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HTLV is a human retrovirus associated with serious diseases such as tropical spastic paraparesis (HAM/TSP) and adult T-cell leukemia/lymphoma (ATL). Although identified more than four decades ago, the molecular mechanisms that explain the clinical progression of the infection are still poorly understood. This study aimed to map gene regulatory networks involved in HTLV infection and its expression modulation, seeking to understand biological processes that favor viral persistence and worsening of symptoms. For this purpose, RNAseq libraries from SRA/NCBI repository were selected with samples from infected and control individuals. After quality control, sequences were aligned to human reference genome and analyzed with the HISAT2, edgeR and PANTHER tools to identify and functionally characterize differentially expressed genes. In addition, protein-protein interaction networks were constructed using the STRING platform. CellDesigner software was used to generate a graphical representation of the main molecular mechanisms involved in HTLV-1 infection. The results revealed pathways associated with immune activation, neuroglial inflammation, energy metabolism and epigenetic mechanisms. Molecules such as NRP-1, FOXP3, SIRT1, NAMPT, IL-27 and proteins of MAPK pathway stand out, which are connected to inflammatory, neurodegenerative processes and cellular transformations. The interaction between these pathways suggests an environment conducive to immune system evasion and the progression of infection severe forms. Therefore, it was possible to conclude that HTLV-1 infection activates a complex set of molecular pathways that favor immune evasion, viral persistence and the development of severe clinical manifestations. Mapping these interactions can guide new diagnostic and therapeutic approaches.

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Transcriptomic Profiling and Regulatory Network Reconstruction Uncovers Central Genes in HTLV Infection Progression

  • 会议论文

  • 发表日期：

    2026年

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  • Laryssa Bandeira de Melo Silva,
  • Gabriel Freitas Araújo,
  • Patrícia Moura,
  • João Pacifico Bezerra Neto

摘要

HTLV is a human retrovirus associated with serious diseases such as tropical spastic paraparesis (HAM/TSP) and adult T-cell leukemia/lymphoma (ATL). Although identified more than four decades ago, the molecular mechanisms that explain the clinical progression of the infection are still poorly understood. This study aimed to map gene regulatory networks involved in HTLV infection and its expression modulation, seeking to understand biological processes that favor viral persistence and worsening of symptoms. For this purpose, RNAseq libraries from SRA/NCBI repository were selected with samples from infected and control individuals. After quality control, sequences were aligned to human reference genome and analyzed with the HISAT2, edgeR and PANTHER tools to identify and functionally characterize differentially expressed genes. In addition, protein-protein interaction networks were constructed using the STRING platform. CellDesigner software was used to generate a graphical representation of the main molecular mechanisms involved in HTLV-1 infection. The results revealed pathways associated with immune activation, neuroglial inflammation, energy metabolism and epigenetic mechanisms. Molecules such as NRP-1, FOXP3, SIRT1, NAMPT, IL-27 and proteins of MAPK pathway stand out, which are connected to inflammatory, neurodegenerative processes and cellular transformations. The interaction between these pathways suggests an environment conducive to immune system evasion and the progression of infection severe forms. Therefore, it was possible to conclude that HTLV-1 infection activates a complex set of molecular pathways that favor immune evasion, viral persistence and the development of severe clinical manifestations. Mapping these interactions can guide new diagnostic and therapeutic approaches.