From the initial sensing of viral nucleotides by pattern recognition receptors, through the induction of type I and III interferons (IFN), upregulation of antiviral effector proteins, and resolution of the inflammatory response, each step of innate immune signaling is under tight control. Though innate immunity is often associated with broad regulation at the level of gene transcription, RNA-centric post-transcriptional processes have emerged as critical mechanisms for ensuring a proper antiviral response. Here, we explore the diverse RNA regulatory mechanisms that modulate the innate antiviral immune response, with a focus on RNA sensing by RIG-I-like receptors (RLR), interferon (IFN) and IFN signaling pathways, viral pathogenesis, and host genetic variation that contributes to these processes. We address the post-transcriptional interactions with RNA-binding proteins, non-coding RNAs, transcript elements, and modifications that control mRNA stability, as well as alternative splicing events that modulate the innate immune antiviral response.
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http://dx.doi.org/10.1111/imr.13019 | DOI Listing |
Blood
January 2025
State Key Laboratory of Experimental Hematology, Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College; Center for Stem Cell Medicine,, Tianjin, China.
Adenosine-to-inosine (A-to-I) RNA editing is a prevalent RNA modification essential for cell survival. The process is catalyzed by the Adenosine Deaminase Acting on RNA (ADAR) enzyme family that converts adenosines in double-stranded RNAs (dsRNAs) into inosines, which are read as guanosines during translation. Deep sequencing has helped to reveal that A-to-I editing occurs across various types of RNAs to affect their functions.
View Article and Find Full Text PDFPLoS Pathog
January 2025
Department of Cancer and Genomic Sciences, College of Medicine and Health, University of Birmingham, Birmingham, United Kingdom.
Upon infection, human papillomavirus (HPV) manipulates host cell gene expression to create an environment that is supportive of a productive and persistent infection. The virus-induced changes to the host cell's transcriptome are thought to contribute to carcinogenesis. Here, we show by RNA-sequencing that oncogenic HPV18 episome replication in primary human foreskin keratinocytes (HFKs) drives host transcriptional changes that are consistent between multiple HFK donors.
View Article and Find Full Text PDFPLoS One
January 2025
Department of Chemistry, Ashoka University, Sonipat, Haryana, India.
Pancreatic Ductal Adenocarcinoma (PDAC) is a devastating disease with poor clinical outcomes, which is mainly because of delayed disease detection, resistance to chemotherapy, and lack of specific targeted therapies. The disease's development involves complex interactions among immunological, genetic, and environmental factors, yet its molecular mechanism remains elusive. A major challenge in understanding PDAC etiology lies in unraveling the genetic profiling that governs the PDAC network.
View Article and Find Full Text PDFMol Biol Rep
January 2025
Medical Sociology and Psychobiology, Department of Health and Physical Activity, University of Potsdam, 14469, Potsdam, Germany.
Background: Depression constitutes a risk factor for osteoporosis, but underlying molecular and cellular mechanisms are not fully understood. MiRNAs influence gene expression and are carried by extracellular vesicles (EV), affecting cell-cell communication.
Aims: (1) Identify the difference in miRNA expression between depressed patients and healthy controls; (2) Analyze associations of these miRNAs with bone turnover markers; (3) Analyze target genes of differentially regulated miRNAs and predict associated pathways regarding depression and bone metabolism.
Neurochem Res
January 2025
Department of Neurology, Affiliated Hospital of Nantong University, Medical School of Nantong University, Nantong, 226001, China.
Our aim was to evaluate the regulation of messenger RNAs (mRNAs) and biological pathways by long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs) in ischemic stroke. We employed weighted gene co-expression network analysis (WGCNA) to construct two co-expression networks for mRNAs with circRNAs and lncRNAs, respectively, to investigate their association with ischemic stroke. We compared the overlap of mRNAs and biological pathways in the stroke-associated modules of the two networks.
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