Duarte Rodrigo R R, Nixon Douglas F, Powell Timothy R
Social, Genetic & Developmental Psychiatry Centre, Institute of Psychiatry, Psychology & Neuroscience, King's College London, London, United Kingdom; Division of Infectious Diseases, Weill Cornell Medicine, Cornell University, New York, NY, the United States of America.
Feinstein Institutes for Medical Research, Northwell Health, Manhasset, NY, the United States of America.
Brain Behav Immun. 2025 Jan;123:765-770. doi: 10.1016/j.bbi.2024.10.020. Epub 2024 Oct 12.
Human endogenous retroviruses (HERVs) are sequences in the human genome that originated from infections with ancient retroviruses during our evolution. Previous studies have linked HERVs to neurodegenerative diseases, but defining their role in aetiology has been challenging. Here, we used a retrotranscriptome-wide association study (rTWAS) approach to assess the relationships between genetic risk for neurodegenerative diseases and HERV expression in the brain, calculated with genomic precision.
We analysed genetic association statistics pertaining to Alzheimer's disease, amyotrophic lateral sclerosis, multiple sclerosis, and Parkinson's disease, using HERV expression models calculated from 792 cortical samples. Robust risk factors were considered those that survived multiple testing correction in the primary analysis, which were also significant in conditional and joint analyses, and that had a posterior inclusion probability above 0.5 in fine-mapping analyses.
The primary analysis identified 12 HERV expression signatures associated with neurodegenerative disease susceptibility. We found one HERV expression signature robustly associated with amyotrophic lateral sclerosis on chromosome 12q14 (MER61_12q14.2) and one robustly associated with multiple sclerosis on chromosome 1p36 (ERVLE_1p36.32a). A co-expression analysis suggested that these HERVs are involved in homophilic cell adhesion via plasma membrane adhesion molecules.
We found HERV expression profiles robustly associated with amyotrophic lateral sclerosis and multiple sclerosis susceptibility, highlighting novel risk mechanisms underlying neurodegenerative disease, and offering potential new targets for therapeutic intervention.
人类内源性逆转录病毒(HERVs)是人类基因组中的序列,起源于我们进化过程中古代逆转录病毒的感染。先前的研究已将HERVs与神经退行性疾病联系起来,但确定它们在病因学中的作用一直具有挑战性。在这里,我们使用全转录组范围的逆转录关联研究(rTWAS)方法,以基因组精度评估神经退行性疾病的遗传风险与大脑中HERV表达之间的关系。
我们使用从792个皮质样本计算得出的HERV表达模型,分析了与阿尔茨海默病、肌萎缩侧索硬化症、多发性硬化症和帕金森病相关的遗传关联统计数据。在初步分析中,经过多次测试校正后仍存在的、在条件分析和联合分析中也具有显著性且在精细定位分析中后验包含概率高于0.5的危险因素被视为稳健的危险因素。
初步分析确定了12个与神经退行性疾病易感性相关的HERV表达特征。我们发现一个HERV表达特征与12号染色体q14区域的肌萎缩侧索硬化症密切相关(MER61_12q14.2),另一个与1号染色体p36区域的多发性硬化症密切相关(ERVLE_1p36.32a)。共表达分析表明,这些HERVs通过质膜粘附分子参与同嗜性细胞粘附。
我们发现HERV表达谱与肌萎缩侧索硬化症和多发性硬化症易感性密切相关,突出了神经退行性疾病潜在的新风险机制,并为治疗干预提供了潜在的新靶点。