PDF(Pubmed)
Abstract：
Hantaan virus (HTNV) is a major public health concern due to its ability to cause hemorrhagic fever with renal syndrome (HFRS) in Eurasia. Symptoms of HFRS include fever, hemorrhage, immune dysfunction and renal impairment, and severe cases can be fatal. T cell-mediated adaptive immune responses play a pivotal role in countering HTNV infection. However, our understanding of HTNV and T cell interactions in the disease progression is limited. In this study, we found that human CD4+ T cells can be directly infected with HTNV, thereby facilitating viral replication and production. Additionally, T-cell immunoglobulin and mucin 1 (TIM-1) participated in the process of HTNV infection of Jurkat T cells, and further observed that HTNV enters Jurkat T cells via the clathrin-dependent endocytosis pathway. These findings not only affirm the susceptibility of human CD4+ T lymphocytes to HTNV but also shed light on the viral tropism. Our research elucidates a mode of the interaction between the virus infection process and the immune system. Critically, this study provides new insights into the pathogenesis of HTNV and the implications for antiviral research.
摘要：
汉坦病毒（HTNV）是主要的公共卫生问题，因为它能够在欧亚大陆引起肾综合征出血热（HFRS）。HFRS的症状包括发烧，出血,免疫功能障碍和肾功能损害，严重的病例可能是致命的。T细胞介导的适应性免疫应答在对抗HTNV感染中起关键作用。然而,我们对疾病进展中HTNV和T细胞相互作用的理解有限.在这项研究中,我们发现人类CD4+T细胞可以直接感染HTNV，从而促进病毒复制和生产。此外,T细胞免疫球蛋白和粘蛋白1(TIM-1)参与了HTNV感染JurkatT细胞的过程,并进一步观察到HTNV通过网格蛋白依赖性胞吞途径进入JurkatT细胞。这些发现不仅肯定了人类CD4T淋巴细胞对HTNV的敏感性，而且还阐明了病毒的嗜性。我们的研究阐明了病毒感染过程与免疫系统之间相互作用的模式。严重的,这项研究为HTNV的发病机制和抗病毒研究提供了新的见解。
