Abstract
Altered expression of protein coding gene (PCG) and long non-coding RNA (lncRNA) have been identified in SARS-CoV-2 infected cells and tissues from COVID-19 patients. The functional role and mechanism (s) of transcriptional regulation of deregulated genes in COVID-19 remain largely unknown. In the present communication, reanalyzing publicly available gene expression data, we observed that 66 lncRNA and 5491 PCG were deregulated in more than one experimental condition. Combining our earlier published results and using different publicly available resources, it was observed that 72 deregulated lncRNA interacted with 3228 genes/proteins. Many targets of deregulated lncRNA could also interact with SARS-CoV-2 coded proteins, modulated by IFN treatment and identified in CRISPR screening to modulate SARS-CoV-2 infection. The majority of the deregulated lncRNA and PCG were targets of at least one of the transcription factors (TFs), interferon responsive factors (IRFs), signal transducer, and activator of transcription (STATs), NFκB, MYC, and RELA/p65. Deregulated 1069 PCG was joint targets of lncRNA and TF. These joint targets are significantly enriched with pathways relevant for SARS-CoV-2 infection indicating that joint regulation of PCG could be one of the mechanisms for deregulation. Over all this manuscript showed possible involvement of lncRNA and mechanisms of deregulation of PCG in the pathogenesis of COVID-19.
Highlights
Coronavirus disease 19 (COVID-19) is caused by infection with severe acute respiratory syndrome corona virus 2 (SARS-CoV-2)
Our analysis showed that at least one of the 15 transcription factors (TFs) could bind to the putative promoters of 68 long non-coding RNA (lncRNA) (Tables S24 and S25)
IRF1, STAT1, STAT3, RELA, and MYC independently or in combination might regulate most of the deregulated lncRNA or protein coding genes (PCG) observed in the present study as the putative promoters of these lncRNA were occupied by these TFs, mostly at the multiple sites
Summary
Coronavirus disease 19 (COVID-19) is caused by infection with severe acute respiratory syndrome corona virus 2 (SARS-CoV-2). A small fraction of infected individuals progress to severe conditions resulting in multi-organ failure which may be fatal [1]. Deregulated macrophages, innate and adaptive immunity result in hyperinflammatory responses, and enhanced expression of various cytokines, and chemokines have been observed in COVID-19 and reviewed [2]. Levels of IFN-I and IFN-III were dependent on anatomical sites, viral load, and severity. Increased level of IFN-III is observed in the upper airways of patients with a high viral burden but reduced disease risk or severity. In the lower airways of patients with severe COVID-19, IFNs are over-represented and show gene pathways associated with increased apoptosis and decreased proliferation [3]
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