PMC:7402624 / 49160-50536
Annnotations
{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7402624","sourcedb":"PMC","sourceid":"7402624","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7402624","text":"Given the association of the UMAP Component 1 with disease severity, we next examined the connections between UMAP Components with individual clinical features. UMAP Component 1 correlated with several clinical measurements of inflammation (e.g., ferritin, hsCRP, IL-6), co-infection, organ failure (APACHE III), and acute kidney disease and renal insufficiency (Fig. 6I). It was interesting, however, that, although D-dimer was elevated, this feature did not correlate with UMAP Component 1, but coagulation complication did (Fig. 6I). Several antibody features also correlated with Component 1 consistent with some of the immune features discussed above. In contrast, Component 2 lacked positive correlation to many of these clinical features of disease and rather was negatively correlated only to eosinophil count, NSAID use, and subsequent treatment with Remdesivir (Fig. 6I). UMAP Component 1, but not Component 2, also correlated with mortality, although there were clearly patients with high Component 2, but low Component 1 who succumbed to COVID-19 disease (Fig. 6E). These data indicate that the immune features captured by UMAP Component 1 have a strong relationship to many features of disease severity, whereas other features of immune dynamics during COVID-19 disease captured by UMAP Component 2 have a distinct relationship with clinical disease 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