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. 2023 Jul 27;11:1229393. doi: 10.3389/fcell.2023.1229393

FIGURE 1.

FIGURE 1

The possible mechanisms of lncRNAs in SARS-CoV-2 infection. Green lines mean upregulating expression or promoting process. Red lines mean downregulating gene expression. Green lncRNAs is antiviral response related lncRNAs. Blue lncRNAs is immune escape related lncRNAs. Red lncRNAs is cytokine storm related lncRNAs. Some lncRNAs boost antiviral responses by triggering innate or adaptive immunity or by increasing the production of antiviral components. NEAT1 relocated splicing factor proline- and glutamine-rich protein (SFPQ) to the paraspeckles, removing the transcriptional inhibitory effects of SFPQ. PIRAT interacts with PU.1 to produce alarmin S100A8/A9. Lnc02384 enhances the expression of IFN-IFN-γ-encoding genes and increases TGFβ-1 mRNA transcript levels by uptaking miR-891a-5p. RORA-AS-7 and RORA-AS-8 regulate RORA genes, LINC-JUND-1 and FOSL2-AS-1 regulate FOSL2 and JUNB, and HIF1A-AS-1 and LINC-HSP90AA1-1 regulate HIF1A, all of which are associated with AP-1 and promote T-cell activation, differentiation and enhancing effects. KCNQ1OT1 interacts with the TLR2 gene which identifies PAMP and functions through MYD88 and TRAF6 to cause NF-κB activation. CHROMR isolated nuclear transcriptional co-blocker IRF2BP2 and IRF-2. Other lncRNAs will aid SARS-CoV-2 in escaping the immune system and escalating bodily tissue harm. LncATV and Lnc-Lsm3b bind and inhibit RIG-I-mediated innate immune activation. LncRNA Lethe binds to NF-κB to inhibit Rela DNA binding and target gene activation. LncRNA LUCAT1 limits the expression of STAT targets and reduces the generation of interferon. LncRNA EGOT and CMPK2 are involved in the control of ISGs. NEAT1 enhances caspase-1 activation by attaching to pro-caspase-1 and encouraging the activation of NLRP3 inflammasomes. NEAT1 as well as competitively binds miR-1246 and releases NAKP, which mediates NF-κB activation. Additionally, upregulated NEAT1 competitively binds Let-7a and releases TLR4 from it, activating TLR4 and stimulating downstream signaling. GAS5 decreases miR-223-3p expression, which increases NLRP3 expression levels and promotes pyroptosis and downregulates miR-23a-3p levels, which can inhibit the TLR4/TNF-α/IL-10 signaling pathway. MALAT1 suppresses the creation of NLRP3 inflammasomes by sponging miR-23C, preventing its repressive impact on the target gene ELAV1. NORAD is involved in the NF-κB signaling pathway through the miR-552-39/MYD88 axis in TNF-α induced apoptosis and inflammation. RAD51-AS1 leads to the expression of pro-inflammatory cytokines.