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Development of a mouse model of rhinovirus infection.

机译：鼻病毒感染的小鼠模型的发展。

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摘要

Rhinoviruses (RVs) are plus-sense, single-stranded RNA viruses in the family Picornaviridae that are causative agents of the majority of upper respiratory tract infections, or "common colds," in humans. RVs infect both the upper and lower respiratory tract, and in addition to the common cold may also cause pneumonia in infants and the elderly, complications in cystic fibrosis patients, and asthma exacerbations. Despite the medical importance of human rhinoviruses, the pathogenesis of rhinovirus-induced illness is poorly understood. An animal model to study rhinovirus pathogenesis would greatly augment efforts to study possible means of preventing or treating RV infections. The major group rhinovirus serotypes bind human intercellular adhesion molecule-1 (ICAM1) for cell entry. While mice also express a homolog of ICAM-1, it is not sufficiently similar to the human ICAM-1 to bind major group RVs. A transgenic mouse expressing human ICAM-1 was developed and infected with mouse-adapted RV16/L and RV39/L. Because the human ICAM-1 transgene was not expressed on the cell surface, however, these mice were not susceptible to infection. The minor group rhinovirus serotypes bind the low-density lipoprotein receptor (LDLR) for cell entry, and can bind mouse LDLR. However, as with the major group serotypes, a post-entry block to replication has been observed in mouse cells. By serial passage through mouse embryonic fibroblasts and mouse lung epithelial cells, variants of RV1A that replicate in mouse cells were selected. The adaptation to growth in mouse cells was mediated by amino acid changes in the 3A non-structural protein. Following chemical permeabilization of the airway, mouse cell-adapted RV1A was capable of infecting mice and producing DC responses to infection in vivo. The availability of a mouse model for RV infection and pathogenesis will permit detailed studies on RV pathogenesis and may identify targets for therapeutic intervention.
机译：鼻病毒（RVs）是Picornaviridae家族中的加有义感的单链RNA病毒，是人类大多数上呼吸道感染或“普通感冒”的病原体。 RVs感染上呼吸道和下呼吸道，除了普通感冒外，还可能引起婴儿和老年人的肺炎，囊性纤维化患者的并发症以及哮喘加重。尽管人类鼻病毒具有医学重要性，但对鼻病毒诱发疾病的发病机理知之甚少。研究鼻病毒发病机理的动物模型将大大增加研究预防或治疗RV感染的可能方法的努力。主要的鼻病毒血清型结合人细胞间粘附分子1（ICAM1）进入细胞。虽然小鼠也表达ICAM-1的同源物，但它与人ICAM-1的相似性不足以结合主要的RVs。开发了表达人ICAM-1的转基因小鼠，并用适应小鼠的RV16 / L和RV39 / L感染。但是，由于人ICAM-1转基因不在细胞表面表达，因此这些小鼠不易感染。小群鼻病毒血清型结合低密度脂蛋白受体（LDLR）进入细胞，并可以结合小鼠LDLR。但是，与主要的血清型一样，在小鼠细胞中已观察到进入后复制的阻滞。通过连续通过小鼠胚胎成纤维细胞和小鼠肺上皮细胞，选择了在小鼠细胞中复制的RV1A变体。小鼠细胞对生长的适应性是由3A非结构蛋白的氨基酸变化介导的。气道化学通透后，适应小鼠细胞的RV1A能够感染小鼠并在体内产生对感染的DC反应。用于RV感染和发病机制的小鼠模型的可用性将允许对RV发病机制进行详细研究，并可能确定治疗干预的靶标。

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  • 作者

    Rasmussen, Angela L.;

  • 作者单位

    Columbia University.;

  • 授予单位 Columbia University.;
  • 学科 Biology Virology.;Health Sciences Immunology.
  • 学位 Ph.D.
  • 年度 2009
  • 页码 136 p.
  • 总页数 136
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

  • 入库时间 2022-08-17 11:38:25

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