Immunosenescence and HIV

The present review discusses the interplay between HIV infection and other environmental factors (e.g. co-infection with CMV) in the acceleration of the aging process of the immune system, leading to 'immunosenescence.'

Basic studies in cell biology demonstrate that replicative senescence is a common pathway of many cell lineages, including those of the immune system, characterized by activation of a unique pro-inflammatory secretory program. In the setting of HIV disease, this process is accelerated, resulting in an immunosuppressed state that diminishes the ability of the immune system to contain virus while at the same time facilitating viral replication and spread. Clinically, these changes result in a lower capacity to respond to new infections as well as an increased frequency of age-associated end-organ disease (e.g. cardiovascular complications, cancer, and neurologic disease).

Accelerated immunosenescence in the setting of HIV disease is associated with increased morbidity and mortality, prompting the need for more investigation into its causes, diagnosis, and treatment.