为什么简单疹1病毒编码的UL49.5蛋白质无法抑制TAP依赖抗原的呈现?
Natalia Karska1, Igor Zhukov2, Andrea D Lipińska3
1Faculty of Chemistry, University of Gdańsk, Wita Stwosza 63, 80-308 Gdańsk, Poland.
Biochimica et biophysica acta. Biomembranes
|July 30, 2023
概括
简单疹病毒1糖蛋白N (gN/UL49.5) 的3D结构在膜环境中确定. 与其他疹病毒不同,HSV-1 gN/UL49.5具有单一的跨膜螺旋,并且不抑制抗原呈现.
科学领域:
- 结构生物学 结构生物学
- 病毒学 病毒学
- 分子生物学分子生物学
背景情况:
- 简单疹病毒1 (HSV-1) 导致人类疾病,产生糖蛋白N (gN/UL49.5).
- 目前尚不清楚HSV-1 gN/UL49.5的功能,特别是其作为与抗原处理 (TAP) 抑制剂相关的载体的作用.
- UL49.5 蛋白质结构在疹病毒物种之间有所不同,需要进行比较分析.
研究的目的:
- 为了阐明HSV-1编码的UL49.5蛋白在内质网膜 (ER) 膜模型中的3D结构.
- 为了比较HSV-1 UL49.5的结构特征与其牛疹病毒1 (BoHV-1) 同类病毒,一种已知的TAP抑制剂.
主要方法:
- 圆形二重化谱光学 圆形二重化谱光学
- 2D核磁共振 (NMR) 是一个二维技术.
- 在膜模拟环境中的多个微秒全原子分子动力学模拟.
主要成果:
- HSV-1 UL49.5的N端在细胞外区域呈现出灵活,无序的结构.
- HSV-1 UL49.5的跨膜域由单个长的α螺旋组成,与BoHV-1 UL49.5.5的两螺旋结构不同.
- HSV-1 UL49.5的C端 (细胞质部分) 显示出一个短,无序的结构.
结论:
- 这项研究为HSV-1 gN/UL49.5.5提供了关键的实验结构数据.
- HSV-1 UL49.5 独特的单螺旋跨膜结构可能解释了它无法抑制TAP-依赖抗原呈现途径的原因.
更多相关视频
09:10siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells
Published on: October 28, 2019
7.3K
09:15Tyramide Signal Amplification for the Immunofluorescent Staining of ZBP1-Dependent Phosphorylation of RIPK3 and MLKL After HSV-1 Infection in Human Cells
Published on: October 20, 2022
2.3K
相关概念视频
Leaky Scanning
During most eukaryotic translation processes, the small 40S ribosome subunit scans an mRNA from its 5' end until it encounters the first start AUG codon. The large 60S ribosomal subunit then joins the smaller one to initiate protein synthesis. The location of the translation initiation is largely determined by the nucleotides near the start codon as there may be multiple translation initiation sites present on the mRNA. Marilyn Kozak discovered that the sequence RCCAUGG (where R stands for...
Immune Response Against Viral Pathogens
The immune system's response to viral infections is a complex and coordinated process involving natural killer (NK) cells, T cell-mediated responses, and antibody-mediated responses.
NK Cells
NK cells are a crucial part of our innate immune system, acting as the first line of defense against viral infections. These cells can recognize and kill infected cells without prior exposure to the virus, effectively slowing down the spread of infection. Additionally, NK cells produce proinflammatory...
NK Cells
NK cells are a crucial part of our innate immune system, acting as the first line of defense against viral infections. These cells can recognize and kill infected cells without prior exposure to the virus, effectively slowing down the spread of infection. Additionally, NK cells produce proinflammatory...
Inhibitors of Viral Protein Synthesis
Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...
Inhibitors of Virion Maturation and Assembly
As part of their replication cycle, certain viruses synthesize long precursor proteins called polyproteins within infected host cells. In human immunodeficiency virus (HIV), two major polyproteins are produced: Gag and Gag-Pol. The Gag polyprotein supplies the structural components of the virus, while Gag-Pol includes essential viral enzymes such as reverse transcriptase, integrase, and protease. After synthesis, these polyproteins move to the host cell membrane, where they assemble into an...
