Virus Attachment and Replication Are Promoted after Acquisition of Host CD28 and CD152 by HIV‐1

Giguère, Jean-François; Diou, Juliette; Madrenas, Joaquim; Tremblay, Michel J.

doi:10.1086/444426

Cited by 8 publications

(3 citation statements)

References 14 publications

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“…The organization of molecules in the VS may inhibit signals that are induced by engagement of CD4 and CKR, or the soluble gp120 in the earlier studies may contain some aggregates. It should be noted that in our planar bilayer system, the target cell engages only gp120 and ICAM-1, while HIV-1 virions can acquire host cell surface molecules like CD28, CD152, CD80, and CD86 (30,31) that can interact with their ligands on the target cells and modulate T-cell activation together with the viral Env. In addition, gp120 can engage ␣4␤7 (1) and other CKRs on T cells and other types of cells (26), all of which may contribute directly or indirectly to Ca 2ϩ influx detected in the T cells.…”

Section: Discussionmentioning

confidence: 99%

Human Immunodeficiency Virus Type 1 Envelope gp120-Induced Partial T-Cell Receptor Signaling Creates an F-Actin-Depleted Zone in the Virological Synapse

Vasiliver-Shamis

Cho

Hioe

et al. 2009

J Virol

129

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Cell-to-cell transmission of human immunodeficiency virus type 1 (HIV-1) occurs via a virological synapse (VS), a tight cell-cell junction formed between HIV-infected cells and target cells in which the HIV-1-infected cell polarizes and releases virions toward the noninfected target cell in a gp120-and intercellular adhesion molecule 1 (ICAM-1)-dependent process. The response of the target cell has been less studied. We utilized supported planar bilayers presenting gp120 and ICAM-1 as a reductionist model for the infected-cell membrane and investigated its effect on the target CD4 T cell. This study shows that HIV-1 gp120 interaction with its receptors is initially organized into microclusters that undergo F-actin-dependent consolidation into a central supramolecular activation complex (cSMAC). Src kinases are active in both gp120 microclusters and in the VS cSMAC. The early T-cell receptor (TCR) signaling machinery is partially activated at the VS, and signaling does not propagate to trigger Ca 2؉ elevation or increase CD69 expression. However, these partial TCR signals act locally to create an F-actin-depleted zone. We propose a model in which the F-actin-depleted zone formed within the target CD4 T cell enhances the reception of virions by releasing the physical barrier for HIV-1 entry and facilitating postentry events.

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Section: Discussionmentioning

confidence: 99%

Human Immunodeficiency Virus Type 1 Envelope gp120-Induced Partial T-Cell Receptor Signaling Creates an F-Actin-Depleted Zone in the Virological Synapse

Vasiliver-Shamis

Cho

Hioe

et al. 2009

J Virol

129

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“…Another example is incorporation of CD28, a T cell specific co-stimulatory glycoprotein and CD152, a high affinity receptor for costimulatory molecules CD80 and CD86 that promotes HIV attachment and replication in T cells. Indirectly, this mechanism can play an important role in infecting antigen presenting cells (APC) utilizing CD28/CD152-CD80/CD86 interactions [42]. These findings demonstrates that acquisition of host specific proteins modulates the virus life cycle, infectivity, and transmission between cells [43].…”

Section: Hiv-mp Interactions: the Viral Life Cyclementioning

confidence: 95%

Human Immunodeficiency Virus-Mononuclear Phagocyte Interactions:Emerging Avenues of Biomarker Discovery, Modes of Viral Persistence and Disease Pathogenesis

Ciborowski

Gendelman²

2006

CHR

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Mononuclear phagocytes (MP; bone marrow monocyte-derived macrophages, histiocytes, alveolar macrophages, Kupffer cells, perivascular macrophages, and microglia) function as sentry and surveillance cells by acting as debris scavengers, killers of microbial pathogens, and regulators of immune responses. Interestingly, these same cells are reservoirs and vehicles of dissemination for the human immunodeficiency virus (HIV). How virus alters the MP immunoregulatory activities so it can complete its own life cycle and affect disease is only recently being unravelled. Physiologic, anatomic and functional changes also underlie virus-MP interactions and include multinucleated giant cell formation, changes in ion channel expression and cell volume, and robust secretory responses with the production of numerous secretory factors affecting tissue injury. The balance between such MP activities and ability to both mobilize an adaptive immune response to thwart viral growth underlies the progression of viral infection and clinical disease. This review serves to discuss the functions of MP in HIV disease by bringing together what is known with what remains unknown. The advent of functional genomics and proteomics has opened the ways to address the intricacies of viral-host interactions and has provided new avenues for therapeutic interventions and disease monitoring that takes advantage of specific intracellular relationships between the virus and its host cell.

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“…ICAM-1) with the matrix domain of gag polyprotein [71]. These selectively acquired functionally active molecules are considered to create selective advantages for HIV transmission and/or infection [44,45,[72][73][74]. Finally, HIV virions may also use the endocytic pathway of macrophages that allows the virus to be taken within multivesicular endosomes [46].…”

Section: Pd-l1 Incorporation Within Hiv Virions Impairs T Follicular ...mentioning

confidence: 99%

Active PD-L1 incorporation within HIV virions functionally impairs T follicular helper cells

et al. 2022

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The limited development of broadly neutralizing antibodies (BnAbs) during HIV infection is classically attributed to an inadequate B-cell help brought by functionally impaired T follicular helper (Tfh) cells. However, the determinants of Tfh-cell functional impairment and the signals contributing to this condition remain elusive. In the present study, we showed that PD-L1 is incorporated within HIV virions through an active mechanism involving p17 HIV matrix protein. We subsequently showed that in vitro produced PD-L1high but not PD-L1low HIV virions, significantly reduced Tfh-cell proliferation and IL-21 production, ultimately leading to a decreased of IgG1 secretion from GC B cells. Interestingly, Tfh-cell functions were fully restored in presence of anti-PD-L1/2 blocking mAbs treatment, demonstrating that the incorporated PD-L1 proteins were functionally active. Taken together, the present study unveils an immunovirological mechanism by which HIV specifically exploits the regulatory potential of PD-L1 to suppress the immune system during the course of HIV infection.

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Virus Attachment and Replication Are Promoted after Acquisition of Host CD28 and CD152 by HIV‐1

Cited by 8 publications

References 14 publications

Human Immunodeficiency Virus Type 1 Envelope gp120-Induced Partial T-Cell Receptor Signaling Creates an F-Actin-Depleted Zone in the Virological Synapse

Human Immunodeficiency Virus Type 1 Envelope gp120-Induced Partial T-Cell Receptor Signaling Creates an F-Actin-Depleted Zone in the Virological Synapse

Human Immunodeficiency Virus-Mononuclear Phagocyte Interactions:Emerging Avenues of Biomarker Discovery, Modes of Viral Persistence and Disease Pathogenesis

Active PD-L1 incorporation within HIV virions functionally impairs T follicular helper cells

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