Purpose of the review: During this era of unprecedented antiretroviral therapeutic efficacy, there is hope for successfully treated individuals to achieve a longevity approaching that of the general population. However, the recent identification of a higher incidence of cardiovascular, bone, metabolic, neurocognitive and other aging comorbidities is of major concern and may compromise that ability. The purpose of this review is to focus on the dynamic process of immune remodelling, known as immune senescence, which occurs during HIV infection, and how it impacts on long-term comorbidities.
Recent findings: Early aging in those with HIV appears to stem from persistent chronic inflammation and residual immune activation despite successful antiretroviral therapy. Multiple similarities exist between the T-cell-senescent phenotypes found in many chronic autoimmune and inflammatory conditions, including HIV disease, and the elderly. The immune risk phenotype is linked to poor clinical outcomes in the elderly and may also have clinical consequences in those with HIV.
Summary: Immune senescence results in functional impairments of immunity and a reduced ability to adapt to metabolic stress. Understanding the factors driving the development of immune senescence is critical for the development of strategies to prevent early aging.