Long noncoding RNAs in respiratory viruses: A review

Abstract

Long noncoding RNAs (lncRNAs) are defined as RNA molecules longer than 200 nucleotides that can regulate gene expression at the transcriptional or post‐transcriptional levels. Both human lncRNAs and lncRNAs encoded by viruses can modulate the expression of host genes which are critical for viral replication, latency, activation of signalling pathways, cytokine and chemokine production, RNAi processing, expression of interferons (IFNs) and interferon‐stimulated genes (ISGs). Studies on lncRNAs as key regulators of host‐virus interactions may give new insights into therapeutic strategies for the treatment of related diseases. This current review focuses on the role of lncRNAs, and their interactions with respiratory viruses including influenza A virus (IAV), respiratory syncytial virus (RSV) and severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2).

Co-Regulation of Protein Coding Genes by Transcription Factor and Long Non-Coding RNA in SARS-CoV-2 Infected Cells: An In Silico Analysis

“…Altered expression of 39 lncRNA was new and expression of 10 lncRNA was reported by other investigators but in opposite direction. Infection with diverse viruses modulates the expression of lncRNA including SARS-CoV-2 [29][30][31]. Increased expression of NEAT1, MALAT1, EGOT, PVT1, MIAT has been also observed in infection with other viruses (Table S1).…”

“…Altered Expression of lncRNA in Cells Infected with Viruses Other Than SARS-CoV-2 Altered expression of lncRNA has been observed in viral infection and reviewed [28]. Infection with influenza virus (IAV), HIV, herpes simplex virus (HSV), hepatitis C virus (HCV), hepatitis B virus (HBV), severe acute respiratory syndrome coronavirus (SARS-CoV), and others alter the expression of host lncRNA and reviewed [29][30][31]. Altered expression of the lncRNAs in different viruses other than SARS-CoV-2 infected cells has been implicated in diverse cellular functions like antiviral activity by modulating viral replication and growth as well as expression of IFNs, and ISGs, possibly by interacting with transcription factors like STAT1, STAT3, NFκB, IRFs and has been reviewed recently [31].…”

“…Infection with influenza virus (IAV), HIV, herpes simplex virus (HSV), hepatitis C virus (HCV), hepatitis B virus (HBV), severe acute respiratory syndrome coronavirus (SARS-CoV), and others alter the expression of host lncRNA and reviewed [29][30][31]. Altered expression of the lncRNAs in different viruses other than SARS-CoV-2 infected cells has been implicated in diverse cellular functions like antiviral activity by modulating viral replication and growth as well as expression of IFNs, and ISGs, possibly by interacting with transcription factors like STAT1, STAT3, NFκB, IRFs and has been reviewed recently [31]. Detail of the literature search for deregulation of lncRNA in viruses other than SARS-CoV-2 infected cells and their possible function is shown in Table S1.…”

“…(A) (top panel): Binding of TFs to the putative promoter (−5 Kb to +1 Kb) of PVT1. Nine TFs IRF1 (binding positions 883 and 870 from the TSS), IRF4 (568, 564), IRF5 (724), MYC(933, 911, 862, 850, 832, 827, 824, 758, 711, 697, 455, 438, 434, 385, 365, 274, 191, 184, 163,126,98,57,45,34,31,21,20,19, 3, −24, −54, −460, −617, −628, −678, −1454), RELA/p65 (974, 949, 932, 900, 894, 875, 863, 841, 831, 826, 806, 791, 679, 678, 677, 669, 657, 652, 652, 643, 633, 627, 626, 620, 612, 611, 603, 597, 596, 565, 341, 247, 18, −8), STAT1 (857,−4693), STAT3 (986, 844, 826, −130), STAT4 (397), STAT5A (941, 928) could bind to the putative promoter. Among the several binding sites observed from ChIPBase, only one site is shown in Figure.…”

Infection of primary nasal epithelial cells differentiates among lethal and seasonal human coronaviruses

“…To date, seven human coronaviruses (HCoVs) are known to infect humans, causing a range of respiratory disease (Coleman and Frieman, 2014; Kesheh et al ., 2022). Three of these HCoVs emerged from animal reservoirs to cause significant public emergencies in the past 20 years and have been categorized as lethal HCoVs due to their propensity to cause life-threatening pneumonia in infected patients (Wang, Grunewald and Perlman, 2020).…”