Abstract
Despite effective antiretroviral therapy (ART), people living with HIV (PLWH) still present persistent chronic immune activation and inflammation. This condition is the result of several factors including thymic dysfunction, persistent antigen stimulation due to low residual viremia, microbial translocation and dysbiosis, caused by the disruption of the gut mucosa, co-infections, and cumulative ART toxicity. All of these factors can create a vicious cycle that does not allow the full control of immune activation and inflammation, leading to an increased risk of developing non-AIDS co-morbidities such as metabolic syndrome and cardiovascular diseases. This review aims to provide an overview of the most recent data about HIV-associated inflammation and chronic immune exhaustion in PLWH under effective ART. Furthermore, we discuss new therapy approaches that are currently being tested to reduce the risk of developing inflammation, ART toxicity, and non-AIDS co-morbidities.
Highlights
36.9 million people are living with the human immunodeficiency virus (HIV) [1].Thanks to antiretroviral therapy (ART) introduction, people living with HIV (PLWH) have a longer life expectancy and decreased morbidity and mortality than untreated patients, but despite effective therapy the virus is not completely eradicated
The persistent status of inflammation and chronic immune activation are some of the causes of endothelial dysfunction, atherosclerosis and hypertension, which affect the functionality of the heart and the vascular system [107] and can be considered as a predictive factor of cardiovascular diseases (CVDs) and cerebral vascular disease development in PLWH under ART
We found that the process of immunosenescence and aging can affect the B cell compartment, characterized by higher frequencies of mature activated B cells (CD19+CD10−CD21−) and double negative B cells (CD19+CD10−CD27−CD21−) in perinatally HIV-infected (perHIV) patients compared with their healthy counterparts and to older healthy control [139,140,141]
Summary
36.9 million people are living with the human immunodeficiency virus (HIV) [1]. The persistence of the virus supports a chronic status of immune activation and inflammation leading to the increased production of pro-inflammatory cytokines [3] and thymus dysfunction [4]. Chronic immune activation and persistent inflammation affect the lymphoid tissue, leading to upregulation of transforming growth factor β (TGF-β), which stimulates collagen production. The chronic inflammation and immune activation induce thymopoiesis, leading to long-term thymic collagen replaces the fibroblastic reticular network modifying the structure and function of lymphoid dysfunction and clonal exhaustion of T cells [42]. Allers et al showed that in patients who initiated ART during acute HIV infection, mucosal CD4+ T cell numbers were well preserved, and markers of microbial translocation and inflammation reversed to normal [66].
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