Publications & Reports

Viremic and virologically suppressed HIV infection increases age-related changes to monocyte activation equivalent to 12 and 4 years of ageing respectively.

Angelovich TA, Hearps AC, Maisa A, Martin GE, Lichtfuss GF, Cheng WJ, Palmer CS, Landay AL, Crowe SM, Jaworowski A
1Centre for Biomedical Research, Burnet Institute, Melbourne, Australia. 2School of Applied Sciences, RMIT University, Melbourne, Australia. 3Department of Infectious Diseases, Monash University, Melbourne, Australia. 4School of Medical Sciences, Univer


BACKGROUND:: Chronic inflammation and immune activation occur in both HIV infection and normal ageing and are associated with inflammatory disease. However, the degree to which HIV influences age-related innate immune changes, and the biomarkers which best reflect them, remains unclear. METHODS AND RESULTS:: We measured established innate immune ageing biomarkers in 309 individuals including 88 virologically-suppressed (VS) and 52 viremic (viral load </= and >50 copies/ml respectively) HIV+ individuals. Levels of soluble (ie. CXCL10, soluble CD163, neopterin) and cellular (ie. proportions of inflammatory CD16+ monocytes) biomarkers of monocyte activation were increased in HIV+ individuals and were only partially ameliorated by viral suppression. Viremic and VS HIV+ individuals show levels of age-related monocyte activation biomarkers that are similar to uninfected controls aged 12 and 4 years older respectively. Viremic HIV infection was associated with an accelerated rate of change of some monocyte activation markers (eg. neopterin) with age, whilst in VS individuals, subsequent age-related changes occurred at a similar rate as in controls, albeit at a higher absolute level. We further identified CXCL10 as a robust soluble biomarker of monocyte activation, highlighting the potential utility of this chemokine as a prognostic marker. IMPLICATIONS:: These findings may partially explain the increased prevalence of inflammatory, age-related diseases in HIV+ individuals and potentially indicate the pathological mechanisms underlying these diseases which persist despite viral suppression.

Supported by National Health and Medical Research Council of Australia (Project Grant 1048536).

Full text (postprint manuscript) available at link on right side of this page.


  • Journal: Journal of Acquired Immune Deficiency Syndromes
  • Published: 02/02/2015
  • Volume: 69
  • Issue: 1
  • Pagination: 11-17


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