在EBV,SARS-CoV-2和HLA等级I分子结合基因之间共享的致病特征和序列,具有潜在的自身免疫作用
Yekbun Adiguzel1, Naim Mahroum2, Sylviane Muller3,4,5
1Department of Medical Biology, School of Medicine, Atilim University, Kizilcasar Mah. 06836 Incek, Golbasi, Ankara, Turkey. yekbun.adiguzel@atilim.edu.tr.
Clinical reviews in allergy & immunology
|July 28, 2023
概括
埃普斯坦-巴尔病毒 (EBV) 和SARS-CoV-2可以通过分子模仿引发自身免疫性疾病. 这些病毒和人类蛋白质之间共享的序列,与特定的HLA基因相结合,可能会增加感染个体的自身免疫风险.
科学领域:
- 免疫学 免疫学 免疫学
- 病毒学 病毒学
- 遗传学 遗传学 是一个
背景情况:
- 爱普斯坦-巴尔病毒 (EBV) 和SARS-CoV-2与自身免疫有关.
- 分子仿真是一种针对病毒诱导的自身免疫性疾病的拟议机制.
- 了解共享的病毒和人类蛋白质序列至关重要.
研究的目的:
- 审查EBV,SARS-CoV-2和自身免疫之间的关系.
- 调查分子模仿作为一种自免疫诱导的常见机制.
- 为了确定与风险增加相关的特定人类白细胞抗原 (HLA) 基因.
主要方法:
- 关于EBV,SARS-CoV-2和自身免疫力的文献综述.
- 分析病毒和人类蛋白质之间共享的8mer序列.
- 在基中预测表位组与特定的HLA等位基结合 (例如,HLA-A*02:01,HLA-B*40:01).
主要成果:
- 在SARS-CoV-2,EBV和人类蛋白质之间确定了共享的5mer序列.
- 发现了与多个HLA等位基因预测的结合亲缘关系的人类序.
- 与特定的HLA血清型相关的突出潜在风险 (例如,HLA-A*02:01,HLA-B*40:01).
结论:
- 分子仿真是一种合理的机制,将SARS-CoV-2和EBV感染与自身免疫性联系起来.
- 特定的HLA基因基因可能会使个体通过这些病毒产生自身免疫反应.
- 对病毒蛋白仿真和HLA关联的进一步研究是有必要的.
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