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<p>The respiratory syncytial virus (RSV) is one of the leading causes of severe respiratory illness in children, responsible for millions of hospitalizations and thousands of deaths annually. Despite extensive research on RSV in pediatric patients, the molecular mechanisms underlying the host response to this infection remain poorly understood. Long non-coding RNAs (lncRNAs) are transcripts longer than 200 nucleotides that do not encode proteins; they regulate gene expression, participating in antiviral immunity, inflammation, cellular responses, and others. Here, we analyzed bulk transcriptome data from pediatric RSV-infected patients and integrated it with single-cell RNA-Seq analysis, focusing on molecular networks involving lncRNAs. We built a network comprising 3,085,980 experimentally validated molecular interactions, from which we created networks to model the molecular systems of healthy and RSV-infected patients. Network analysis revealed hundreds of lncRNAs responsive to RSV infection, some of which interact with infection-related genes and proteins. The lncRNA interactors in the RSV network were associated with mRNA metabolism and the regulation of nucleobase-containing compound metabolic processes. Network analysis highlighted SOX2-OT, C5orf64, and MEG3 as candidate lncRNAs potentially involved in pediatric RSV infection through regulation or interaction with genes associated with respiratory diseases. Furthermore, the lncRNAs OIP5-AS1 and LINC00342 were associated with mild RSV infections. Single-cell RNA-Seq data revealed lncRNA markers with elevated expression in CD16- NK and regulatory T cells, and reduced expression in ILC3 cells during infection. We offered insight into the RSV-induced remodeling of lncRNA networks, with implications for the development of novel biomarkers and therapeutic strategies in viral respiratory diseases.</p>

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Analysis of LncRNAs in children infected with respiratory syncytial virus using the transcriptome, single-cell RNA-Seq, and networks

  • 期刊论文

  • 发表日期：

    2025年7月10日

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  • Ana Beatriz Rodrigues,
  • Matheus Rodrigues Sauda,
  • Agatha MS Kubo,
  • Jeferson dos Santos Souza,
  • Tatiana de Campos Melo,
  • Rejane MT Grotto,
  • Guilherme Targino Valente

摘要

The respiratory syncytial virus (RSV) is one of the leading causes of severe respiratory illness in children, responsible for millions of hospitalizations and thousands of deaths annually. Despite extensive research on RSV in pediatric patients, the molecular mechanisms underlying the host response to this infection remain poorly understood. Long non-coding RNAs (lncRNAs) are transcripts longer than 200 nucleotides that do not encode proteins; they regulate gene expression, participating in antiviral immunity, inflammation, cellular responses, and others. Here, we analyzed bulk transcriptome data from pediatric RSV-infected patients and integrated it with single-cell RNA-Seq analysis, focusing on molecular networks involving lncRNAs. We built a network comprising 3,085,980 experimentally validated molecular interactions, from which we created networks to model the molecular systems of healthy and RSV-infected patients. Network analysis revealed hundreds of lncRNAs responsive to RSV infection, some of which interact with infection-related genes and proteins. The lncRNA interactors in the RSV network were associated with mRNA metabolism and the regulation of nucleobase-containing compound metabolic processes. Network analysis highlighted SOX2-OT, C5orf64, and MEG3 as candidate lncRNAs potentially involved in pediatric RSV infection through regulation or interaction with genes associated with respiratory diseases. Furthermore, the lncRNAs OIP5-AS1 and LINC00342 were associated with mild RSV infections. Single-cell RNA-Seq data revealed lncRNA markers with elevated expression in CD16- NK and regulatory T cells, and reduced expression in ILC3 cells during infection. We offered insight into the RSV-induced remodeling of lncRNA networks, with implications for the development of novel biomarkers and therapeutic strategies in viral respiratory diseases.