来自杂志 Immunogenetics 的文献。
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小年 (2024-08-31 21:29):
#paper The impact of HLA polymorphism on herpesvirus infection and disease DOI :10.1007/s00251-022-01288-z 文章探讨了 HLA 多态性对感染和疾病的影响。以疱疹病毒为切入口,讲述了HLA 的遗传变异与疱疹病毒感染和疾病的易感性密切相关。 文章通过对 HHV 的感染和疾病信息的总结,以及对 HLA 免疫功能的介绍,阐述了 HLA - HHV 协同进化的证据。通过 GWAS 和病例 - 对照研究,确定了与不同疱疹病毒相关的 HLA 等位基因,并探讨了 HLA 等位基因协调可变免疫反应的机制。文章发现,A * 01 和 A * 02 等位基因分别与疱疹病毒感染和疾病的易感性和抵抗力普遍相关,其他 HLA 等位基因与特定疱疹病毒或疾病的关联存在差异。文章强调了 HLA 在疱疹病毒免疫中的重要性,但也指出相关研究存在局限性,未来需要进一步深入研究。 这里这里有趣的是文章讲了疱疹病毒与人类有古老的共同进化关系,由此延伸,如果去找那先与人类关系紧密又比较“古老”的病毒和疾病,应该能发现更多类似的跟我们免疫系统有着共同进化关系的病毒和疾病,说不定能挖出来些东西。
Abstract:
AbstractHuman Leukocyte Antigens (HLA) are cell surface molecules, central in coordinating innate and adaptive immune responses, that are targets of strong diversifying natural selection by pathogens. Of these pathogens, human … >>>
AbstractHuman Leukocyte Antigens (HLA) are cell surface molecules, central in coordinating innate and adaptive immune responses, that are targets of strong diversifying natural selection by pathogens. Of these pathogens, human herpesviruses have a uniquely ancient relationship with our species, where coevolution likely has reciprocating impact on HLA and viral genomic diversity. Consistent with this notion, genetic variation at multiple HLA loci is strongly associated with modulating immunity to herpesvirus infection. Here, we synthesize published genetic associations of HLA with herpesvirus infection and disease, both from case/control and genome-wide association studies. We analyze genetic associations across the eight human herpesviruses and identify HLA alleles that are associated with diverse herpesvirus-related phenotypes. We find that whereas most HLA genetic associations are virus- or disease-specific, HLA-A*01 and HLA-A*02 allotypes may be more generally associated with immune susceptibility and control, respectively, across multiple herpesviruses. Connecting genetic association data with functional corroboration, we discuss mechanisms by which diverse HLA and cognate receptor allotypes direct variable immune responses during herpesvirus infection and pathogenesis. Together, this review examines the complexity of HLA-herpesvirus interactions driven by differential T cell and Natural Killer cell immune responses. <<<
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