HIV infection and aging of the innate immune system
Anna C. Hearps A , Thomas A. Angelovich A , Anthony Jaworowski A B C , John Mills D E , Alan L. Landay F and Suzanne M. Crowe A C D G
+ Author Affiliations
- Author Affiliations
A AIDS Pathogenesis Research Unit, Centre for Virology, Burnet Institute for Medical Research and Public Health, Melbourne, Vic. 3004, Australia.
B Department of Immunology, Monash University, Melbourne, Vic. 3004, Australia.
C Department of Medicine, Monash University, Melbourne, Vic. 3004, Australia.
D Department of Infectious Diseases, Alfred Hospital, Melbourne, Vic. 3004, Australia.
E Department of Epidemiology & Community Health, Monash University, Melbourne, Vic. 3004, Australia.
F Department of Immunology and Microbiology, Rush University Medical Center, Chicago, IL 60612, USA.
G Corresponding author. Email: crowe@burnet.edu.au
Sexual Health 8(4) 453-464 https://doi.org/10.1071/SH11028
Submitted: 22 February 2011 Accepted: 6 May 2011 Published: 30 September 2011
Abstract
The increased life expectancy of HIV-infected individuals due to improved treatment has revealed an unexpected increase in non-AIDS comorbidities that are typically associated with older age including cardiovascular disease, dementia and frailty. The majority of these diseases arise as the result of dysregulated systemic inflammation, and both the aged and HIV-infected individuals exhibit elevated basal levels of inflammation. In the elderly, increased inflammation and age-related diseases are associated with a state of impaired immunity called immunosenescence, which is thought to result from a lifetime of immune stimulation. It is now apparent that HIV induces premature immunosenescence within T-cells; however, the impact of HIV on aging of cells of the innate arm of the immune system is unknown. Innate immune cells play a central role in inflammation and are thus critical for the pathogenesis of inflammatory diseases. Limited evidence suggests HIV infection mimics age-related changes to innate immune cells; however, the extent of this effect and the mechanism underlying these changes remain to be defined. This review focuses on the impact of HIV infection on the function and aging of innate immune cells and discusses potential drivers of premature immunosenescence including chronic endotoxaemia, residual viraemia, telomere attrition and altered cellular signalling.
Additional keywords: AIDS, immunosenescence, inflammation.
References
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