Investigation of NEAT1, IFNG‐AS1, and NRIR expression in Crimean–Congo hemorrhagic fever

Bayyurt, Burcu; Bakır, Mehmet; Engin, Aynur; Öksüz, Caner; Arslan, Serdal

doi:10.1002/jmv.26606

Cited by 9 publications

(13 citation statements)

References 20 publications

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“…NEAT1 is a well-studied lncRNA known to play important anti-viral roles. In most studies, however, NEAT1 is upregulated upon viral infections (Prinz et al 2019) and downregulation has only been described in dengue and Crimean Congo hemorrhagic fever (Pandey et al 2017;Bayyurt et al 2021). Our results suggest that NEAT1 depletion may be specific to severe hemorrhagic fevers and it is the first time that such downregulation is shown to occur specifically in monocytes.…”

Section: Cell-type Dynamic Regulation Of Lncrnas Upon Ebov Infectionmentioning

confidence: 58%

In vivo single-cell profiling of lncRNAs during Ebola virus infection

Santus

García-Pérez

Sopena-Rios

et al. 2022

Preprint

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Long non-coding RNAs (lncRNAs) are pivotal mediators of systemic immune response to viral infection, yet most studies concerning their expression and functions upon immune stimulation are limited to in vitro bulk cell populations. This strongly constrains our understanding of how lncRNA expression varies at single-cell resolution, and how their cell-type specific immune regulatory roles may differ compared to protein-coding genes. Here, we perform the first in-depth characterization of lncRNA expression variation at single-cell resolution during Ebola virus (EBOV) infection in vivo. Using bulk RNA-sequencing from 119 samples and 12 tissue types, we significantly expand the current macaque lncRNA annotation. We then profile lncRNA expression variation in immune circulating single-cells during EBOV infection and find that lncRNAs' expression in fewer cells is a major differentiating factor from their protein-coding gene counterparts. Upon EBOV infection, lncRNAs present dynamic and mostly cell-type specific changes in their expression profiles especially in monocytes, the main cell type targeted by EBOV. Such changes are associated with gene regulatory modules related to important innate immune responses such as interferon response and purine metabolism. Within infected cells, several lncRNAs have positively and negatively correlated expression with viral load, suggesting that expression of some of these lncRNAs might be directly hijacked by EBOV to attack host cells. This study provides novel insights into the roles that lncRNAs play in the host response to acute viral infection and paves the way for future lncRNA studies at single-cell resolution.

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Section: Cell-type Dynamic Regulation Of Lncrnas Upon Ebov Infectionmentioning

confidence: 58%

In vivo single-cell profiling of lncRNAs during Ebola virus infection

Santus

García-Pérez

Sopena-Rios

et al. 2022

Preprint

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“…6a). NRIR and BISPR transcripts are virus-responsive lncRNAs involved in the regulation of the innate immune response and interferon signaling [52, 68]. MIR155HG has been also described as a regulator of the cellular response against influenza viruses [53] and recently characterized as upregulated in a cellular model of SARS-CoV-2 infection [69].…”

Section: Resultsmentioning

confidence: 99%

“…Using in vitro models of hepatitis C virus (HCV) infection, the knockdown of NRIR gene resulted in a marked reduction in HCV replication in interferon-stimulated hepatocytes, suggesting that it could affect the antiviral role of interferon [82]. In other viral infections such the Crimean-Congo hemorrhagic fever, NRIR has been also shown to be upregulated [68]. The molecular partners associated with NRIR regulatory action are still not characterized, however preliminary evidence suggested that NRIR could act via recruitment of chromatin-remodeling enzymes [51, 82].…”

Section: Discussionmentioning

confidence: 99%

The interplay between lncRNAs, RNA-binding proteins and viral genome during SARS-CoV-2 infection reveals strong connections with regulatory events involved in RNA metabolism and immune response

Enguita

Leitão

McDonald

et al. 2022

Preprint

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Viral infections are complex processes based on an intricate network of molecular interactions. The infectious agent hijacks components of the cellular machinery for its profit, circumventing the natural defense mechanisms triggered by the infected cell. The successful completion of the replicative viral cycle within a cell depends on the function of viral components versus the cellular defenses. Non-coding RNAs (ncRNAs) are important cellular modulators, either promoting or preventing the progression of viral infections. Among these ncRNAs, the long non-coding RNA (lncRNA) family is especially relevant due to their intrinsic functional properties and ubiquitous biological roles. Specific lncRNAs have been recently characterized as modulators of the cellular response during infection of human host cells by single stranded RNA viruses. However, the role of host lncRNAs in the infection by human RNA coronaviruses such as SARS-CoV-2 remains uncharacterized. In the present work, we have performed a transcriptomic study of a cohort of patients with different SARS-CoV-2 viral load. Our results revealed the existence of a SARS-CoV-2 infection-dependent pattern of transcriptional up-regulation in which specific lncRNAs are an integral component. To determine the role of these lncRNAs, we performed a functional correlation analysis complemented with the study of the validated interactions between lncRNAs and RNA-binding proteins (RBPs). This combination of in silico functional association studies and experimental evidence allowed us to identify a lncRNA signature composed of six elements - NRIR, BISPR, MIR155HG, FMR1-IT1, USP30-AS1, and U62317.2 - associated with the regulation of SARS-CoV-2 infection. We propose a competition mechanism between the viral RNA genome and the regulatory lncRNAs in the sequestering of specific RBPs that modulates the interferon response and the regulation of RNA surveillance by nonsense-mediated decay (NMD).

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“…Also, NEAT1 levels were negatively correlated with dengue severity ( Pandey et al, 2017 ). In addition, Bayyurt and his group found that NEAT1 was down-regulated in Crimean–Congo hemorrhagic fever (CCHF) patients and fatal groups compared with controls ( Bayyurt et al, 2020 ).…”

Section: Discussionmentioning

confidence: 99%