AI Article Synopsis
- * Severe and critical cases showed a significant reduction in type I interferon (IFN) responses, leading to high viral loads and heightened inflammation.
- * The inflammation was linked to increased production of tumor necrosis factor-α and interleukin-6, indicating potential targets for combined treatment strategies in severe COVID-19 cases.
Article Abstract
Coronavirus disease 2019 (COVID-19) is characterized by distinct patterns of disease progression that suggest diverse host immune responses. We performed an integrated immune analysis on a cohort of 50 COVID-19 patients with various disease severity. A distinct phenotype was observed in severe and critical patients, consisting of a highly impaired interferon (IFN) type I response (characterized by no IFN-β and low IFN-α production and activity), which was associated with a persistent blood viral load and an exacerbated inflammatory response. Inflammation was partially driven by the transcriptional factor nuclear factor-κB and characterized by increased tumor necrosis factor-α and interleukin-6 production and signaling. These data suggest 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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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7402632 | PMC |
| http://dx.doi.org/10.1126/science.abc6027 | DOI Listing |
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