Noncoding RNAs: modulators and modulatable players during infection-induced stress response

Chattopadhyay, Partha; Vasudevan, Janani Srinivasa; Pandey, Rajesh

doi:10.1093/bfgp/elaa026

Cited by 10 publications

(5 citation statements)

References 196 publications

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“…Noncoding RNAs (ncRNAs) are emerging as an essential biomolecule in controlling different cellular functions and cell survival. ncRNAs can play a pro-viral role by regulating cellular antiviral response or their regulation can help host cells to counteract viral replication [110]. For example, IFN-α induced lncISG15 and lncBST2 (also called lncRNA-BISPR) are reported as positive regulators of ISGs ISG15 and BST2 [111].…”

Section: Noncoding Rna: Lncrna and Mirnamentioning

confidence: 99%

Interplay between Hepatitis E Virus and Host Cell Pattern Recognition Receptors

Devhare

Madiyal

Mukhopadhyay

et al. 2021

IJMS

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Hepatitis E virus (HEV) usually causes self-limiting acute hepatitis, but the disease can become chronic in immunocompromised individuals. HEV infection in pregnant women is reported to cause up to 30% mortality, especially in the third trimester. Additionally, extrahepatic manifestations like neuronal and renal diseases and pancreatitis are also reported during the course of HEV infection. The mechanism of HEV pathogenesis remains poorly understood. Innate immunity is the first line of defense triggered within minutes to hours after the first pathogenic insult. Growing evidence based on reverse genetics systems, in vitro cell culture models, and representative studies in animal models including non-human primates, has implicated the role of the host’s innate immune response during HEV infection. HEV persists in presence of interferons (IFNs) plausibly by evading cellular antiviral defense. This review summarizes our current understanding of recognizing HEV-associated molecular patterns by host cell Pattern Recognition Receptors (PRRs) in eliciting innate immune response during HEV infection as well as mechanisms of virus-mediated immune evasion.

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Section: Noncoding Rna: Lncrna and Mirnamentioning

confidence: 99%

Interplay between Hepatitis E Virus and Host Cell Pattern Recognition Receptors

Devhare

Madiyal

Mukhopadhyay

et al. 2021

IJMS

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“…Diverse biological processes and pathways associated with deregulated lncRNA in SARS-CoV-2 infection have been reported and reviewed. These pathways include oxidative stress, immune responses [42], NLRP3 inflammasome [43,44], TNF signaling pathway, IL-17 signaling pathway, cytokine-cytokine receptor interaction, NOD-like receptor signaling pathway, Influenza A, chemokine signaling pathway, RIG-I-like receptor signaling pathway, MAPK signaling pathway, NF-kappa B signaling pathway, Toll-like receptor signaling pathway, AGE-RAGE signaling pathway in diabetic complications, FoxO signaling pathway, apoptosis, epithelial cell signaling in Helicobacter pylori infection and cellular senescence [35], viral defense response, innate immune response, and inflammatory response [9].…”

Section: Possible Functional Role Of the Deregulated Lncrna In Viral ...mentioning

confidence: 99%

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

Saha

Laha

Chatterjee

et al. 2021

ncRNA

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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.

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“…Many studies have highlighted the functional role of lncRNAs in several infectious diseases. Viruses can utilize lncRNAs to regulate the signaling pathways involved in innate immunity ( Wang et al, 2020 ), cell metabolism ( Khatun et al, 2020 ), and cell stress ( Chattopadhyay et al, 2021 ), to survive and replicate in host cells. Like other viruses, it is conceivable that some lncRNAs for virus replication that are regulated by ALV-J infection exist, which has not been documented.…”

Section: Discussionmentioning

confidence: 99%

An Endogenous Retroviral LTR-Derived Long Noncoding RNA lnc-LTR5B Interacts With BiP to Modulate ALV-J Replication in Chicken Cells

Chen

Zhao

et al. 2021

Front. Microbiol.

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Infection with the avian leukosis virus subgroup J (ALV-J) impairs host genes and facilitates the establishment of chronic infection and the viral life cycle. However, the involvement of long noncoding RNAs (lncRNAs) in ALV-J infection remains largely unknown. In this study, we identified a novel chicken lncRNA derived from LTR5B of the ERV-L family (namely lnc-LTR5B), which is significantly downregulated in ALV-J infected cells. lnc-LTR5B was localized in the cytoplasm and was relatively high expressed in the chicken lung and liver. Notably, the replication of ALV-J was inhibited by the overexpression of lnc-LTR5B but enhanced when lnc-LTR5B expression was knocked down. We further confirmed that lnc-LTR5B could bind to the binding immunoglobulin protein (BiP), a master regulator of endoplasmic reticulum (ER) function. Mechanistically, lnc-LTR5B serves as a competing endogenous RNA for BiP, restricting its physical availability. Upon ALV-J infection, the reduction of lnc-LTR5B released BiP, which facilitated its translocation to the cell surface. This is crucial for ALV-J entry as well as pro-survival signaling. In conclusion, we identified an endogenous retroviral LTR-activated lnc-LTR5B that is involved in regulating the cell surface translocation of BiP, and such regulatory machinery can be exploited by ALV-J to complete its life cycle and propagate.

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Noncoding RNAs: modulators and modulatable players during infection-induced stress response

Cited by 10 publications

References 196 publications

Interplay between Hepatitis E Virus and Host Cell Pattern Recognition Receptors

Interplay between Hepatitis E Virus and Host Cell Pattern Recognition Receptors

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

An Endogenous Retroviral LTR-Derived Long Noncoding RNA lnc-LTR5B Interacts With BiP to Modulate ALV-J Replication in Chicken Cells

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