LncRNAs harbouring regulatory motifs within repeat elements modulate immune response towards COVID‐19 disease severity and clinical outcomes

SEE PDF] The patient demographics and clinical data are summarised in File S1: Table S1, wherein, the median Ct value of E/RdRp gene was significantly different between recovered/mortality and RS/SOB patients, respectively (Figure 1B,C). Integration of lncRNA–miRNA–mRNA regulatory potential revealed that by virtue of LINC00174:11 downregulation in mortality, miR-1910-3p-mediated elevation of NF-kB signalling and cytokine storm were possible.1 Downregulation of RNASEH1-AS1:23 and ROR1-AS1:6 may modulate heightened immune, inflammatory and stress response, as well as viral replication during mortality, mediated by miR-218-5p and miR-375.2,3 DEG and GSEA analysis of study cohort in conjunction with LncRNA–miRNA–mRNA interaction network, highlight heightened inflammatory response (Files S3–S5; Figure 2C,D). Downregulation of LINC00504:9 and RNASEH1-AS1:23 suggests a decreased inflammatory and antiviral response in the mortality patients, whereas downregulation of MALAT1:9 suggests an increased innate immune response in the mortality, contrary to other findings.6 Upregulation of LUCAT1:3 in mortality indicates activation of interferon immunity, whereas downregulated LINC01537 reflects increased iNOS-mediated stress and decreased T-cell activation in mortality.7,8 MALAT1:9 upregulation in the severe (vs. moderate) indicates decreased immune response in severe, whereas UGDH-AS1:11 downregulation suggests decreased antiviral response and increased disease severity in the severe.5 Finally, LINC00273 downregulation in the mortality group (vs. severe) could possibly explain the decreased early innate immune response in mortality.