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Review
. 2016 Dec;13(6):309-317.
doi: 10.1007/s11904-016-0332-x.

Aging of the Liver: What This Means for Patients with HIV

Austin W Chan  1 , Yuval A Patel  2 , Steve Choi  3
Affiliations
Review

Aging of the Liver: What This Means for Patients with HIV

Austin W Chan et al. Curr HIV/AIDS Rep. 2016 Dec.

Abstract

As the HIV population continues to live longer as a result of antiretroviral therapy, liver-related mortality has become one of the leading causes of non-AIDS related death in this patient population. The liver possesses a remarkable regenerative capacity but undergoes complex biological changes in response to aging and inflammation that result in decreased cellular regeneration and a tipping of the scales towards fibrogenesis. Patients with HIV infection have serological evidence of ongoing inflammation, with elevations in some biomarkers persisting despite adequate virologic control. In addition, HIV-co-infected patients have markers of advanced age on liver biopsy and increased prevalence of fibrosis as compared to an age-matched HCV mono-infected cohort. In this review, we will discuss the biology of aging, age-related changes in the liver, and the relevant mechanisms by which HIV causes inflammation in the context of accelerated aging, fibrosis of the liver, and other viral co-infection.

Keywords: Aging; Co-infections; Fibrogenesis; HIV; Immunosenescence; Liver.

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Figures

Fig. 1
Fig. 1
Senescent cells develop the senescent-associated secretory phenotype (SASP). Senescent cells secrete significant amounts of IL-6 and IL-8, cytokines which can act in both an autocrine or paracrine manner to promote cellular senescence. IL-6 through IL-6 receptor (IL-6R) and/or IL-8 (through CXCR2) act in concert with cellular stress induced by reactive oxidative species (ROS) to induce the senescent phenotype
See this image and copyright information in PMC

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