Noppert Grace, Wragg Kathleen, Li Chihua, Duchowny Kate, Mody Lona, Aiello Allison E, Nyquist Linda, O'Brien Martin, Yung Raymond, Goldstein Daniel
Institute for Social Research, University of Michigan, Ann Arbor, Michigan, USA.
Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Open Forum Infect Dis. 2024 Nov 29;11(12):ofae693. doi: 10.1093/ofid/ofae693. eCollection 2024 Dec.
There is an increasing awareness that aging of the immune system, or immunosenescence, is a key biological process underlying many of the hallmark diseases of aging and age-related decline broadly. While immunosenescence can be in part due to normal age-related changes in the immune system, emerging evidence posits that viral infections may be biological stressors of the immune system that accelerate the pace of immunosenescence.
We used a convenience sample of 42 individuals aged 65 years and older to examine correlations between antiviral immunoglobulin G (IgG) levels for 4 human herpesviruses (cytomegalovirus [CMV], herpes simplex virus [types 1 and 2], and Epstein-Barr virus) and multiple indicators of T-cell immunosenescence.
We found that most of the sample (n = 33) was antiviral IgG positive for 2 or more of the 4 herpesvirus infections. We also examined correlations between both the total number of viruses for which an individual had antiviral IgG and each individual virus and multiple indicators of T-cell immunosenescence, particularly p16 expression. The strongest correlations were observed between the total number of viruses for which an individual had detectable antiviral IgG and p16 mean fluorescent intensity (MFI) among CD27-CD28-CD57+ CD4+ cells ( = 0.60; < .001) and between anti-CMV IgG and p16 MFI of CD27-CD57+ CD4+ cells ( = 0.59; < .001).
Broadly, our findings offer compelling preliminary evidence for future investigations to incorporate multiple indicators of persistent viral infections and a more comprehensive set of markers of T-cell immunosenescence in population-based studies of aging.
人们越来越意识到,免疫系统衰老,即免疫衰老,是许多衰老标志性疾病及广泛的与年龄相关衰退背后的关键生物学过程。虽然免疫衰老部分可能归因于免疫系统正常的年龄相关变化,但新出现的证据表明,病毒感染可能是加速免疫衰老进程的免疫系统生物应激源。
我们使用了一个由42名65岁及以上个体组成的便利样本,来研究4种人类疱疹病毒(巨细胞病毒[CMV]、单纯疱疹病毒[1型和2型]以及爱泼斯坦-巴尔病毒)的抗病毒免疫球蛋白G(IgG)水平与T细胞免疫衰老的多个指标之间的相关性。
我们发现,大多数样本(n = 33)对4种疱疹病毒感染中的2种或更多种呈抗病毒IgG阳性。我们还研究了个体具有抗病毒IgG的病毒总数以及每种病毒与T细胞免疫衰老的多个指标(特别是p16表达)之间的相关性。在个体具有可检测抗病毒IgG的病毒总数与CD27-CD28-CD57+ CD4+细胞中的p16平均荧光强度(MFI)之间(r = 0.60;P <.001)以及抗CMV IgG与CD27-CD57+ CD4+细胞的p16 MFI之间(r = 0.59;P <.001)观察到最强的相关性。
总体而言,我们的研究结果为未来的研究提供了令人信服的初步证据,即在基于人群的衰老研究中纳入持续性病毒感染的多个指标以及更全面的T细胞免疫衰老标志物。