Socioeconomic Disadvantage Related to Infection Burden and Immune Aging

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Epstein-Barr virus (EBV), computer illustration. EBV, also known as human herpes virus 4, is 1 of 8 herpes viruses that infects humans. It is best known as the cause of infectious mononucleosis (glandular fever), but is also associated with some forms of cancer, including Burkitt's lymphoma. In both infections, the virus infects one type of white blood cell, the B lymphocytes. Infection with EBV is common and usually harmless; additional factors potentiate the development of more serious diseases.

Socioeconomic status (SES) affects many aspects of health. For instance, SES disadvantage has been associated with higher-risk living environments, such as overcrowded housing or substandard sanitation; increased chronic stress; and decreased access to health care. For immune health specifically, the cumulative effects of chronic stressors and repeated exposure to infections may accelerate biological aging, even in young adults. Understanding how these processes are impacted by SES is essential for identifying early contributors to chronic disease risk.

What were the researchers studying and why?

Persistent infection burden can lead to chronic immune activation, which can gradually wear down the immune system. This deterioration, known as immunosenescence, is typically measured at one time point, even though major contributors—such as chronic stress and repeated exposure to infection—occur across the life course. As SES disadvantage across the life course is associated with a heavier burden of persistent infections, the researchers sought to determine whether SES and infection burden contribute to signs of premature immune aging in young adults.

How did the researchers conduct the study?

The research team analyzed data from the National Longitudinal Study of Adolescent to Adult Health (Add Health). Add Health is a nationally representative longitudinal study of more than 20,000 adolescents who were in grades 7–12 during the 1994–95 school year and have been followed across six waves of data collection, most recently in 2022–25. The study provides insights into risk and preventive health factors from adolescence through the life course.

Participants provided detailed information about their socioeconomic circumstances from childhood through early adulthood, including early-life economic hardship, educational attainment, and mobility across socioeconomic strata. Blood samples were used to assess persistent infection burden through biomarkers indicating exposure to four common pathogens: cytomegalovirus (CMV), Epstein-Barr virus (EBV), herpes simplex virus type 1 (HSV-1), and Helicobacter pylori (H. Pylori). 

The researchers also measured cellular immunosenescence by examining levels of the antibody immunoglobulin G (IgG) and ratios of immune cell phenotypes (CD4+, CD8+, naïve, and memory T Cells) that are known to shift with aging and chronic immune stimulation. They then investigated the associations between these SES measures and biological indicators using multivariable logistic models.

What did the study results show?

The study found that young adults who experienced greater socioeconomic disadvantage throughout their lives were more likely to have a higher burden of persistent infections (CMV OR = 1.6 95 % CI: 1.3, 2.0; HSV-1 OR = 1.9 95 % CI: 1.5, 2.5; H. Pylori OR = 2.3 95 % CI: 1.8, 2.9). For all infections but EBV, individuals with disadvantaged SES also showed higher antibody concentrations later in life than those with non-disadvantaged SES (CMV β = 13.0, 95 % CI: 7.4, 18.7; HSV-1 β = 1.4, 95 % CI: 0.9, 1.9; H. Pylori β = 8.6, 95 % CI: 5.0, 12.1), suggesting that some individuals’ immune systems may be aging more rapidly than expected. Life-course socioeconomic disadvantage (β = 0.2, 95 % CI: 0.02)—especially the decline of socioeconomic status (β = 0.3, 95 % CI: 0.1, 0.4 )—was associated with higher CD4+ memory-to-naïve T-cell ratios, indicating shifts in immune cell composition.

People with both life-course disadvantage and elevated infection burden exhibited the clearest markers of immunosenescence. These findings indicate that early-life social environments may influence biological aging through pathways involving chronic immune activation and infectious exposures, revealing a mechanism through which differences in SES can impact long-term health.

What is the potential impact of these findings?

This study offers new insight into how exposures and stressors associated with lower SES may become biologically embedded and demonstrates that these factors begin to affect long-term immune function at an earlier stage of life than previously appreciated. The findings underscore the importance of designing interventions to address socioeconomic conditions and reduce environmental and infectious exposures in childhood. Additional research is needed to determine how widespread these patterns are and to identify strategies for mitigating early immune aging. Doing so may not only improve immediate well-being but also protect against early immune decline and later disease vulnerability.

Citation

Momkus, J., Harris, K. M., Yang, Y. C., Martin, C. L., Edwards, J. K., & Aiello, A. E. (2025). Life course socioeconomic disadvantage and persistent infection burden: links to cellular immunosenescence in U.S. young adults. Social Science & Medicine, 383, 118398. https://doi.org/10.1016/j.socscimed.2025.118398