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Human long noncoding RNA, VILMIR, is induced by major respiratory viral infections and modulates the host interferon response

ABSTRACT: Human long noncoding RNA, VILMIR, is induced by major respiratory viral infections and modulates the host interferon response

PROVIDER: PRJNA1089571 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28388508_1.fastq.gz	Fastqsanger.gz
	SRR28388508_2.fastq.gz	Fastqsanger.gz
	SRR28388509_1.fastq.gz	Fastqsanger.gz
	SRR28388509_2.fastq.gz	Fastqsanger.gz
	SRR28388510_1.fastq.gz	Fastqsanger.gz

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Human long noncoding RNA, VILMIR, is induced by major respiratory viral infections and modulates the host interferon response

Project description:Long noncoding RNAs (lncRNAs) are a newer class of noncoding transcripts identified as key regulators of biological processes. Here we aimed to identify novel lncRNA targets that play critical roles in major human respiratory viral infections by systematically mining large-scale transcriptomic datasets. Using bulk RNA-sequencing (RNA-seq) analysis, we identified a previously uncharacterized lncRNA, named virus inducible lncRNA modulator of interferon response (VILMIR), that was consistently upregulated after in vitro influenza infection across multiple human epithelial cell lines and influenza A virus subtypes. VILMIR was also upregulated after SARS-CoV-2 and RSV infections in vitro. We experimentally confirmed the response of VILMIR to influenza infection and interferon-beta (IFN-β) treatment in the A549 human epithelial cell line and found the expression of VILMIR was robustly induced by IFN-β treatment in a dose and time-specific manner. Single cell RNA-seq analysis of bronchoalveolar lavage fluid (BALF) samples from COVID-19 patients uncovered that VILMIR was upregulated across various cell types including at least five immune cells. The upregulation of VILMIR in immune cells was further confirmed in the human T cell and monocyte cell lines, SUP-T1 and THP-1, after IFN-β treatment. Finally, we found that knockdown of VILMIR expression reduced the magnitude of host transcriptional responses to IFN-β treatment in A549 cells. Together, our results show that VILMIR is a novel interferon-stimulated gene (ISG) that regulates the host interferon response and may be a potential therapeutic target for human respiratory viral infections upon further mechanistic investigation.

2024-04-17 | GSE261920 | GEO

Human long noncoding RNA, VILMIR, is induced by major respiratory viral infections and modulates the host interferon response

Project description:Long noncoding RNAs (lncRNAs) are a newer class of noncoding transcripts identified as key regulators of biological processes. Here we aimed to identify novel lncRNA targets that play critical roles in major human respiratory viral infections by systematically mining large-scale transcriptomic datasets. Using bulk RNA-sequencing (RNA-seq) analysis, we identified a previously uncharacterized lncRNA, named virus inducible lncRNA modulator of interferon response (VILMIR), that was consistently upregulated after in vitro influenza infection across multiple human epithelial cell lines and influenza A virus subtypes. VILMIR was also upregulated after SARS-CoV-2 and RSV infections in vitro. We experimentally confirmed the response of VILMIR to influenza infection and interferon-beta (IFN-β) treatment in the A549 human epithelial cell line and found the expression of VILMIR was robustly induced by IFN-β treatment in a dose and time-specific manner. Single cell RNA-seq analysis of bronchoalveolar lavage fluid (BALF) samples from COVID-19 patients uncovered that VILMIR was upregulated across various cell types including at least five immune cells. The upregulation of VILMIR in immune cells was further confirmed in the human T cell and monocyte cell lines, SUP-T1 and THP-1, after IFN-β treatment. Finally, we found that knockdown of VILMIR expression reduced the magnitude of host transcriptional responses to both IFN-β treatment and influenza A virus infection in A549 cells. Together, our results show that VILMIR is a novel interferon-stimulated gene (ISG) that regulates the host interferon response and may be a potential therapeutic target for human respiratory viral infections upon further mechanistic investigation.

2025-03-20 | GSE288251 | GEO

Human long noncoding RNA, VILMIR, is induced by major respiratory viral infections and modulates the host interferon response

Project description:Human long noncoding RNA, VILMIR, is induced by major respiratory viral infections and modulates the host interferon response

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Long noncoding RNA INCA1 regulates tumor interferon signaling

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Long noncoding RNA INCA1 regulates tumor interferon signaling.

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Long noncoding RNA INCA1 regulates tumor interferon signaling

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Project description:Respiratory viruses, particularly coronaviruses (CoVs) and influenza A viruses (IAVs), have driven global pandemics, with zoonotic spillover posing ongoing threats to public health. SARS-CoV-2, the cause of COVID-19, emerged in 2019, devastating global health and claiming over 7 million lives, while the 2009 influenza pandemic caused at least 200,000 deaths. The innate immune system serves as the first line of defense, where type I interferons (IFNs) and interferon-stimulated genes (ISGs) play pivotal antiviral roles. Impaired IFN-I responses are linked to severe COVID-19 and influenza, underscoring their importance: life-threatening COVID-19 cases often involve genetic defects in IFN pathways or neutralizing autoantibodies that dampen IFN activity, whereas children’s resilience to severe infection correlates with robust IFN responses. Recombinant IFNs show therapeutic potential, though timing is critical. Key ISGs like OAS1 and OASL further illustrate IFN-mediated protection, highlighting the need to dissect how individual ISGs aid viral clearance and mitigate disease. In this context, we identified GALNT2, an O-GalNAc transferase, as a novel ISG that enhances viral clearance and reduces susceptibility and severity in both SARS-CoV-2 and IAV infections.

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A novel interferon stimulated gene GALNT2 is required to restrict respiratory virus infections

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Assessment Of Long Noncoding RNA CCAT1 In Colorectal Cancer Patients

Project description:1. Evaluate the diagnostic value of long noncoding RNA (CCAT1) expression by RT-PCR in peripheral blood in colorectal cancer patients versus normal healthy control personal. 2. Evaluate the clinical utility of detecting long noncoding RNA (CCAT1) expression in diagnosis of colorectal cancer patients & its relation to tumor staging. 3. Evaluate the clinical utility of detecting long noncoding RNA (CCAT1) expression in precancerous colorectal diseases. 4. Compare long noncoding RNA (CCAT1) expression with traditional marker; carcinoembryonic antigen (CEA) and Carbohydrate antigen 19-9 (CA19-9) in diagnosis of colorectal cancer.

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Long noncoding RNA INCA1 regulates tumor interferon signaling [CLIP-seq]

Project description:Tumor interferon signaling regulates the expression of immunosuppressive molecules and promotes cancer immune evasion. Although the role of long noncoding RNAs (lncRNAs) in the regulation of gene expression is now emerging, their function in tumor interferon signaling remains unexplored. We have identified the interferon-γ (IFNγ)-stimulated non-coding RNA 1 (INCA1) as a novel lncRNA expressed form the PD-L1 locus. INCA1 is expressed in multiple tumor types and its levels increase after IFNγ stimulation. Silencing INCA1 decreased the expression of several interferon-stimulated genes (ISGs). We discovered that the transcripts of some ISGs are negatively regulated by HNRNPH1. We demonstrate that binding of INCA1 to HNRNPH1 is required for ISG expression. Overall, our findings reveal a mechanism of tumor interferon signaling regulation mediated by the lncRNA INCA1.

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