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How Does Hiv Affect The Immune System

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Innate Immunity Against Hiv 1 Infection

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World Aids Day

Research Unit in Congenital and Perinatal Infections, Academic Department of Pediatrics (DPUO), Department of Immunology and Infectious Diseases, Bambino Gesu Children’s Hospital, 00165 Rome, Italy

Submission Received: 30 January 2019 / Revised: 19 February 2019 / Accepted: 26 February 2019 / Published: 27 February 2019

Despite effective antiretroviral therapy (ART), people living with HIV (PLWH) still have persistent chronic immune activation and inflammation. This condition is the result of multiple factors including thymic dysfunction, persistent antigen stimulation due to low waste, microbial translocation and dysbiosis, disruption of the intestinal mucosa, co-infections, and cumulative ART toxicity. All these factors can create a vicious cycle that does not allow full control of immune activation and inflammation, increasing the risk of developing non-AIDS co-morbidities such as metabolic syndrome and cardiovascular diseases. The purpose of this review is to provide an overview of the most recent data on HIV-associated inflammation and chronic immune exhaustion in PLWH under effective ART. In addition, we discuss new therapy approaches that are currently being tested to reduce the risk of developing inflammation, ART toxicity, and non-AIDS co-morbidities.

Globally, 36.9 million people are living with human immunodeficiency virus (HIV) [1]. Thanks to the introduction of antiretroviral therapy (ART), people living with HIV (PLWH) live longer and have lower morbidity and mortality than untreated patients, but the virus is not completely eradicated despite effective therapy. is Consequently, HIV is now considered a chronic disease rather than a fatal disease in countries where ART is available [2]. Persistence of the virus favors a chronic state of immune activation and inflammation leading to increased production of pro-inflammatory cytokines [3] and thymus dysfunction [4] . Furthermore, persistent inflammation increases tissue damage in PLWH, particularly in the gastrointestinal tract, allowing microbial components to enter the circulatory system (microbial translocation), exacerbating inflammation [ 5 ]. This immunological status increases the risk for PLWH of developing non-AIDS-related co-morbidities that are commonly associated with immunosenescence, commonly seen in the elderly [ 6 ]. In addition, HIV infection and long-term ART have been associated with the development of metabolic syndrome (METS) [7, 8], which is a combination of metabolic disorders including hypertension, hyperglycemia, changes in fat distribution, cholesterol includes a small amount of growth. High-density lipoprotein (LDL) and triglycerides, cholesterol and a reduced level of high-density lipoprotein (HDL) and cause cardiovascular diseases (CVD) such as heart disease, stroke, and diabetes [8, 9, 10]. can The goal of this review is to provide an overview of the most recent findings on the relationship between immune activation associated with metabolic complications in PLWH and the relationship between HIV and inflammation associated with non-AIDS co-morbidities.

Hiv Symptoms At Each Stage Of The Disease

Within weeks of HIV infection, the virus begins a massive invasion of the gut, leading to a significant depletion of memory CD4+ T cells. Such reduction follows disruption of tight junctions in the intestinal epithelium, which may not be fully restored even with early ART initiation (within six months of infection) [ 11 , 12 ]. Intestinal disruption leads to an imbalance of intestinal microbiota composition (dysbiosis) and the release of bacterial products into the circulation (microbial translocation) that induce chronic immune activation and inflammation [ 5 , 13 , 14 , 15 ]. Regarding dysbiosis, several studies have shown that, compared to healthy controls (HCs), PLWH present an altered microbiota composition with a decrease in pro-inflammatory and potentially pathogenic bacteria and beneficial ones [16, 17, 18]. In particular, Larsen et al. showed that certain species of Pravotella, abundant in the microbiota of PLWH, exacerbate Th17-mediated mucosal inflammation, having a pro-inflammatory effect [19], while Bacteroides, which are decreased in these patients, produce anti-inflammatory cytokines. are capable of [20] ]. Indeed, Paquin-Proulx et al. have shown that some Bacteroidetes are associated with the production of natural killer T cells in the gut, leading to a reduction in immune activation [21]. In addition, Vujkovic-Civjin et al. found a positive correlation between Prevotella and immune activation, while the abundance of Bacteroides was negatively correlated with markers of inflammation in PLWH under ART or ART-naïve PLWH, their protection against inflammation [18]. highlights the effect.

As mentioned above, microbial translocation is another important cause of chronic inflammation. In particular, lipopolysaccharides (LPS), a component of the Gram-negative bacterial cell wall, are released from the leaky gut and are able to trigger a strong immune response. Indeed, LPS binds CD14, found either in soluble form or anchored on the surface of monocytes and macrophages. The newly formed complex LPS/CD14 activates Toll-like receptor-4 (TLR4), leading to the production of pro-inflammatory cytokines [ 22 , 23 , 24 , 25 ]. In addition, this binding is also responsible for triggering the coagulation cascade, increasing the production of procoagulant tissue factors [6]. Indeed, it has been shown that soluble CD14 (sCD14) remains elevated in PLWH even with effective ART [ 26 ], and that it is associated with the risk of developing CVDs [ 27 , 28 , 29 ]. Overall, microbial translocation can be considered one of the major drivers of morbidity and mortality in HIV infection, as its role is to induce and maintain persistent inflammation [ 5 , 30 , 31 , 32 ]. As summarized in Figure 1 , several mechanisms contribute to chronic inflammation in PLWH.

Chronic immune activation and persistent inflammation also affect lymphoid tissue, leading to elevation of transforming growth factor β (TGF-β), which stimulates collagen production. Collagen alters the fibroblastic reticular network that modifies the structure and function of lymphoid tissue with progressive loss of naïve T cells [ 33 , 34 , 35 ]. As demonstrated by Sánchez et al., initiation of ART did not reverse lymphoid tissue fibrosis, perhaps due to persistent inflammation and low levels of virus replication [ 36 ].

Sustained antigen stimulation produces other inflammatory biomarkers such as interleukin (IL)-6, IL-1β, tumor necrosis factor (TNF)-α, and C-reactive protein (CPR). Recently, it has been shown by Grund et al. that IL-6 and D-Dimer are independently associated with non-AIDS co-morbidity in PLWH, suggesting that lowering these biomarkers may be aimed at reducing morbidity and mortality in PLWH under ART [37]. can help in It has also been shown that intercellular adhesion molecule (ICAM)-1, vascular cell adhesion molecule (VCAM)-1 and D-dimer, markers of CVDs [38, 39, 40], and monocyte chemotactic protein osteopontin (OPN), related As for the risk of dementia, elevated in PLWH [41].

What Complications Can Occur With Hiv?

Persistent inflammation also affects thymus function, which is essential for achieving full immune recovery. Indeed, HIV infection in untreated adults causes chronic inflammation and immune activation that induces thymopoiesis, leading to long-term thymic dysfunction and clonal exhaustion of T cells [ 42 ]. Furthermore, HIV-induced pro-inflammatory molecules sustain an abnormal development of regulatory T cells (Tregs) in the thymus, resulting in a lack of control of HIV and opportunistic pathogen infections [ 42 ]. In addition, thymic atrophy and fibrosis lead to a decreased receptivity to IL-7 that appears to be associated with sustained expression of type I interferon and decreased expression of IL-7Rα due to IL-1β and IL-6, cell Associated with death and thymopoiesis. inhibition [43]. With initiation of ART, thymic function is only partially preserved. however,

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