Details

Autor(en) / Beteiligte

• Ma, Ruixue
• Zheng, Xuyang
• Gu, Tianle
• Liu, Ziyu
• Hou, Shiyuan
• Sun, Danni
• Ding, Yaxin
• Wang, Fang
• Ying, Qikang
• Ma, Xiaohan
• Kang, Huarui
• Liu, Rongrong
• Lian, Jianqi
• Wu, Xingan

Titel

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

Ist Teil von

• Virus research, 2024-08, Vol.346, p.199394-199394, Article 199394

Ort / Verlag

Netherlands: Elsevier B.V

Erscheinungsjahr

2024

Link zum Volltext

Quelle

Alma/SFX Local Collection

Beschreibungen/Notizen

• •Primary human CD4+T cells and Jurkat T cells can be infected with HTNV.•A specific anti-TIM-1 antibody resulted in a significant decrease in HTNV infection of Jurkat T cells.•Knocking down TIM-1 resulted in a substantial decrease of HTNV infection of Jurkat T cells.•Overexpression of TIM-1 markedly enhanced the infection of HTNV of Jurkat T cells.•HTNV enters Jurkat T cells via the clathrin-dependent endocytosis pathway. 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.