Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
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.

PubMed Disclaimer

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

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Walensky RP, Paltiel AD, Losina E, Mercincavage LM, Schackman BR, Sax PE, et al. The survival benefits of AIDS treatment in the United States. J Infect Dis. 2006;194(1):11–9. doi:10.1086/505147. - DOI - PubMed
    1. Palella FJ Jr, Baker RK, Moorman AC, Chmiel JS, Wood KC, Brooks JT, et al. Mortality in the highly active antiretroviral ther- apy era: changing causes of death and disease in the HIV outpatient study. J Acquir Immune Defic Syndr. 2006;43(1):27–34. doi:10.1097/01.qai.0000233310.90484.16. - DOI - PubMed
    1. Smith CJ, Ryom L, Weber R, Morlat P, Pradier C, Reiss P, et al. Trends in underlying causes of death in people with HIV from 1999 to 2011 (D:A:D): a multicohort collaboration. Lancet (London, England). 2014;384(9939):241–8. doi:10.1016/s0140-6736(14)60604-8. - DOI - PubMed
    1. HIV Surveillance Report 2014. In: HIV surveillance report. CDC division of HIV/AIDS Prevention. 2015. http://www.cdc.gov/hiv/library/reports/surveillance/. Accessed 7/15/2016 26.
    1. May MT, Ingle SM, Costagliola D, Justice AC, de Wolf F, Cavassini M, et al. Cohort profile: Antiretroviral Therapy Cohort Collaboration (ART-CC). Int J Epidemiol. 2014;43(3): 691–702. doi:10.1093/ije/dyt010. - DOI - PMC - PubMed

MeSH terms

Substances