and organ injury.

A key explanation for the inability to address this controversy has been the lack of diagnostic tools to evaluate immune function in COVID-19 infections.

-- ELISpot, a highly sensitive, functional immunoassay was employed in 27 COVID-19, 51 septic, 18 critically-ill non-septic (CINS), and 27 healthy controls to evaluate adaptive and innate immune status by quantitating T cell IFN-gamma and monocyte TFN-alpha production.
-- Circulating T cell subsets were profoundly reduced in COVID-19 patients.
-- Additionally, stimulated blood mononuclear cells produced less than 40% to 50% of the IFN-gamma and TNF-alpha observed in septic and CINS patients, consistent with markedly impaired immune effector cell function.
-- Approximately 25% of COVID-19 patients had increased IL-6 levels greater than 1,000 pg/mL that were not associated with elevations in other canonical pro-inflammatory cytokines.

Collectively, these findings support the hypothesis that COVID-19 suppresses host functional adaptive and innate immunity. Importantly, Interleukin-7 administered ex vivo restored T cell IFN-gamma production in COVID-19 patients. Thus, ELISpot may functionally characterize host immunity in COVID-19 and inform prospective therapies.

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