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HIV pyroptosis

Sara A Bumgardner, Lin Zhang, Alora S LaVoy, Barbara Andre, Chad B Frank, Akinobu Kajikawa, Todd R Klaenhammer, Gregg A Dean
Safe and efficacious orally-delivered mucosal vaccine platforms are desperately needed to combat the plethora of mucosally transmitted pathogens. Lactobacillus spp. have emerged as attractive candidates to meet this need and are known to activate the host innate immune response in a species- and strain-specific manner. For selected bacterial isolates and mutants, we investigated the role of key innate immune pathways required for induction of innate and subsequent adaptive immune responses. Co-culture of murine macrophages with L...
2018: PloS One
Alessandra Bandera, Michela Masetti, Massimiliano Fabbiani, Mara Biasin, Antonio Muscatello, Nicola Squillace, Mario Clerici, Andrea Gori, Daria Trabattoni
Background: Inflammasome-mediated activation of caspase-1 regulates inflammatory responses and pyroptosis. We analyzed possible associations between inflammasome-related genes and immune reconstitution in HIV-infected antiretroviral therapy (ART)-treated patients. Methods: Cross-sectional, case-control study. HIV-infected patients on ART for ≥24 months with HIV-RNA<50 cp/mL for ≥12 months were enrolled and defined as immunological responders (IR) or non-responders (INR) if CD4 count was ≥500 or ≤350 cells/μL, respectively...
2018: Frontiers in Immunology
Fareed Ahmad, Neha Mishra, Gerrit Ahrenstorf, Bernardo S Franklin, Eicke Latz, Reinhold E Schmidt, Lukas Bossaller
OBJECTIVE: The formation of large intracellular protein aggregates of the inflammasome adaptor protein ASC (apoptosis-associated speck-like protein containing a caspase-recruitment domain; also know as PYCARD) is a hallmark of inflammasome activation. ASC speck-forming cells release the highly proinflammatory cytokine IL-1β in addition to ASC specks into the extracellular space during pyroptotic cell death. There ASC specks can propagate inflammation to other nonactivated cells or tissues...
January 28, 2018: AIDS
Ruian Ke, Mian-Er Cong, David Li, J Gerardo García-Lerma, Alan S Perelson
Progressive T cell depletion during chronic human immunodeficiency virus type 1 (HIV) infection is a key mechanism that leads to the development of AIDS. Recent studies have suggested that most T cells in the tissue die through pyroptosis triggered by abortive infection, i.e., infection of resting T cells in which HIV failed to complete reverse transcription. However, the contribution of abortive infection to T cell loss and how quickly abortively infected cells die in vivo , key parameters for a quantitative understanding of T cell population dynamics, are not clear...
September 15, 2017: Journal of Virology
Dominik Wodarz, David N Levy
A long-lived reservoir of latently infected T cells prevents antiretroviral therapy from eliminating HIV-1 infection. Furthering our understanding of the dynamics of latency generation and maintenance is therefore vital to improve treatment outcome. Using mathematical models and experiments, we suggest that the death of latently infected cells brought about by pyroptosis, or to a lesser extent by superinfection, might be key mechanisms to account for the size and composition of the latent reservoir. Pyroptosis is a form of cell death that occurs in a resting (and thus latently infected) T cell when a productively infected cell attempts cell-to-cell transmission of virus...
June 19, 2017: Scientific Reports
Gilad Doitsh, Nicole L K Galloway, Xin Geng, Zhiyuan Yang, Kathryn M Monroe, Orlando Zepeda, Peter W Hunt, Hiroyu Hatano, Stefanie Sowinski, Isa Muñoz-Arias, Warner C Greene
No abstract text is available yet for this article.
April 6, 2017: Nature
Rentian Cai, Li Liu, Bin Luo, Jiangrong Wang, Jiayin Shen, Yinzhong Shen, Renfang Zhang, Jun Chen, Hongzhou Lu
Both Caspase 1-induced cell death and Caspase 3-induced cell death were reported to be the causes of CD4+ T cell depletion in HIV infection. We measured by flow cytometry the expression of key proteins associated with pyroptosis (Caspase 1), apoptosis (Caspase 3, Caspase 8, Caspase 9), and immune activation in peripheral T cells. The percentages of CD4+ T cells that expressed Caspase 1 and Caspase 3 were significantly higher in untreated human immunodeficiency virus 1 (HIV-1) patients compared with healthy control (Caspase 1: 19...
February 2017: AIDS Research and Human Retroviruses
Xue Wang, Christelle Mbondji-Wonje, Jiangqin Zhao, Indira Hewlett
HIV-1 infection-induced apoptosis is able to ensure viral replication. The death of some CD4+ T cells residing in lymphoid tissues can be induced by HIV-1 infection through caspase-1 driven pyroptosis with release of cytokine of IL-1β and IL-18. It is not well known whether IL-1β and IL-18 affect HIV-1 replication in lymphocytic cells. Using susceptible lymphocytic cell line, Jurkat cells, and primary peripheral blood mononuclear cells (PBMCs), we studied the effects of IL-1β and IL-18 on HIV-1 replication...
May 13, 2016: Biochemical and Biophysical Research Communications
Gilad Doitsh, Warner C Greene
Although the replicative life cycle of HIV within CD4 T cells is understood in molecular detail, less is known about how this human retrovirus promotes the loss of CD4 T lymphocytes. It is this cell death process that drives clinical progression to acquired immune deficiency syndrome (AIDS). Recent studies have highlighted how abortive infection of resting and thus nonpermissive CD4 T cells in lymphoid tissues triggers a lethal innate immune response against the incomplete DNA products generated by inefficient viral reverse transcription in these cells...
March 9, 2016: Cell Host & Microbe
Sunpeng Wang, Patricia Hottz, Mauro Schechter, Libin Rong
The progressive loss of CD4+ T cell population is the hallmark of HIV-1 infection but the mechanism underlying the slow T cell decline remains unclear. Some recent studies suggested that pyroptosis, a form of programmed cell death triggered during abortive HIV infection, is associated with the release of inflammatory cytokines, which can attract more CD4+ T cells to be infected. In this paper, we developed mathematical models to study whether this mechanism can explain the time scale of CD4+ T cell decline during HIV infection...
December 2015: PLoS Computational Biology
Shabirul Haque, Xiqian Lan, Hongxiu Wen, Rivka Lederman, Amrita Chawla, Mohamed Attia, Ramchandra P Bongu, Mohammad Husain, Joanna Mikulak, Moin A Saleem, Waldemar Popik, Ashwani Malhotra, Praveen N Chander, Pravin C Singhal
Dysregulated growth and loss of podocytes are important features of HIV-associated nephropathy. Recently, HIV was reported to induce a new type of programed cell death, pyroptosis, in T lymphocytes through induction of Nod-like receptor protein 3 (NLRP3) inflammasome complexes. We evaluated the role of HIV in podocyte NLRP3 inflammasome formation both in vivo and in vitro. Renal cortical sections of HIV-transgenic mice (Tg26) displayed increased expression of NLRP3, ASC (a CARD protein), caspase-1, and IL-1β proteins, confirming NLRP3 inflammasome complex formation in podocytes of Tg26 mice...
February 2016: American Journal of Pathology
Shelly J Krebs, Jintanat Ananworanich
PURPOSE OF REVIEW: The purpose of this review is to outline recent data pertaining to mechanisms of immune activation in acute infection and describe new developments that seek to determine if early antiretroviral treatment can mitigate chronic immune activation. RECENT FINDINGS: Following the detection of HIV RNA, highly activated CD8 T cells expand and peak approximately 2 weeks following peak viral load whereas levels of proinflammatory soluble markers coincide with a rise in viral load...
March 2016: Current Opinion in HIV and AIDS
Wuxun Lu, Andrew J Demers, Fangrui Ma, Guobin Kang, Zhe Yuan, Yanmin Wan, Yue Li, Jianqing Xu, Mark Lewis, Qingsheng Li
UNLABELLED: Lymphoid tissues (LTs) are the principal sites where human immunodeficiency virus type 1 (HIV-1) replicates and virus-host interactions take place, resulting in immunopathology in the form of inflammation, immune activation, and CD4(+) T cell death. The HIV-1 pathogenesis in LTs has been extensively studied; however, our understanding of the virus-host interactions in the very early stages of infection remains incomplete. We investigated virus-host interactions in the rectal draining lymph nodes (dLNs) of rhesus macaques at different times after intrarectal inoculation (days postinoculation [dpi]) with simian immunodeficiency virus (SIV)...
January 15, 2016: Journal of Virology
Isa Muñoz-Arias, Gilad Doitsh, Zhiyuan Yang, Stefanie Sowinski, Debbie Ruelas, Warner C Greene
Progression to AIDS is driven by CD4 T cell depletion, mostly involving pyroptosis elicited by abortive HIV infection of CD4 T cells in lymphoid tissues. Inefficient reverse transcription in these cells leads to cytoplasmic accumulation of viral DNAs that are detected by the DNA sensor IFI16, resulting in inflammasome assembly, caspase-1 activation, and pyroptosis. Unexpectedly, we found that peripheral blood-derived CD4 T cells naturally resist pyroptosis. This resistance is partly due to their deeper resting state, resulting in fewer HIV-1 reverse transcripts and lower IFI16 expression...
October 14, 2015: Cell Host & Microbe
Nicole Lk Galloway, Gilad Doitsh, Kathryn M Monroe, Zhiyuan Yang, Isa Muñoz-Arias, David N Levy, Warner C Greene
The progressive depletion of CD4 T cells underlies clinical progression to AIDS in untreated HIV-infected subjects. Most dying CD4 T cells correspond to resting nonpermissive cells residing in lymphoid tissues. Death is due to an innate immune response against the incomplete cytosolic viral DNA intermediates accumulating in these cells. The viral DNA is detected by the IFI16 sensor, leading to inflammasome assembly, caspase-1 activation, and the induction of pyroptosis, a highly inflammatory form of programmed cell death...
September 8, 2015: Cell Reports
Jingjing Song, Yanmei Jiao, Tong Zhang, Yonghong Zhang, Xiaojie Huang, Hongjun Li, Hao Wu
Over 95% of CD4 cell death occurs by Caspase-1-mediated pyroptosis during HIV infection. Caspase-3-mediated apoptosis accounts for the death in a small proportion of infected CD4 cells. To date, there have been no reports on the dynamics of Caspase-1 and Caspase-3 and their relationship with disease progression in acute HIV-1 infection. In this study, two distinct HIV-1 patient groups were enrolled. The CD4High group maintained a CD4 level above 450 cells/μl while CD4 levels in the CD4Low group dropped below 250 cells/μl within 2 years after infection...
2015: PloS One
Jing Zou, Wenjiao Li, Anisha Misra, Fei Yue, Kun Song, Qi Chen, Guanghua Guo, Jinglin Yi, Jason T Kimata, Leyuan Liu
Tetherin has been characterized as a key factor that restricts viral particles such as HIV and hepatitis C virus on plasma membranes, acts as a ligand of the immunoglobulin-like transcript 7 (ILT7) receptor in tumor cells, and suppresses antiviral innate immune responses mediated by human plasmacytoid dendritic cells. However, the normal cellular function of Tetherin without viral infection is unknown. Here we show that Tetherin not only serves as a substrate of autophagy but itself regulates the initiation of autophagy...
March 13, 2015: Journal of Biological Chemistry
Joseph A Church
No abstract text is available yet for this article.
November 2014: Pediatrics
Nadine van Montfoort, David Olagnier, John Hiscott
Retroviruses can selectively trigger an array of innate immune responses through various PRR. The identification and the characterization of the molecular basis of retroviral DNA sensing by the DNA sensors IFI16 and cGAS has been one of the most exciting developments in viral immunology in recent years. DNA sensing by these cytosolic sensors not only leads to the initiation of the type I interferon (IFN) antiviral response and the induction of the inflammatory response, but also triggers cell death mechanisms including pyroptosis and apoptosis in retrovirus-infected cells, thereby providing important insights into the pathophysiology of chronic retroviral infection...
December 2014: Cytokine & Growth Factor Reviews
Amanda K Steele, Eric J Lee, Jennifer A Manuzak, Stephanie M Dillon, John David Beckham, Martin D McCarter, Mario L Santiago, Cara C Wilson
BACKGROUND: Early HIV-1 infection causes massive CD4+ T cell death in the gut and translocation of bacteria into the circulation. However, the programmed cell death (PCD) pathways used by HIV-1 to kill CD4+ T cells in the gut, and the impact of microbial exposure on T cell loss, remain unclear. Understanding mucosal HIV-1 triggered PCD could be advanced by an ex vivo system involving lamina propria mononuclear cells (LPMCs). We therefore modeled the interactions of gut LPMCs, CCR5-tropic HIV-1 and a commensal gut bacterial species, Escherichia coli...
2014: Retrovirology
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