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Review
. 2010 Nov;5(6):498-503.
doi: 10.1097/COH.0b013e32833ed6f4.

Biomarkers of immune dysfunction in HIV

Affiliations
Review

Biomarkers of immune dysfunction in HIV

Daniel E Nixon et al. Curr Opin HIV AIDS. 2010 Nov.

Abstract

Purpose of review: HIV infection is characterized by chronic immune system activation and inflammatory cytokine production. This review will highlight recent developments using plasma and cellular biomarkers of immune system activation and dysfunction to predict mortality and opportunistic disease in HIV-infected individuals.

Recent findings: HIV infection results in features characteristic of early aging of the immune system or 'immune senescence', driven by chronic antigen exposure and immune system activation. Microbial translocation of gut bacterial components is associated with chronic immune activation and possibly systemic inflammation. Antiretroviral therapy may not fully normalize this condition. Baseline elevations of certain biomarkers of inflammation or coagulopathy, notably interleukin-6 (IL-6), C-reactive protein (CRP), and D-dimer, have been associated with mortality or opportunistic disease, after adjustment for appropriate variables, in several large randomized clinical trials. It is not known if elevated IL-6 or CRP causes this morbidity and mortality or if they are simply surrogate markers of a global inflammatory state.

Summary: Several inflammatory biomarkers appear to add to our ability to predict mortality or opportunistic disease in HIV-infected individuals. Before biomarkers will be useful, it will be necessary to identify interventions that moderate biomarker levels, and then determine if this moderation attenuates disease outcomes.

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References

    1. Lifson AR, Belloso WH, Carey C, et al. Determination of the underlying cause of death in three multicenter international HIV clinical trials. HIV Clin Trials. 2008;9:177–185. - PMC - PubMed
    1. Deeks SG, Phillips AN. HIV infection, antiretroviral treatment, ageing, and non-AIDS related morbidity. BMJ. 2009;338:a3172. - PubMed
    1. Baker J, Ayenew W, Quick H, et al. High-density lipoprotein particles and markers of inflammation and thrombotic activity in patients with untreated HIV infection. J Infectious Dis. 2010;201:285–292. - PMC - PubMed
    1. Funderburg NT, Mayne E, Sieg SF, et al. Increased tissue factor expression on circulating monocytes in chronic HIV infection: relationship to in vivo coagulation and immune activation. Blood. 2010;115:161–167. This study examines the induction of cell surface monocyte TF expression by LPS and its association with sCD14 and <sc>d</sc>-dimer.

    1. Neuhaus J, Jacobs DR, Jr, Baker JV, et al. Markers of inflammation, coagulation, and renal function are elevated in adults with HIV infection. J Infect Dis. 2010;201:1788–1795. This is a comparison of biomarkers from HIV-infected patients participating in SMART with two non-HIV-infected populations using the same reference lab. Demonstrated that baseline biomarkers in HIV-infected patients are higher than noninfected as well as the effects of HAART on biomarker levels.

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