Wu Erli, Cheng Ming, Yang Shouxiang, Yuan Wanting, Gu Mengyun, Lu Dandan, Zhang Lei, Wang Qingqing, Sun Xiaoyu, Shao Wei
Stomatologic Hospital & College, Anhui Medical University, Key Lab. of Oral Diseases Research of Anhui Province, Hefei, 230032, China.
Arrail Dental Group, Beijing, 100012, China.
Heliyon. 2024 Aug 6;10(16):e35904. doi: 10.1016/j.heliyon.2024.e35904. eCollection 2024 Aug 30.
To explore the causal association between () infection, herpesvirus infection and periodontitis (PD) from a genetic perspective using Mendelian randomization (MR).
The PD data were derived from genome-wide association study (GWAS) from the Dental Endpoints (GLIDE) consortium, and the FinnGen Biobank provided data on and herpesvirus infections. In addition, we examined GWAS data for subtypes of and herpesvirus infection. Inverse variance weighting (IVW) was selected as a major analysis technique, and weighted median (WM), weighted model, simple model, and MR-Egger regression were added as supplementary methods. To verify the findings, the effects of pleiotropy and heterogeneity were assessed.
Genetically predicted infection (OR = 0.914, 95%CI = 0.693-1.205, P = 0.523), anti- VacA (OR = 0.973, 95%CI = 0.895-1.057, P 0.515), anti- CagA (OR = 1.072, 95%CI = 0.986-1.164; P = 0.102), Epstein-Barr virus (EBV) infection (OR = 1.026, 95%CI = 0.940-1.120, P = 0.567), Herpes simplex virus (HSV) infection (OR = 0.962, 95%CI = 0.883-1.048, P = 0.372), cytomegalovirus (CMV) infection (OR = 1.025, 95%CI = 0.967-1.088, P = 0.415), EBV nuclear antigen-1 (EBNA1) (OR = 1.061, 95%CI = 0.930-1.209, P = 0.378), EBV virus capsid antigen (VCA) (OR = 1.043, 95CI% = 0.890-1.222, P = 0.603), HSV-1 (OR = 1.251, 95%CI = 0.782-2.001, P = 0.351), HSV-2 (OR = 1.020, 95%CI = 0.950-1.096, P = 0.585), CMV IgG (OR = 0.990, 95CI% = 0.882-1.111, P = 0.861) were not associated with PD, indicated that and herpesvirus infection had no causal relationship to PD. Reverse studies also found no cause effect of PD on or herpesvirus infection. The results of the sensitivity analysis suggested the robustness of the MR results.
This study offered preliminary proof that and herpesvirus infections were not causally linked to PD, and vice versa. However, more robust instrumental variables (IVs) and larger samples of GWAS data were necessary for further MR analysis.
采用孟德尔随机化（MR）方法从遗传学角度探讨（）感染、疱疹病毒感染与牙周炎（PD）之间的因果关系。
PD数据来源于牙科终点（GLIDE）联盟的全基因组关联研究（GWAS），芬兰生物银行提供了关于和疱疹病毒感染的数据。此外，我们还研究了和疱疹病毒感染亚型的GWAS数据。选择逆方差加权（IVW）作为主要分析技术，并增加加权中位数（WM）、加权模型、简单模型和MR-Egger回归作为补充方法。为验证研究结果，评估了多效性和异质性的影响。
遗传预测的感染（OR = 0.914，95%CI = 0.693 - 1.205，P = 0.523）、抗VacA（OR = 0.973，95%CI = 0.895 - 1.057，P = 0.515）、抗CagA（OR = 1.072，95%CI = 0.986 - 1.164；P = 0.102）、爱泼斯坦-巴尔病毒（EBV）感染（OR = 1.026，95%CI = 0.940 - 1.120，P = 0.567）、单纯疱疹病毒（HSV）感染（OR = 0.962，95%CI = 0.883 - 1.048，P = 0.372）、巨细胞病毒（CMV）感染（OR = 1.025，95%CI = 0.967 - 1.088，P = 0.415）、EBV核抗原-1（EBNA1）（OR = 1.061，95%CI = 0.930 - 1.209，P = 0.378）、EBV病毒衣壳抗原（VCA）（OR = 1.043，95CI% = 0.890 - 1.222，P = 0.603）、HSV-1（OR = 1.251，95%CI = 0.782 - 2.001，P = 0.351）、HSV-2（OR = 1.020，95%CI = 当文档中出现不完整信息时，需保持原文格式，如（）、VacA、CagA、CI%等。95%CI = 0.950 - 1.096，P = 0.585）、CMV IgG（OR = 0.990，95CI% = 0.882 - 1.111，P = 0.861）与PD均无关联，表明和疱疹病毒感染与PD无因果关系。反向研究也未发现PD对或疱疹病毒感染有因果效应。敏感性分析结果表明MR结果具有稳健性。
本研究提供了初步证据，表明和疱疹病毒感染与PD无因果联系，反之亦然。然而，进一步的MR分析需要更稳健的工具变量（IVs）和更大样本量的GWAS数据。
