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<p>Bats are recognized for harboring a diverse array of viruses without manifesting disease symptoms. In this study, we explored the single-cell atlas of wild <i>Rhinolophus affinis</i> (<i>R. affinis</i>) using Viral-Track and identified transcript expression of eight viral species in the <i>R. affinis</i> lung and three viral species in the kidney. Within the <i>R. affinis</i> lung, these viruses were detected across all cell types except ciliated cells. Compared to uninfected cells, virus-infected cells exhibited activation of pathways associated with protein synthesis, tissue repair, and immune responses, as evidenced by increased expression of corresponding genes. Ligand-receptor based analysis revealed that viral infection reshapes intercellular communication networks in the bat lung, with infected fibroblasts and infected proliferative T cells exhibiting enhanced signaling linked to tissue remodeling and immune activation. Through gene module analysis, we identified an immune cell activation-related module by high expression of <i>CD14</i>, <i>CD74</i>, and <i>MRC1</i>, as well as an antiviral related module by elevated expression of <i>SAMHD1</i>, <i>SLC11A1</i>, <i>TYROBP</i>, and <i>IL18</i> in <i>R. affinis</i> pulmonary macrophages. Additionally, a cross-species single-cell transcriptomic comparative analysis demonstrated that <i>R. affinis</i> pulmonary macrophages exhibit elevated expression of pro-inflammatory genes (<i>IRF9</i>, <i>DDX5</i>, <i>IL6ST</i> and <i>ITGA4</i>), which are associated with antiviral activity and immune activation, and anti-inflammatory genes (<i>IRF2</i>, <i>PTPRE</i> and <i>GPR65</i>), which play critical roles in mitigating excessive immune responses. Compared to the other species, <i>R. affinis</i> pulmonary macrophages exhibited upregulation of genes enriched in pathways related to vacuolar acidification and negative regulation of response to external stimulus. These findings suggest that the <i>R. affinis</i> lung possesses a unique immune system that enables it to balance immune responses during viral infections, thereby preventing excessive immune damage and maintaining lung tissue homeostasis. Our study provides valuable insights into the viral infection risk organs in <i>R. affinis</i> and their distinctive antiviral immune responses.</p>

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Single-cell analysis of intermediate horseshoe bat (Rhinolophus affinis) organs reveals viral infections and antiviral immune signatures

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月7日

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  • Tianhang Lv,
  • Jianhui Zhang,
  • Zhiwan Zheng,
  • Xiaohui Fan

摘要

Bats are recognized for harboring a diverse array of viruses without manifesting disease symptoms. In this study, we explored the single-cell atlas of wild Rhinolophus affinis (R. affinis) using Viral-Track and identified transcript expression of eight viral species in the R. affinis lung and three viral species in the kidney. Within the R. affinis lung, these viruses were detected across all cell types except ciliated cells. Compared to uninfected cells, virus-infected cells exhibited activation of pathways associated with protein synthesis, tissue repair, and immune responses, as evidenced by increased expression of corresponding genes. Ligand-receptor based analysis revealed that viral infection reshapes intercellular communication networks in the bat lung, with infected fibroblasts and infected proliferative T cells exhibiting enhanced signaling linked to tissue remodeling and immune activation. Through gene module analysis, we identified an immune cell activation-related module by high expression of CD14, CD74, and MRC1, as well as an antiviral related module by elevated expression of SAMHD1, SLC11A1, TYROBP, and IL18 in R. affinis pulmonary macrophages. Additionally, a cross-species single-cell transcriptomic comparative analysis demonstrated that R. affinis pulmonary macrophages exhibit elevated expression of pro-inflammatory genes (IRF9, DDX5, IL6ST and ITGA4), which are associated with antiviral activity and immune activation, and anti-inflammatory genes (IRF2, PTPRE and GPR65), which play critical roles in mitigating excessive immune responses. Compared to the other species, R. affinis pulmonary macrophages exhibited upregulation of genes enriched in pathways related to vacuolar acidification and negative regulation of response to external stimulus. These findings suggest that the R. affinis lung possesses a unique immune system that enables it to balance immune responses during viral infections, thereby preventing excessive immune damage and maintaining lung tissue homeostasis. Our study provides valuable insights into the viral infection risk organs in R. affinis and their distinctive antiviral immune responses.