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基孔肯雅病毒包膜蛋白进入人类细胞与蚊子细胞的决定因素。

Determinants of human versus mosquito cell entry by the Chikungunya virus envelope proteins.

作者信息

Ju Xiaohui, Hannon William W, Kaszuba Tomasz, Radford Caelan E, Larsen Brendan B, Nelson Samantha S, Nelson Christopher A, Baltazar-Perez Israel, Zimmerman Ofer, Fremont Daved H, Diamond Michael S, Bloom Jesse D

机构信息

Basic Sciences Division and Computational Biology Program, Fred Hutchinson Cancer Center, Seattle, WA 98109, USA.

Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.

出版信息

bioRxiv. 2025 Aug 25:2025.08.25.672233. doi: 10.1101/2025.08.25.672233.

Abstract

Chikungunya virus (CHIKV) infects both humans and mosquitoes during its transmission cycle. How the virus's envelope proteins mediate entry in cells from such different species is unclear. MXRA8 is a receptor for CHIKV in mammalian cells, but the receptor(s) in mosquito cells remains unknown. Here we use pseudovirus deep mutational scanning to measure how nearly all amino-acid mutations to the CHIKV envelope proteins affect entry in MXRA8-expressing human and mosquito cells. Most mutations similarly affect entry in both types of cells, and our comprehensive measurements of these effects define functional constraints related to protein folding and fusion activity. However, some mutations differentially affect entry in MXRA8-expressing human cells versus mosquito cells. Sites where mutations specifically impair entry in MXRA8-expressing human cells are often involved in MXRA8 binding, and we hypothesize sites where mutations specifically impair entry in mosquito cells are involved in binding the unknown mosquito receptor(s). We use the deep mutational scanning data to design loss-of-tropism mutant viruses that are impaired in their ability to infect either mosquito cells or MXRA8-expressing human cells. Our findings provide insights into the species-specific determinants of CHIKV cell entry that can help guide receptor identification and vaccine development.

摘要

基孔肯雅病毒(CHIKV)在其传播周期中会感染人类和蚊子。该病毒的包膜蛋白如何介导进入如此不同物种的细胞尚不清楚。MXRA8是CHIKV在哺乳动物细胞中的一种受体,但蚊子细胞中的受体仍然未知。在这里,我们使用假病毒深度突变扫描来测量CHIKV包膜蛋白几乎所有的氨基酸突变如何影响进入表达MXRA8的人类和蚊子细胞。大多数突变对两种类型细胞的进入都有类似影响,我们对这些影响的全面测量定义了与蛋白质折叠和融合活性相关的功能限制。然而,一些突变对表达MXRA8的人类细胞和蚊子细胞的进入有不同影响。突变特异性损害进入表达MXRA8的人类细胞的位点通常参与MXRA8结合,我们推测突变特异性损害进入蚊子细胞的位点参与结合未知的蚊子受体。我们利用深度突变扫描数据设计了嗜性丧失突变病毒,这些病毒感染蚊子细胞或表达MXRA8的人类细胞的能力受损。我们的研究结果为CHIKV细胞进入的物种特异性决定因素提供了见解,有助于指导受体鉴定和疫苗开发。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a5d/12407778/31f11ed24c96/nihpp-2025.08.25.672233v1-f0007.jpg

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