Causal Impact of Immune Phenotypes on Herpes Zoster and Postherpetic Neuralgia: Insights from Mendelian Randomization Analysis

疱疹后神经痛 医学 孟德尔随机化 皮肤病科 免疫系统 孟德尔遗传 表型 神经痛 免疫学 木瓦 病毒学 生物信息学 遗传学 药理学 神经病理性疼痛 病毒 生物 遗传变异 基因 基因型
作者
Zhangren Yan,Dandan Shen,Xiaoqian Qiu,Bohua Ai,Chengjie Xiong
出处
期刊:Clinical, Cosmetic and Investigational Dermatology [Dove Medical Press]
卷期号:Volume 18: 919-928
标识
DOI:10.2147/ccid.s502861
摘要

Previous research has investigated the contribution of immunological cells to both herpes zoster (HZ) and postherpetic neuralgia (PHN). This Mendelian randomization (MR) study seeks to further assess the cause-and-effect connection among 731 immune cell phenotypes and HZ and PHN providing partial causal evidence. The data for HZ and PHN were sourced from the FinnGen database, and the 731 immune cell phenotypes were drawn from GWAS. Five analytical methods, primarily utilizing the inverse variance weighted (IVW) approach, were selected to assess the cause-and-effect connection in relation to exposure and outcomes. Finally, sensitivity analyses were undertaken to verify the robustness as well as validity of the data. The MR analysis utilizing the IVW method revealed that in the forward Mendelian randomization, two immune cell phenotypes of T cells were negatively connected with HZ(P < 0.05, OR < 1). In comparison, two other immune cell phenotypes were advantageously linked with PHN(P < 0.05, OR > 1). In the reverse Mendelian randomization, HZ was positively associated with five immune cell phenotypes from T cells and NK cells (P < 0.05, OR > 1). PHN demonstrated a positive association with nine immune cell phenotypes from T cells, myeloid cells, B cells, CDC, and monocytes (P < 0.05, OR > 1), while showing a negative association with the remaining 11 immune cells (P < 0.05, OR < 1). Likewise, No evidence of disparity, horizontal pleiotropy, or backward causality was found. This study employs Mendelian randomization analysis to elucidate the complex causal relationships between various immune cell phenotypes and the development of HZ and PHN. The findings provide insights into the immune mechanisms underlying disease progression, advancing our understanding of immune-mediated pathways and their potential implications for future therapeutic strategies.

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