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Background  Systemic inflammation is a characteristic of both HIV-1 infection and aging (“inflammaging”). Intestinal epithelial barrier damage (IEBD) and microbial translocation (MT) contribute to HIV-associated inflammation, but their impact on inflammaging remains unclear.    Methods  Plasma biomarkers for IEBD (iFABP), MT (LPS, sCD14), T-cell activation (sCD27), and inflammation (hsCRP, IL-6) were measured in 88 HIV-1 uninfected (HIV neg ) and 83 treated, HIV-1-infected (HIV pos ) adults from 20–100 years old.    Results  Age positively correlated with iFABP (r = 0.284,  p  = 0.008), sCD14 (r = 0.646,  p  = <0.0001) and LPS (r = 0.421,  p  = 0.0002) levels in HIV neg  but not HIV pos  subjects. Age also correlated with sCD27, hsCRP, and IL-6 levels regardless of HIV status. Middle-aged HIV pos  subjects had elevated plasma biomarker levels similar to or greater than those of elderly HIV neg  subjects with the exception of sCD14. Clustering analysis described an inflammaging phenotype (IP) based on iFABP, sCD14, sCD27, and hsCRP levels in HIV neg  subjects over 60 years of age. The IP in HIV neg  subjects was used to develop a classification model that was applied to HIV pos  subjects to determine whether HIV pos  subjects under 60 years of age were IP+. HIV pos  IP+ subjects were similar in age to IP- subjects but had a greater risk of cardiovascular disease (CVD) based on Framingham risk score ( p  =  0.01).    Conclusions  We describe a novel IP that incorporates biomarkers of IEBD, MT, immune activation as well as inflammation. Application of this novel IP in HIV-infected subjects identified a group at higher risk of CVD.

Contribution of Intestinal Barrier Damage, Microbial Translocation and HIV-1 Infection Status to an Inflammaging Signature