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      Hematopoietic Stem/Progenitor Cells and the Pathogenesis of HIV/AIDS

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          Abstract

          The interaction between human immunodeficiency virus (HIV) and hematopoietic stem/progenitor cells (HSPCs) has been of great interest. However, it remains unclear whether HSPCs can act as viral reservoirs. Many studies have reported the presence of latently infected HSPCs in the bone marrow of HIV-infected patients, whereas many other investigators have reported negative results. Hence, further evidence is required to elucidate this controversy. The other arm of HSPC investigations of HIV infection involves dynamics analysis in the early and late stages of infection to understand the impact on the pathogenesis of acquired immunodeficiency syndrome. Several recent studies have suggested reduced amounts and/or functional impairment of multipotent, myeloid, and lymphoid progenitors in HIV infection that may contribute to hematological manifestations, including anemia, pancytopenia, and T-cell depletion. In addition, ongoing and future studies on the senescence of HSPCs are expected to further the understanding of HIV pathogenesis. This mini review summarizes reports describing the basic aspects of hematopoiesis in response to HIV infection and offers insights into the association of HIV infection/exposure of the host HSPCs and hematopoietic potential.

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          Most cited references121

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          Identification of clonogenic common lymphoid progenitors in mouse bone marrow.

          The existence of a common lymphoid progenitor that can only give rise to T cells, B cells, and natural killer (NK) cells remains controversial and constitutes an important gap in the hematopoietic lineage maps. Here, we report that the Lin(-)IL-7R(+)Thy-1(-)Sca-1loc-Kit(lo) population from adult mouse bone marrow possessed a rapid lymphoid-restricted (T, B, and NK) reconstitution capacity in vivo but completely lacked myeloid differentiation potential either in vivo or in vitro. A single Lin(-)IL-7R(+)Thy-1(-)Sca-1loc-Kit(lo) cell could generate at least both T and B cells. These data provide direct evidence for the existence of common lymphoid progenitors in sites of early hematopoiesis.
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            Massive infection and loss of memory CD4+ T cells in multiple tissues during acute SIV infection.

            It has recently been established that both acute human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV) infections are accompanied by a dramatic and selective loss of memory CD4+ T cells predominantly from the mucosal surfaces. The mechanism underlying this depletion of memory CD4+ T cells (that is, T-helper cells specific to previously encountered pathogens) has not been defined. Using highly sensitive, quantitative polymerase chain reaction together with precise sorting of different subsets of CD4+ T cells in various tissues, we show that this loss is explained by a massive infection of memory CD4+ T cells by the virus. Specifically, 30-60% of CD4+ memory T cells throughout the body are infected by SIV at the peak of infection, and most of these infected cells disappear within four days. Furthermore, our data demonstrate that the depletion of memory CD4+ T cells occurs to a similar extent in all tissues. As a consequence, over one-half of all memory CD4+ T cells in SIV-infected macaques are destroyed directly by viral infection during the acute phase-an insult that certainly heralds subsequent immunodeficiency. Our findings point to the importance of reducing the cell-associated viral load during acute infection through therapeutic or vaccination strategies.
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              Delta-like 4 is indispensable in thymic environment specific for T cell development

              The thymic microenvironment is required for T cell development in vivo. However, in vitro studies have shown that when hematopoietic progenitors acquire Notch signaling via Delta-like (Dll)1 or Dll4, they differentiate into the T cell lineage in the absence of a thymic microenvironment. It is not clear, however, whether the thymus supports T cell development specifically by providing Notch signaling. To address this issue, we generated mice with a loxP-flanked allele of Dll4 and induced gene deletion specifically in thymic epithelial cells (TECs). In the thymus of mutant mice, the expression of Dll4 was abrogated on the epithelium, and the proportion of hematopoietic cells bearing the intracellular fragment of Notch1 (ICN1) was markedly decreased. Corresponding to this, CD4 CD8 double-positive or single-positive T cells were not detected in the thymus. Further analysis showed that the double-negative cell fraction was lacking T cell progenitors. The enforced expression of ICN1 in hematopoietic progenitors restored thymic T cell differentiation, even when the TECs were deficient in Dll4. These results indicate that the thymus-specific environment for determining T cell fate indispensably requires Dll4 expression to induce Notch signaling in the thymic immigrant cells.
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                Author and article information

                Contributors
                Journal
                Front Cell Infect Microbiol
                Front Cell Infect Microbiol
                Front. Cell. Infect. Microbiol.
                Frontiers in Cellular and Infection Microbiology
                Frontiers Media S.A.
                2235-2988
                21 February 2020
                2020
                : 10
                : 60
                Affiliations
                Department of Immunology, Faculty of Medicine, Kindai University , Osaka, Japan
                Author notes

                Edited by: Samuel K. Campos, The University of Arizona, United States

                Reviewed by: Julià Blanco, IrsiCaixa, Spain; Larisa Y. Poluektova, University of Nebraska Medical Center, United States

                *Correspondence: Tetsuo Tsukamoto ttsukamoto@ 123456med.kindai.ac.jp

                This article was submitted to Virus and Host, a section of the journal Frontiers in Cellular and Infection Microbiology

                Article
                10.3389/fcimb.2020.00060
                7047323
                32154191
                90a418df-ccb7-471f-8d53-c7a340178827
                Copyright © 2020 Tsukamoto.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 19 November 2019
                : 06 February 2020
                Page count
                Figures: 1, Tables: 0, Equations: 0, References: 131, Pages: 10, Words: 8075
                Categories
                Cellular and Infection Microbiology
                Mini Review

                Infectious disease & Microbiology
                human immunodeficiency virus,acquired immunodeficiency syndrome,hematopoietic stem/progenitor cells,hematopoiesis,senescence

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