This study aims to take advantage of a unique opportunity to add immunoassays for several common pathogens to a sub-sample of the Whitehall II epidemiological cohort in order to study the interaction of the social environment, psychosocial stress, immune function, and cellular aging. The biological changes that occur in response to chronic stress appear to parallel those observed in aging. While stress is known to elicit a variety of biological responses that can contribute to the development of disease, the specific mechanisms linking stressors to aging are not well understood. Immune system changes are one of the hallmarks of aging. Age-associated alterations in systemic immunity, referred to as """"""""immunosenescence"""""""", are thought to contribute to the increased incidence and severity of infectious disease in older persons. Latent viral infections such as cytomegalovirus (CMV) and herpes simplex virus-1 (HSV-1) are increasingly implicated as causative agents of immunosenescence, as well as contributors to chronic health conditions characterized by inflammation including dementia and cardiovascular disease. In addition, clear and consistent relationships between psychosocial stress and reactivation of latent infections have been reported. On a separate front, psychosocial stress has recently been linked to cellular aging via telomere length. Telomeres are complex DNA-protein structures that cap and stabilize the physical ends of chromosomes, decreasing in length after each cell division. These two distinct threads of research suggest different pathways through which psychosocial stress might be related to accelerated aging: latent infections and telomeres. Socioeconomic status has been found to be related to both prevalence and immune response to latent pathogens as well as telomere length. Animal evidence suggests that infections may play a role in telomere shortening, but thus far no human studies have examined the relationships between psychosocial stressors, immune response to infection and telomere length. Such a study would greatly increase our understanding of how stress changes the body over the life course and could identify novel strategies for intervention.
This study will increase our understanding of how psychosocial stress accelerates the aging process. We propose to bring together research on two pathways that have been linked to both socioeconomic status and psychosocial stress: the role of latent pathogens in age-related immunosenescence, and the role of telomere shortening in cellular aging. Identifying associations and interactions between psychosocial stress, immune function, and telomere length could lead to novel areas of prevention and intervention in the chronic diseases of aging.
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