Cytokine Biomarkers of Inflammatory Response in COVID-19 Patients

Event Date

June 11, 2020 | 1:00-2:00 pm EDT

Discussions:

Ultrasensitive SIMOA™ Immunoassays Impacting COVID-19, Infectious Diseases, and Immunology

Kevin Hrusovsky, President, Chairman and CEO, Quanterix

Dan Sikkema, PhD, Vice President, Accelerator and Pharma Services, Quanterix

As COVID-19 pandemic preparedness initiatives ramp up to address the current crisis, one area of focus has been the improvement of testing methods to re-open society. Differentiating early symptoms from other respiratory pathogens that have a similar clinical presentation, identifying those patients at risk for severe symptoms such as “cytokine storm”, and determining immunity status have been hallmarks of scientific efforts over the past several months. The Quanterix SIMOA™ platform is an ultra-sensitive immunoassay system that is typically 100-1000-fold more sensitive than most ELISA systems. This level of sensitivity offers the ability to detect and quantitate key cytokines involved early in the disease progression and provides insight like “a radar system” into “prediction” of subsequent immune complications. Here we describe efforts around frontline immunological and serologic assessments of COVID-19 patients and examples of historical approaches for auto-immune, vaccine, and infectious disease research using SIMOA technology.

Impaired Type I Interferon Activity and Exacerbated Inflammatory Responses in Severe Covid-19 Patients

Darragh Duffy, PhD, Scientific Manager, LabEx Milieu Interieur, Institut Pasteur

Coronavirus disease 2019 (Covid-19) is characterized by distinct patterns of disease progression implying diverse host immune responses. We performed an integrated immune analysis on a cohort of fifty Covid19 patients with various disease severity. A unique phenotype in severe and critical patients was identified. It consisted of a profoundly impaired interferon (IFN) type I response characterized by no IFN-b and low IFN-a production and activity, associated with a persistent blood virus load and exacerbated inflammatory response. The cytokine storm was partially driven by the transcriptional factor NFkB and characterized by increased tumor necrosis factor (TNF)- a and interleukin (IL)-6 production and signaling. We propose that type-I IFN deficiency in the blood could be a hallmark of severe Covid-19 and provide a rationale for combined therapeutic approaches.

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