...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of Mathematical Biology >Modeling the role of macrophages in HIV persistence during antiretroviral therapy
【24h】

Modeling the role of macrophages in HIV persistence during antiretroviral therapy

机译：抗逆转录病毒治疗期间巨噬细胞在艾滋病毒持续性中的作用

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

HIV preferentially infects activated CD4+ T cells. Current antiretroviral therapy cannot eradicate the virus. Viral infection of other cells such as macrophages may contribute to viral persistence during antiretroviral therapy. In addition to cell-free virus infection, macrophages can also get infected when engulfing infected CD4+ T cells as innate immune sentinels. How macrophages affect the dynamics of HIV infection remains unclear. In this paper, we develop an HIV model that includes the infection of CD4+ T cells and macrophages via cell-free virus infection and cell-to-cell viral transmission. We derive the basic reproduction number and obtain the local and global stability of the steady states. Sensitivity and viral dynamics simulations show that even when the infection of CD4+ T cells is completely blocked by therapy, virus can still persist and the steady-state viral load is not sensitive to the change of treatment efficacy. Analysis of the relative contributions to viral replication shows that cell-free virus infection leads to the majority of macrophage infection. Viral transmission from infected CD4+ T cells to macrophages during engulfment accounts for a small fraction of the macrophage infection and has a negligible effect on the total viral production. These results suggest that macrophage infection can be a source contributing to HIV persistence during suppressive therapy. Improving drug efficacies in heterogeneous target cells is crucial for achieving HIV eradication in infected individuals.
机译：HIV优先感染活性CD4 + T细胞。目前的抗逆转录病毒治疗不能消除病毒。在抗逆转录病毒治疗期间，诸如巨噬细胞等其他细胞的病毒感染可能导致病毒持久性。除了无细胞病毒感染外，巨噬细胞还可以在吞噬受感染的CD4 + T细胞时感染，因为本体免疫哨兵。巨噬细胞如何影响HIV感染的动态仍然不清楚。在本文中，我们开发了一种艾滋病毒模型，其包括通过无细胞病毒感染和细胞对细胞病毒传输感染CD4 + T细胞和巨噬细胞。我们派生了基本的再现号码并获得稳定状态的本地和全球稳定性。敏感性和病毒动力学模拟表明，即使通过治疗完全阻断CD4 + T细胞的感染，病毒仍然可以持续存在，并且稳态病毒载荷对治疗效果的变化不敏感。对病毒复制的相对贡献分析表明，无细胞病毒感染导致大多数巨噬细胞感染。从感染的CD4 + T细胞到巨噬细胞的病毒透射率占巨噬细胞感染的一小部分，对总病毒生产具有可忽略的影响。这些结果表明，巨噬细胞感染可以是抑制治疗期间有助于艾滋病毒持久性的来源。改善异质靶细胞中的药物效果对于在感染的个体中实现艾滋病毒灭绝是至关重要的。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号