How Hiv Affect The Immune System – Retrospective identification and genetic characterization of porcine circovirus 3 (PCV3) strains detected in Brazil between 2006 and 2007.
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How Hiv Affect The Immune System
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Immune Responses To Viral Gene Therapy Vectors: Molecular Therapy
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The Effects Of Hiv/aids On The Immune System
Congenital and Perinatal Infections Research Unit, Academic Department of Pediatrics (DPUO), Department of Immunology and Infectious Diseases, Children’s Hospital Bambina Gesù, 00165 Rome, Italy
Received: 30 January 2019 / Revised: 19 February 2019 / Accepted: 26 February 2019 / Published: 27 February 2019
Despite the benefits of antiretroviral therapy (ART), people living with HIV (PLHIV) continue to have persistent and chronic immunosuppression. This condition is caused by many factors, including thymic dysfunction, continuous antigen stimulation due to low residual viremia, microbial translocation and dysbacteriosis from intestinal mucosal damage, co-infection, and accumulated ART toxicity. All of these factors can create a vicious circle that prevents the immune system and the disease from being fully controlled, leading to a high risk of AIDS diseases such as metabolic syndrome and cardiovascular disease. This review is designed to provide an overview of the most recent data on HIV-related morbidity and mortality in PLHIV on ART. In addition, we discuss new therapies that are currently being tested to reduce the risk of inflammation, ART toxicity, and non-AIDS comorbidities.
Worldwide, 36.9 million people are living with human immunodeficiency virus (HIV) [1]. Thanks to the introduction of antiretroviral therapy (ART), people living with HIV (PLHIV) have longer lives and reduced morbidity and mortality than untreated patients, but but even with good results, this disease is not completely eradicated. Therefore, HIV is now considered a chronic disease leading to death in countries with ART [2]. Viral persistence maintains a weakened immune system and inflammation, leading to increased production of pro-inflammatory cytokines [3] and thymic dysfunction [4]. In addition, chronic inflammation causes tissue damage in PLWH, especially in the colon, allowing microbial material to enter the bloodstream (microbial translocation), causing further pain [5]. This immunosuppression increases the risk of non-AIDS comorbidities in PLHIV, which is often associated with immunospermia, which is more common in adults [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 diseases that include high blood pressure, hyperglycemia, changes in fat, and weight gain. cholesterol. high-density lipoprotein (LDL) and triglycerides, as well as lowering high-density lipoprotein (HDL) cholesterol and can lead to cardiovascular diseases (CVD), such as heart disease, stroke and diabetes [8 , 9, 10]. The purpose of this review is to provide an overview of the recent findings regarding the relationship between HIV and the immune system and non-AIDS comorbidities associated with the metabolic problems in PLWH.
Hiv And Your Cbc (complete Blood Count)
Within weeks of HIV infection, the virus begins a massive attack on the gut, leading to a massive loss of memory CD4+ T cells. Such depletion is accompanied by disruption of the tight junctions in the intestinal epithelium, which may not recover completely even at the early start of ART (within six months of the disease) [11 , 12]. Intestinal dysfunction leads both to the imbalance of the intestinal microbiota (dysbacteriosis) and the release of bacterial products into the circulation (microbial translocation), which weakens the body and pain [5, 13, 14, 15]. Regarding dysbacteriosis, several studies have shown that, compared to healthy individuals (HC), PLHIV have an altered microbiota composition with an increase in pro-inflammatory bacteria and the ability to for disease and reduction of results [16, 17. , 18] a. In particular, Larsen et al. showed that some Prevotella bacteria, which are abundant in the microbiota of PLHIV, enhance Th17-mediated mucosal inflammation, have a protective effect [19], while Bacteroides, which is reduced in patients, has ability to produce anti-cytokines. [20]. ]. Indeed, Paquin-Proulx et al. showed that some Bacteroides genera interfere with the production of anti-inflammatory T cells in the gut, leading to a decrease in immune response [21]. In addition, Vujkovic-Cvijin et al. found a positive relationship between Prevotella and immunity, while Bacteroides abundance was associated with signs of inflammation in PLHIV on ART or ART-naive PLHIV, indicating their protective effect [18].
As mentioned above, the movement of microbes is another important cause of inflammation. In particular, lipopolysaccharide (LPS), part of the cell wall of gram-negative bacteria, is released from the intestinal lumen and has the ability to initiate the immune system. In fact, LPS binds CD14, which is in soluble form or binds to the surface of monocytes and macrophages. The newly formed LPS/CD14 complex 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 activating the coagulation cascade by increasing the production of procoagulant tissue [6]. Indeed, soluble CD14 (sCD14) has been shown to persist in PLWH despite effective ART [ 26 ] and is associated with CVD risk [ 27 , 28 , 29 ]. In general, microbial adaptation can be considered an important factor in the morbidity and mortality of HIV infection, since its role is to promote and maintain chronic disease [5, 30, 31, 32]. As shown in Figure 1, several mechanisms contribute to inflammation in PLWH.
Physical activity and chronic pain also affect the lymphoid tissue, resulting in the development of growth factor β (TGF-β), which promotes collagen production. Collagen replaces the fibroblastic reticular network, modifies the structure and function of lymphoid tissue with impaired growth of T cells [33, 34, 35]. As shown by Sanchez et al., the administration of ART does not reverse the lymphoid tissue, possibly due to the persistent inflammation and low level of infection [36].
Continued antigen stimulation increases other inflammatory biomarkers such as interleukin (IL)-6, IL-1β, tumor necrosis factor (TNF)-α, and C-reactive protein (CPR). This was recently shown by Grund et al. that IL-6 and D-dimer are independently associated with non-AIDS comorbidities in PLWH, suggesting that treatment to reduce these biomarkers may help reduce morbidity and mortality in PLWH on ART [37]. Intercellular adhesion molecule (ICAM)-1, vascular cell adhesion molecule (VCAM)-1 and D-dimer, CVD markers [38, 39, 40], and monocyte chemotactic protein osteopontin (OPN) have also been shown to be associated with dementia risk, increased in PLWH [41].
How Does Hiv/aids Affect The Mouth?
Chronic inflammation also affects the functioning of the thymus gland, which is necessary to achieve full immunity. Indeed, in untreated adults, HIV infection causes chronic inflammation and inactivation of thymopoiesis, leading to long-term thymic failure and clonal depletion of T cells [ 42 ]. Moreover, HIV-induced pro-inflammatory molecules promote the abnormal development of regulatory T cells (Tregs) in the thymus, leading to uncontrolled HIV and opportunistic infections [42]. In addition, thymic atrophy and fibrosis lead to a decrease in IL-7, which appears to be associated with continued expression of type I interferons and reduced IL-1β- and IL-6-induced IL-7Rα expression. associated with cell death and thymopoiesis. protection [43]. With the introduction of ART, the function of the thymus gland is only partially preserved. However, early treatment in adults is necessary to prevent thymic dysfunction before the damage becomes irreversible [4]. In addition,
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