首页> 外文OA文献 >Rapid Onset of Intestinal Epithelial Barrier Dysfunction in Primary Human Immunodeficiency Virus Infection Is Driven by an Imbalance between Immune Response and Mucosal Repair and Regeneration▿
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Rapid Onset of Intestinal Epithelial Barrier Dysfunction in Primary Human Immunodeficiency Virus Infection Is Driven by an Imbalance between Immune Response and Mucosal Repair and Regeneration▿

机译:免疫应答与黏膜修复和再生之间的不平衡驱动原发性人类免疫缺陷病毒感染中肠道上皮屏障功能障碍的迅速发作▿

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摘要

Gut-associated lymphoid tissue (GALT) is an early target for human immunodeficiency virus type 1 (HIV-1) infection and is a site for severe CD4+ T-cell depletion. HIV-associated enteropathy is well-documented in chronic HIV-1 infection. However, the initial host responses to HIV infection in GALT and the early molecular correlates of HIV enteropathogenesis have not been characterized during primary HIV infection. In this study, we provide evidence of viral replication in GALT resident CD4+ T cells and macrophages in primary-stage patients and identify early patterns of host mucosal responses and changes in the molecular microenvironment through gene expression profiling. High levels of viral replication in GALT and marked CD4+ T-cell depletion correlated with decreased expression levels of genes regulating epithelial barrier maintenance and digestive/metabolic functions. These changes coincided with a marked increase in the transcription of immune activation-, inflammation-, and apoptosis-associated genes. Our findings indicate that HIV-induced pathogenesis in GALT emerges at both the molecular and cellular levels prior to seroconversion in primary HIV infection, potentially setting the stage for disease progression by impairing the ability to control viral replication and repair and regenerate intestinal mucosal tissues.
机译:肠道相关淋巴样组织(GALT)是人类免疫缺陷病毒1型(HIV-1)感染的早期靶标,并且是严重CD4 + T细胞耗竭的部位。与艾滋病毒有关的肠病在慢性HIV-1感染中有据可查。但是,在原发性HIV感染期间,尚未鉴定出宿主对GALT中HIV感染的最初反应以及HIV肠道发病的早期分子相关性。在这项研究中,我们提供了在初级阶段患者中GALT驻留CD4 + T细胞和巨噬细胞中病毒复制的证据,并通过基因表达谱鉴定了宿主黏膜反应的早期模式和分子微环境的变化。 GALT中高水平的病毒复制和明显的CD4 + T细胞耗竭与调节上皮屏障维持和消化/代谢功能的基因的表达水平下降相关。这些变化与免疫激活,炎症和凋亡相关基因的转录显着增加相吻合。我们的研究结果表明,HIV诱发的GALT发病机理在原发性HIV感染发生血清转化之前在分子和细胞水平上均已出现,可能通过削弱控制病毒复制,修复和再生肠道粘膜组织的能力而为疾病发展奠定基础。

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