一个与COVID-19中嗅觉丧失相关的表观遗传位置
Elif Sibel Aslan1,2, Kenneth White3, Gulsen Meral4,5
1Department of Molecular Biology and Genetics, Biruni University, Merkezefendi, 75 Sk No:1-13 M.G., 34015 Istanbul, Turkey.
Diagnostics (Basel, Switzerland)
|January 8, 2025
概括
感染COVID-19可能会导致持续的气味丧失 (厌味症). 这项研究发现,阿诺斯米亚患者的UGT1A1基因的DNA甲基化水平较低,这表明嗅觉功能障碍的潜在表观遗传生物标志物.
科学领域:
- 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.
- 嗅觉神经科学是一种神经科学.
- 病毒病原体的产生
背景情况:
- 持续的嗅觉丧失 (无闻症) 是SARS-CoV-2感染的常见,长期症状.
- 与COVID-19相关的厌氧症背后的机制尚不清楚.
- 接近UGT2A1/UGT2A2的遗传变异与厌氧有关,但表观遗传因素仍未被探索.
研究的目的:
- 为了研究COVID-19患者的UGT1A1基因中的DNA甲基化变化,有或没有嗅觉丧失.
- 探索表观遗传学在COVID-19后嗅觉功能障碍的发展和持续中的作用.
主要方法:
- 分析来自COVID-19幸存者的两个匹配队列 (每组20名患者) 的血液样本中的DNA甲基化模式.
- 群体根据嗅觉功能进行了分层:正常的嗅觉 (normmosmia) 与嗅觉丧失 (anosmia).
- 年龄和性别在队列之间匹配,以控制混变量.
主要成果:
- 与诺莫斯米亚组相比,在阿诺斯米亚组的UGT1A1位点观察到显著较低的DNA甲基化水平.
- 在患有嗅觉丧失 (p < 0.0001) 的患者中,中位 UGT1A1 甲基化率下降了 14%.
- 这些表观基因组变化表明UGT1A1甲基化在COVID-19诱导的无氧化症病原体中的潜在作用.
结论:
- 这项研究提供了表观遗传变化的新证据,特别是UGT1A1中的DNA甲基化,与COVID-19中嗅觉丧失相关.
- 在SARS-CoV-2感染后,UGT1A1甲基化状态可能作为嗅觉功能障碍的潜在生物标志物.
- 这些发现为未来针对持久性厌氧症的有针对性的干预措施的研究奠定了基础,强调了遗传,表观遗传和环境因素的相互作用.
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