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      Immune Activation, Inflammation, and Non-AIDS Co-Morbidities in HIV-Infected Patients under Long-Term ART

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          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.

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          Most cited references131

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          Metabolic syndrome and risk of incident cardiovascular events and death: a systematic review and meta-analysis of longitudinal studies.

          The purpose of this research was to assess the association between the metabolic syndrome (MetSyn) and cardiovascular events and mortality by meta-analyses of longitudinal studies. Controversy exists regarding the cardiovascular risk associated with MetSyn. We searched electronic reference databases through March 2005, studies that referenced Reaven's seminal article, abstracts presented at meetings in 2003 to 2004, and queried experts. Two reviewers independently assessed eligibility. Longitudinal studies reporting associations between MetSyn and cardiovascular events or mortality were eligible. Two reviewers independently used a standardized form to collect data from published reports. Authors were contacted. Study quality was assessed by the control of selection, detection, and attrition biases. We found 37 eligible studies that included 43 cohorts (inception 1971 to 1997) and 172,573 individuals. Random effects meta-analyses showed MetSyn had a relative risk (RR) of cardiovascular events and death of 1.78 (95% confidence interval [CI] 1.58 to 2.00). The association was stronger in women (RR 2.63 vs. 1.98, p = 0.09), in studies enrolling lower risk (<10%) individuals (RR 1.96 vs. 1.43, p = 0.04), and in studies using factor analysis or the World Health Organization definition (RR 2.68 and 2.06 vs. 1.67 for National Cholesterol Education Program definition and 1.35 for other definitions; p = 0.005). The association remained after adjusting for traditional cardiovascular risk factors (RR 1.54, 95% CI 1.32 to 1.79). The best available evidence suggests that people with MetSyn are at increased risk of cardiovascular events. These results can help clinicians counsel patients to consider lifestyle interventions, and should fuel research of other preventive interventions.
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            The Immune Response to Prevotella Bacteria in Chronic Inflammatory Disease.

            The microbiota plays a central role in human health and disease by shaping immune development, immune responses, metabolism, and protecting from invading pathogens. Technical advances that allow comprehensive characterization of microbial communities by genetic sequencing have sparked the hunt for disease modulating bacteria. Emerging studies in humans have linked increased abundance of Prevotella species at mucosal sites to localized and systemic disease, including periodontitis, bacterial vaginosis, rheumatoid arthritis, metabolic disorders, and low-grade systemic inflammation. Intriguingly, Prevotella abundance is reduced within the lung microbiota of asthma and COPD. Increased Prevotella abundance is associated with augmented Th17-mediated mucosal inflammation, which is in line with the marked capacity of Prevotella in driving Th17 immune responses in vitro. Studies indicate, that Prevotella predominantly activate TLR2 leading to production of Th17-polarizing cytokines by antigen presenting cells, including IL-23 and IL-1. Furthermore, Prevotella stimulate epithelial cells to produce IL-8, IL-6 and CCL20, which can promote mucosal Th17 immune responses and neutrophil recruitment. Prevotella-mediated mucosal inflammation leads to systemic dissemination of inflammatory mediators, bacteria, and bacterial products, which in turn may affect systemic disease outcomes. Studies in mice support a causal role of Prevotella as colonization experiments promote clinical and inflammatory features of human disease. When compared to strict commensal bacteria, Prevotella exhibit increased inflammatory properties as demonstrated by augmented release of inflammatory mediators from immune cells and various stromal cells. These findings indicate that some Prevotella strains may be clinically important pathobionts that can participate in human disease by promoting chronic inflammation. This article is protected by copyright. All rights reserved.
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              Intestinal microbiota, microbial translocation, and systemic inflammation in chronic HIV infection.

              Despite effective antiretroviral therapy (ART), patients with chronic human immunodeficiency virus (HIV) infection have increased microbial translocation and systemic inflammation. Alterations in the intestinal microbiota may play a role in microbial translocation and inflammation.
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                Author and article information

                Journal
                Viruses
                Viruses
                viruses
                Viruses
                MDPI
                1999-4915
                27 February 2019
                March 2019
                : 11
                : 3
                : 200
                Affiliations
                [1 ]Research Unit in Congenital and Perinatal Infections, Academic Department of Pediatrics (DPUO), Division of Immunology and Infectious Diseases, Bambino Gesù Children’s Hospital, 00165 Rome, Italy; sonia.zicari@ 123456opbg.net (S.Z.); nicola.cotugno@ 123456opbg.net (N.C.); alessandra.ruggiero@ 123456opbg.net (A.R.); salvatore.rocca@ 123456opbg.net (S.R.); paola.zangari@ 123456opbg.net (P.Z.); emma.manno@ 123456opbg.net (E.C.M.)
                [2 ]Department of Systems Medicine, University of Rome Tor Vergata, 00133 Rome, Italy; libera.sessa@ 123456gmail.com (L.S.); elena.morrocchi@ 123456gmail.com (E.M.)
                [3 ]Department of Laboratories, Division of Virology, Bambino Gesù Children’s Hospital, 00165 Rome, Italy; carlo.concato@ 123456opbg.net
                Author notes
                [* ]Correspondence: paolo.palma@ 123456opbg.net ; Tel.: +390668593080
                [†]

                These authors contributed equally to this work.

                Author information
                https://orcid.org/0000-0003-3995-9537
                https://orcid.org/0000-0002-3066-4719
                Article
                viruses-11-00200
                10.3390/v11030200
                6466530
                30818749
                49d2a51a-0311-4948-845a-394569854c92
                © 2019 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 30 January 2019
                : 26 February 2019
                Categories
                Review

                Microbiology & Virology
                inflammation,immune activation,premature aging,metabolic syndrome,hiv,art,non-aids co-morbidities

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