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Effects of infection with measles virus on interferon signaling in human lung epithelial cells.

机译：麻疹病毒感染对人肺上皮细胞干扰素信号传导的影响。

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摘要

Measles virus (MV) remains responsible for a large percentage of the global vaccine preventable mortality in children. It is a highly contagious disease spread via the respiratory route and results in immunosuppression, making the host susceptible to secondary infections and causing increased morbidity and mortality. MV utilizes accessory proteins V and C to modulate the host innate immune response, specifically type I IFN. This effect, however, varies with the attenuation of the infecting MV strain. The outcome of MV infection also depends on the cell type being infected because wild type (WT) strains are limited in their receptor usage compared with attenuated strains WT strains use CD150/SLAM, while attenuated strains can use both CD150/SLAM and CD46. MV infection is initiated in respiratory epithelial cells, but these cells do not possess the CD150/SLAM receptor, and have an unidentified third receptor for WT MV infection.;Using A-549 (non-polarized) and Calu-3 (polarized) lung epithelial cells, the level of MV replication and subsequent IFN induction by WT and attenuated strains of MV were investigated. All MV strains studied replicated in lung epithelial cells, with WT strains replicating to higher levels. However, the vaccine (Edmonston) and lab-adapted (Chicago-1) strains of MV induced higher levels of type I IFN secretion, with IFN-beta being the major contributor, while the WT strain (Bilthoven) was best able to avoid induction of the innate IFN response. Antibody to IFN-alpha enhanced the protective ability of MV viral supernatant fluids against challenge virus infection, while antibody to IFN-beta abrogated all protection. Induction of upstream mRNAs for IFN signaling molecules RIG-I, IRF-3, and IRF-7 was independent of the virus attenuation state, but was strain-specific. IRF-7 mRNA was increased after infection to a greater degree than IRF-3 mRNA. The response of polarized lung epithelial cells to infection with different MV strains is a system more closely resembling the initiation of infection.
机译：麻疹病毒（MV）仍占儿童全球疫苗可预防死亡率的很大比例。它是一种高度传染性的疾病，通过呼吸道传播，导致免疫抑制，使宿主易感继发感染，并增加发病率和死亡率。 MV利用辅助蛋白V和C调节宿主固有的免疫应答，特别是I型IFN。然而，这种效果随感染MV株的衰减而变化。 MV感染的结果还取决于被感染的细胞类型，因为野生型（WT）菌株与减毒菌株相比受体使用受到限制，WT菌株使用CD150 / SLAM，而减毒菌株可以同时使用CD150 / SLAM和CD46。 MV感染始于呼吸道上皮细胞，但这些细胞不具有CD150 / SLAM受体，并且具有未确定的WT MV感染的第三种受体。;使用A-549（非极化）和Calu-3（极化）肺研究了上皮细胞，MV复制水平以及随后的WT和MV减毒株对IFN的诱导。所有研究的MV菌株都在肺上皮细胞中复制，而WT菌株则复制到更高水平。然而，疫苗（埃德蒙斯顿）和实验室适应性（芝加哥-1）MV菌株诱导更高水平的I型IFN分泌，其中IFN-β是主要贡献者，而WT菌株（Bilthoven）最能避免诱导天生的IFN反应。 IFN-α抗体增强了MV病毒上清液对攻击病毒感染的保护能力，而IFN-β抗体则取消了所有保护作用。 IFN信号分子RIG-1，IRF-3和IRF-7的上游mRNA的诱导与病毒的减毒状态无关，但具有菌株特异性。感染后IRF-7 mRNA的增加程度大于IRF-3 mRNA。极化的肺上皮细胞对不同MV菌株感染的反应是一个更类似于感染起始的系统。

著录项

  • 作者

    Siwek, Martina Marie.;

  • 作者单位

    The Johns Hopkins University.;

  • 授予单位 The Johns Hopkins University.;
  • 学科 Biology Virology.;Health Sciences Immunology.
  • 学位 Ph.D.
  • 年度 2009
  • 页码 155 p.
  • 总页数 155
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 预防医学、卫生学;
  • 关键词

  • 入库时间 2022-08-17 11:38:28

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