Immunosenescence and HIV.
OBJECTIVE
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.'


RESULTS
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).


CONCLUSIONS
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.
HIV/AIDS Program, Department of Medicine, University of California, San Francisco, CA, USA.
Steven G
SG
Deeks
Eric
E
Verdin
Joseph M
JM
McCune
D000375:Aging / Q000276:immunology*; D000818:Animals; D016922:Cellular Senescence / Q000502:physiology; D015658:HIV Infections / Q000276:immunology*; D006801:Humans; D007107:Immune System / Q000502:physiology*