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Immune senescence, or the aging of the immune system, particularly its effect on changes in lymphocyte development and function, predisposes older adults to a higher risk of latent virus reactivation. The varicella-zoster virus, for example, the agent responsible for chickenpox in children, remains dormant in nerve cells in the trigeminal and dorsal root ganglia and reactivates in later life to cause shingles and post-herpetic neuralgia.
Other persistent viral infections include Epstein-Barr virus, herpes simplex virus-1 and -2, and cytomegalovirus (CMV).
Age-related immune senescent remodeling likely involves both the innate and adaptive immune system and may contribute to the immune system’s functional decline; chronic inflammatory state; and risk for frailty, chronic disease, and functional decline in older adults.
Researchers in the Johns Hopkins Division of Geriatric Medicine and Gerontology are focused on understanding the basic biological and physiological changes related to aging and frailty in the human immune system, with a special emphasis on the translational aspects of immunosenescence that have the most relevance to frailty and late-life decline.
Current research studies
- Vaccine-induced immune protection against influenza and its underlying mechanisms in frail older adults
- Persistent viral infection and age-related restriction of T cell repertoire diversity
- T cell phenotypic remodeling in aging and frailty
- Innate immune remodeling and monocyte/macrophage activation
- Aging and HIV