T-cell immunoglobulin and mucin 1 (TIM-1) mediates infection of Hantaan virus in Jurkat T cells

IF 2.5 4区 医学 Q3 VIROLOGY
Ruixue Ma , Xuyang Zheng , Tianle Gu , Ziyu Liu , Shiyuan Hou , Danni Sun , Yaxin Ding , Fang Wang , Qikang Ying , Xiaohan Ma , Huarui Kang , Rongrong Liu , Jianqi Lian , Xingan Wu
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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.

T 细胞免疫球蛋白和粘蛋白 1 (TIM-1) 在 Jurkat T 细胞中介导汉坦病毒感染。
汉坦病毒(HTNV)可在欧亚大陆引起出血热并发肾综合征(HFRS),因此是一个重大的公共卫生问题。出血热肾综合征的症状包括发热、出血、免疫功能障碍和肾功能损害,严重病例可导致死亡。T 细胞介导的适应性免疫反应在对抗 HTNV 感染中发挥着关键作用。然而,我们对 HTNV 和 T 细胞在疾病进展过程中的相互作用了解有限。在这项研究中,我们发现人类 CD4+ T 细胞可直接感染 HTNV,从而促进病毒的复制和产生。此外,T细胞免疫球蛋白和粘蛋白1(TIM-1)参与了HTNV感染Jurkat T细胞的过程,并进一步观察到HTNV通过凝集素依赖性内吞途径进入Jurkat T细胞。这些发现不仅证实了人类 CD4+ T 淋巴细胞对 HTNV 的易感性,还揭示了病毒的趋向性。我们的研究阐明了病毒感染过程与免疫系统之间的相互作用模式。重要的是,这项研究为 HTNV 的发病机制和抗病毒研究提供了新的见解。
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来源期刊
Virus research
Virus research 医学-病毒学
CiteScore
9.50
自引率
2.00%
发文量
239
审稿时长
43 days
期刊介绍: Virus Research provides a means of fast publication for original papers on fundamental research in virology. Contributions on new developments concerning virus structure, replication, pathogenesis and evolution are encouraged. These include reports describing virus morphology, the function and antigenic analysis of virus structural components, virus genome structure and expression, analysis on virus replication processes, virus evolution in connection with antiviral interventions, effects of viruses on their host cells, particularly on the immune system, and the pathogenesis of virus infections, including oncogene activation and transduction.
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