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Biosocial Mechanisms of Accelerated Aging: Persistent Infections and the Immune System
Biosocial Mechanisms of Accelerated Aging: Persistent Infections and the Immune System
상세정보
- 자료유형
- 학위논문 서양
- 최종처리일시
- 20260202104710
- ISBN
- 9798291555187
- DDC
- 614.4
- 서명/저자
- Biosocial Mechanisms of Accelerated Aging: Persistent Infections and the Immune System
- 발행사항
- [Sl] : The University of North Carolina at Chapel Hill, 2025
- 발행사항
- Ann Arbor : ProQuest Dissertations & Theses, 2025
- 형태사항
- 212 p
- 주기사항
- Source: Dissertations Abstracts International, Volume: 87-02, Section: B.
- 주기사항
- Advisor: Aiello, Allison E.
- 학위논문주기
- Thesis (Ph.D.)--The University of North Carolina at Chapel Hill, 2025.
- 초록/해제
- 요약Persistent infections and immune system aging are increasingly recognized as critical mechanisms underlying the development of age-related disease and health disparities. Yet, limited research has examined how these processes unfold prior to midlife or how socioeconomic disadvantage spanning early life and young adulthood may shape infection susceptibility, burden, and immune aging trajectories. This dissertation investigates the associations between life-course socioeconomic status (SES), persistent infections, and biomarkers of immunosenescence and biological aging in a nationally representative cohort of U.S. adults in early midlife, aiming to advance understanding of biosocial pathways that contribute to accelerated aging.Using data from the National Longitudinal Study of Adolescent to Adult Health (Add Health, we investigated these relationships in young adulthood and early midlife. We examined persistent infection outcomes (seropositivity and IgG antibody concentrations for CMV, EBV, HSV-1, and H. Pylori) in Wave IV (median age 28), and immune cell distributions and epigenetic markers of biological age acceleration at Wave V (median age 38). We estimated the associations between life-course socioeconomic disadvantage and both persistent infection and cellular immunosenescence outcomes, as well as associations between infection measures and cellular immunosenescence and biological age acceleration. Multivariable linear and logistic regression models were used to examine these associations. Survey weights and multiple sensitivity analyses were applied to assess generalizability and robustness of results.Results showed that persistent SES disadvantage from adolescence to young adulthood was strongly associated with higher odds of CMV, HSV-1, and H. Pylori infection, elevated CMV and HSV-1 IgG antibody concentrations, and more aged immune cell profiles as measured by increased CD4+ and CD8+ memory-to-naive T cell ratios. Further, CMV emerged as the infection most robustly associated with both immunosenescence and epigenetic age acceleration. While other infections (HSV-1, EBV, H. Pylori) demonstrated weaker and more variable associations, they were still linked to epigenetic aging outcomes.These findings underscore that biological aging processes begin manifesting well before midlife and are shaped by interacting features of social environment and biological determinants. The study highlights the importance of integrating social and biomedical frameworks in aging research and public health, and points to early-life intervention as a promising strategy to reduce infection-related immune decline and promote healthy aging trajectories across the life course.
- 일반주제명
- Epidemiology
- 일반주제명
- Aging
- 일반주제명
- Immunology
- 키워드
- Immunosenescence
- 키워드
- Life course
- 기타저자
- The University of North Carolina at Chapel Hill Epidemiology
- 기본자료저록
- Dissertations Abstracts International. 87-02B.
- 전자적 위치 및 접속
- 로그인 후 원문을 볼 수 있습니다.
MARC
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■006m o d
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■020 ▼a9798291555187
■035 ▼a(MiAaPQ)AAI32118151
■040 ▼aMiAaPQ▼cMiAaPQ
■0820 ▼a614.4
■1001 ▼aMomkus, Jennifer.
■24510▼aBiosocial Mechanisms of Accelerated Aging: Persistent Infections and the Immune System
■260 ▼a[Sl]▼bThe University of North Carolina at Chapel Hill▼c2025
■260 1▼aAnn Arbor▼bProQuest Dissertations & Theses▼c2025
■300 ▼a212 p
■500 ▼aSource: Dissertations Abstracts International, Volume: 87-02, Section: B.
■500 ▼aAdvisor: Aiello, Allison E.
■5021 ▼aThesis (Ph.D.)--The University of North Carolina at Chapel Hill, 2025.
■520 ▼aPersistent infections and immune system aging are increasingly recognized as critical mechanisms underlying the development of age-related disease and health disparities. Yet, limited research has examined how these processes unfold prior to midlife or how socioeconomic disadvantage spanning early life and young adulthood may shape infection susceptibility, burden, and immune aging trajectories. This dissertation investigates the associations between life-course socioeconomic status (SES), persistent infections, and biomarkers of immunosenescence and biological aging in a nationally representative cohort of U.S. adults in early midlife, aiming to advance understanding of biosocial pathways that contribute to accelerated aging.Using data from the National Longitudinal Study of Adolescent to Adult Health (Add Health, we investigated these relationships in young adulthood and early midlife. We examined persistent infection outcomes (seropositivity and IgG antibody concentrations for CMV, EBV, HSV-1, and H. Pylori) in Wave IV (median age 28), and immune cell distributions and epigenetic markers of biological age acceleration at Wave V (median age 38). We estimated the associations between life-course socioeconomic disadvantage and both persistent infection and cellular immunosenescence outcomes, as well as associations between infection measures and cellular immunosenescence and biological age acceleration. Multivariable linear and logistic regression models were used to examine these associations. Survey weights and multiple sensitivity analyses were applied to assess generalizability and robustness of results.Results showed that persistent SES disadvantage from adolescence to young adulthood was strongly associated with higher odds of CMV, HSV-1, and H. Pylori infection, elevated CMV and HSV-1 IgG antibody concentrations, and more aged immune cell profiles as measured by increased CD4+ and CD8+ memory-to-naive T cell ratios. Further, CMV emerged as the infection most robustly associated with both immunosenescence and epigenetic age acceleration. While other infections (HSV-1, EBV, H. Pylori) demonstrated weaker and more variable associations, they were still linked to epigenetic aging outcomes.These findings underscore that biological aging processes begin manifesting well before midlife and are shaped by interacting features of social environment and biological determinants. The study highlights the importance of integrating social and biomedical frameworks in aging research and public health, and points to early-life intervention as a promising strategy to reduce infection-related immune decline and promote healthy aging trajectories across the life course.
■590 ▼aSchool code: 0153.
■650 4▼aEpidemiology
■650 4▼aAging
■650 4▼aImmunology
■653 ▼aBiosocial pathways
■653 ▼aEpigenetic age acceleration
■653 ▼aImmunosenescence
■653 ▼aLife course
■653 ▼aPersistent infections
■653 ▼aSocioeconomic disadvantage
■690 ▼a0766
■690 ▼a0982
■690 ▼a0493
■71020▼aThe University of North Carolina at Chapel Hill▼bEpidemiology.
■7730 ▼tDissertations Abstracts International▼g87-02B.
■790 ▼a0153
■791 ▼aPh.D.
■792 ▼a2025
■793 ▼aEnglish
■85640▼uhttp://www.riss.kr/pdu/ddodLink.do?id=T17358494▼nKERIS▼z이 자료의 원문은 한국교육학술정보원에서 제공합니다.
