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      Clinical symptoms and immune injury reflected by low CD4/CD8 ratio should increase the suspicion of HIV coinfection with tuberculosis

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          Abstract

          Background

          Patients who are coinfected with human immunodeficiency virus 1 (HIV) and Mycobacterium tuberculosis (TB) benefit from timely diagnosis and treatment. In the present study frequencies of CD3 +, CD4 +, and CD8 + T cells among peripheral blood mononuclear cells (PBMCs) of patients in the Kashi region of China infected with HIV, TB, and both HIV and TB (HIV-TB) were investigated to provide a basis for rapid identification of coinfected patients.

          Methods

          A total of 62 patients with HIV, TB, or HIV-TB who were first hospitalized at our institution were included in the study, as were 30 controls. PBMCs were isolated, and the frequencies of CD3 +, CD4 +, and CD8 + T cells were determined via flow cytometry.

          Results

          The frequency of CD4 + T cells and the CD4/CD8 ratio were significantly lower in the HIV-TB group than in the other three groups. In fever patients the frequency of CD4 + T cells and the CD4/CD8 ratio were significantly lower in the HIV-TB group than in the HIV group and the TB group. In patients who exhibited rapid weight loss there were no significant differences in the frequency of CD4 + T cells or the CD4/CD8 ratio between the groups. The results of treatment were compared in the HIV, TB, and HIV-TB groups after 7 days, and there were obvious improvements in the frequency of CD4 + T cells and the CD4/CD8 ratio.

          Conclusion

          Clinical symptoms and the degree of immune injury can heighten suspicion for HIV-TB coinfection.

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          Most cited references16

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          Cell death by pyroptosis drives CD4 T-cell depletion in HIV-1 infection.

          Gilad Doitsh, Nicole Galloway, Xin Geng … (2014)
          The pathway causing CD4 T-cell death in HIV-infected hosts remains poorly understood although apoptosis has been proposed as a key mechanism. We now show that caspase-3-mediated apoptosis accounts for the death of only a small fraction of CD4 T cells corresponding to those that are both activated and productively infected. The remaining over 95% of quiescent lymphoid CD4 T cells die by caspase-1-mediated pyroptosis triggered by abortive viral infection. Pyroptosis corresponds to an intensely inflammatory form of programmed cell death in which cytoplasmic contents and pro-inflammatory cytokines, including IL-1β, are released. This death pathway thus links the two signature events in HIV infection-CD4 T-cell depletion and chronic inflammation-and creates a pathogenic vicious cycle in which dying CD4 T cells release inflammatory signals that attract more cells to die. This cycle can be broken by caspase 1 inhibitors shown to be safe in humans, raising the possibility of a new class of 'anti-AIDS' therapeutics targeting the host rather than the virus.
          Article 0 comments Cited 198 times – based on 0 reviews     Review now
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            Emerging concepts in the immunopathogenesis of AIDS.

            Daniel Douek, Mario Roederer, R Koup (2008)
            There is an intense interplay between HIV and the immune system, and the literature is replete with studies describing various immunological phenomena associated with HIV infection. Many of these phenomena seem too broad in scope to be attributable either to HIV-infected cells or to the HIV-specific immune response. Recently, a more fundamental understanding of how HIV affects various T cells and T cell compartments has emerged. This review covers the role of immune activation in HIV immunopathogenesis, how that activation could be mediated directly by HIV replicating within and damaging the gut mucosal barrier, how HIV affects multiple T cell functions and phenotypes, and how chronic HIV replication induces immune modulatory pathways to negatively regulate certain functions in HIV-specific T cells.
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              Pathogenesis of HIV-1 and Mycobacterium tuberculosis co-infection

              Lucy C. K. Bell, Mahdad Noursadeghi (2018)
              Co-infection with Mycobacterium tuberculosis is the leading cause of death in individuals infected with HIV-1. It has long been known that HIV-1 infection alters the course of M. tuberculosis infection and substantially increases the risk of active tuberculosis (TB). It has also become clear that TB increases levels of HIV-1 replication, propagation and genetic diversity. Therefore, co-infection provides reciprocal advantages to both pathogens. In this Review, we describe the epidemiological associations between the two pathogens, selected interactions of each pathogen with the host and our current understanding of how they affect the pathogenesis of TB and HIV-1/AIDS in individuals with co-infections. We evaluate the mechanisms and consequences of HIV-1 depletion of T cells on immune responses to M. tuberculosis. We also discuss the effect of HIV-1 infection on the control of M. tuberculosis by macrophages through phagocytosis, autophagy and cell death, and we propose models by which dysregulated inflammatory responses drive the pathogenesis of TB and HIV-1/AIDS.
              Article 0 comments Cited 130 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Li Li
                DaYong Zheng
                XiaoGuang Zou
                Journal
                Journal ID (nlm-ta): Heliyon
                Journal ID (iso-abbrev): Heliyon
                Title: Heliyon
                Publisher: Elsevier
                ISSN (Electronic): 2405-8440
                Publication date PMC-release: 04 March 2023
                Publication date Collection: March 2023
                Publication date (Electronic): 04 March 2023
                Volume: 9
                Issue: 3
                Electronic Location Identifier: e14219
                Affiliations
                [a ]Department of Respiratory and Critical Care Medicine, First People's Hospital of Kashi, Kashi, China
                [b ]Department of Clinical Research Center of Infectious Diseases (Pulmonary Tuberculosis), First People's Hospital of Kashi, Kashi, China
                [c ]Department of Infectious Diseases, First People's Hospital of Kashi, Kashi, China
                [d ]State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Xinjiang Medical University, Urumqi, China
                Author notes
                [∗ ]Corresponding author. Department of Respiratory and Critical Care Medicine, First People's Hospital of Kashi, Kashi, China lili5511@ 123456yeah.net
                [∗∗ ]Corresponding author. zdy525679@ 123456163.com
                [∗∗∗ ]Corresponding author. ZXGKS11@ 123456yeah.net
                [1]

                These authors contributed equally to this work: Li Li, Zulipikaer Abudureheman and XueMei Zhong (Co-first author).

                Article
                Publisher Item ID: S2405-8440(23)01426-3 Publisher ID: e14219
                DOI: 10.1016/j.heliyon.2023.e14219
                PMC ID: 10015191
                PubMed ID: 36938418
                SO-VID: 3e5eaf13-da38-4345-9f35-9054493d42ed
                Copyright © © 2023 The Authors
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 28 April 2022
                Date revision received : 29 January 2023
                Date accepted : 24 February 2023
                Categories
                Subject: Research Article

                Keywords: cd4/cd8 ratio,cd4+ t cells,hiv-tb coinfection
                Data availability:
                Keywords: cd4/cd8 ratio, cd4+ t cells, hiv-tb coinfection

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