Abstract
Although antiretroviral therapy effectively controls human immunodeficiency virus (HIV) replication, a residual chronic immune activation/inflammation persists throughout the disease. This aberrant immune activation and inflammation are considered an accelerator of non-AIDS-related events and one of the driving forces of CD4+ T cell depletion. Unfortunately, HIV-associated immune activation is driven by various factors, while the mechanism of excessive inflammation has not been formally clarified. To date, several clinical interventions or treatment candidates undergoing clinical trials have been proposed to combat this systemic immune activation/inflammation. However, these strategies revealed limited results, or their nonspecific anti-inflammatory properties are similar to previous interventions. Here, we reviewed recent learnings of immune activation and persisting inflammation associated with HIV infection, as well as the current directions to overcome it. Of note, a more profound understanding of the specific mechanisms for aberrant inflammation is still imperative for identifying an effective clinical intervention strategy.
Highlights
With the development of well-tolerated and highly effective antiretroviral therapy (ART), human immunodeficiency virus (HIV)/AIDS has changed from a fatal disease into a chronic and controllable condition [1]
People living with HIV (PLWH) after successful ART still showed a higher level of immune activation, characterized by elevated biomarkers such as IL-6, D-dimer, C-reactive protein (CRP), and sCD14 [3, 4]
Chronic immune system activation is a hallmark of HIV infection and better predicts disease outcome than plasma viral load [5]
Summary
With the development of well-tolerated and highly effective antiretroviral therapy (ART), HIV/AIDS has changed from a fatal disease into a chronic and controllable condition [1]. The life expectancy of HIV-infected patients with a high CD4+ T cell count and an undetectable viral after ART is gradually approaching that of the uninfected population [2]. Abnormal immune activation and inflammation are accompanied by the whole infection process, and antiviral therapy alone is challenging to solve these clinical problems. Chronic immune system activation is a hallmark of HIV infection and better predicts disease outcome than plasma viral load [5]. Clinical data suggested that only up to 30% of patients after ART present a modest rise of CD4+ T cell levels, far from effective immune reconstitution. HIV-related immune activation and inflammation are a systematic and long-term process, and many other factors and mechanisms are involved. This review will systematically elucidate the current mechanisms and therapeutic strategies/drugs for HIV-related immune activation and inflammation
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