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The HIV-1 proviral landscape reveals that Nef contributes to HIV-1 persistence in effector memo CD4+ T cells - Peeref

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<ul class="nav navbar-nav navbar-right" style="display: inline-flex; align-items: center; margin-left: 20px;"> <li id="language" class="d-none d-xl-inline-flex"> <a href="javascript:"> <div class="current"> <i class="ivu-icon ivu-icon-md-globe"></i> EN </div> </a> <div class="selection"> <a rel="alternate" hreflang="en" href="https://www.peeref.com/works/35097577" > <span>English</span> </a> <a rel="alternate" hreflang="zh" href="https://www.peeref.com/zh/works/35097577" > <span>中文</span> </a> </div> </li> </ul> </ul> </div> </nav> <main> <div id="top-info-banner" class="container-fluid mb-0"> <div class="container"> <div class="d-flex align-items-center" style="margin-top: 30px;"> <span class="text-white"> <strong class="f18">☆</strong> <span class="f16">4.8</span> </span> <span class="mx-3"></span> <span class="tag">Article</span> </div> <h1 class="title title-for-article"> The HIV-1 proviral landscape reveals that Nef contributes to HIV-1 persistence in effector memo CD4+ T cells </h1> <div class="help-links-left"> <p class="pub-info"> JOURNAL OF CLINICAL INVESTIGATION (2022) </p> </div> </div> </div> <div id="article-sticky-navbar"> <div class="container"> <div class="d-flex justify-content-between flex-wrap flex-md-nowrap"> <div class="d-flex align-items-center mb-2"> <ul class="nav nav-underline f16 font-weight-bold"> <li class="active"> <a href="javascript:;"> Overview </a> </li> <li class=""> <a href="https://www.peeref.com/works/35097577/comments"> Write a Review </a> </li> </ul> </div> <div class="d-flex align-items-center justify-content-md-end flex-wrap flex-md-nowrap"> <div class="mr-3 mt-3 mt-md-0 flex-shrink-0"> <a href="https://doi.org/10.1172/JCI154422" target="_blank" class="btn btn-warning btn-circle"> <i class="ivu-icon ivu-icon-md-copy f16"></i> <strong>Get Full Text</strong> </a> </div> <div class="mr-3 mt-3 mt-md-0 flex-shrink-0"> <a href="https://www.peeref.com/works/35097577/add-to-collection" class="btn btn-success btn-circle"> 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</div> </div> <div id="article-details" class="container"> <div class="col-md-4 px-0 pr-md-3"> <div class="f15 panel-box rounded shadow-none border"> <div class="mb-3 pb-3"> <h4 class="mt-0">Journal</h4> <div class="f16"> <h5 class="title f16"> <a href="https://www.peeref.com/journals/4315/journal-of-clinical-investigation"> JOURNAL OF CLINICAL INVESTIGATION </a> </h5> <span> Volume 132, Issue 7, Pages - </span> </div> </div> <div class="mb-3 pb-3"> <h4 class="mt-0">Publisher</h4> <div class="f16"> <h5 class="title f16 text-primary"> AMER SOC CLINICAL INVESTIGATION INC </h5> <div class="my-2"> DOI: 10.1172/JCI154422 </div> </div> </div> <div class="mb-3 pb-3"> <h4 class="mt-0">Keywords</h4> <div class="f16"> - </div> </div> <div class="mb-3 pb-3"> <h4 class="mt-0">Categories</h4> <div class="f16"> <span class="d-block"> <a href="https://www.peeref.com/works/list?category=Medicine%2C+Research+%26+Experimental" target="_blank" class="text-dark btn btn-link p-0 text-left"> Medicine, Research &amp; Experimental </a> </span> </div> </div> <div class="mb-3 pb-3"> <h4 class="mt-0">Funding</h4> <div class="f16"> <ol class=""> <li>Delaney AIDS Research Enter-prise to Find a Cure [1U19AI096109, 1UM1AI126611-01, 1UM1AI164560-01]</li> <li>amfAR Research Consortium on HIV Eradication Collaborative Research grant from the Foundation for AIDS Research [amfAR 108074-50-RGRL]</li> <li>Australian Centre for HIV and Hepatitis Virology Research (ACH2) [2015-43]</li> <li>Australian National Health and Medical Research Council [APP1061681, APP1149990]</li> <li>Sydney Medical School Foundation, The University of Sydney Institute for Infectious Diseases</li> </ol> </div> </div> </div> <div class="f15 panel-box rounded shadow-none border"> <h4 class="mt-0 text-center">Ask authors/readers for more resources</h4> <div class="requests"> <div class="requests-item"> <div class="icon"> <img src="https://peeref-open.s3.amazonaws.com/images/file.png" alt=""> </div> <h4>Protocol</h4> <p> <a href="https://www.peeref.com/works/35097577/resource" class="btn btn-outline-primary btn-sm"> Community support </a> </p> </div> <div class="requests-item"> <div class="icon"> <img src="https://peeref-open.s3.amazonaws.com/images/experiment.png" alt=""> </div> <h4>Reagent</h4> <p> <a href="https://www.peeref.com/works/35097577/resource" class="btn btn-outline-primary btn-sm"> Community support </a> </p> </div> </div> </div> </div> <div class="col-md-8 px-0 pl-md-3"> <div id="article-summary-panel" class="mb-4"> <ul class="nav nav-tabs" style="list-style: none; padding-left: 0;"> <li class="active"> <a href="#ai_summary" data-toggle="tab" class="summary-tab mx-0 f16 text-dark"> <strong>Automated Summary</strong> <strong class="text-danger ml-1"><i>New</i></strong> </a> </li> <li class=""> <a href="#raw_abstract" data-toggle="tab" class="abstract-tab mx-0 f16 text-dark"> <strong>Abstract</strong> </a> </li> </ul> <div class="tab-content border border-top-0"> <div id="ai_summary" class="tab-pane active"> <div class="summary-panel panel-box mb-0 rounded shadow-none"> <div class="f16">Through studying CD4(+) T cells of HIV-1 patients, the importance of effector memory T cells in the persistence of HIV-1 has been identified, and Nef has been suggested as a potential therapeutic target.</div> </div> </div> <div id="raw_abstract" class="tab-pane "> <div class="abstract-panel panel-box mb-0 rounded shadow-none"> <div class="f16">Despite long-term antiretroviral therapy (ART), HIV-1 persists within a reservoir of CD4(+) T cells that contribute to viral rebound if treatment is interrupted. Identifying the cellular populations that contribute to the HIV-1 reservoir and understanding the mechanisms of viral persistence are necessary to achieve an effective cure. In this regard, through Full-Length Individual Proviral Sequencing, we observed that the HIV-1 proviral landscape was different and changed with time on ART across naive and memory CD4(+) T cell subsets isolated from 24 participants. We found that the proportion of genetically intact HIV-1 proviruses was higher and persisted overtime in effector memory CD4(+) T cells when compared with naive, central, and transitional memory CD4(+) T cells, Interestingly, we found that escape mutations remained stable over time within effector memory T cells during therapy. Finally, we provided evidence that Nef plays a role in the persistence of genetically intact HIV-1. These findings posit effector memory T cells as a key component of the HIV-1 reservoir and suggest Nef as an attractive therapeutic target.</div> </div> </div> </div> </div> <div class="f15 panel-box rounded shadow-none border"> <h4 class="mt-0 heading-count">Authors</h4> <div class="mb-3"> <article-authors tid="35097577" list="[{&quot;name&quot;:&quot;Gabriel Duette&quot;,&quot;sequence&quot;:1},{&quot;name&quot;:&quot;Bonnie Hiener&quot;,&quot;sequence&quot;:2},{&quot;name&quot;:&quot;Hannah Morgan&quot;,&quot;sequence&quot;:3},{&quot;name&quot;:&quot;Fernando G. Mazur&quot;,&quot;sequence&quot;:4},{&quot;name&quot;:&quot;Vennila Mathivanan&quot;,&quot;sequence&quot;:5},{&quot;name&quot;:&quot;Bethany A. Horsburgh&quot;,&quot;sequence&quot;:6},{&quot;name&quot;:&quot;Katie Fisher&quot;,&quot;sequence&quot;:7},{&quot;name&quot;:&quot;Orion Tong&quot;,&quot;sequence&quot;:8},{&quot;name&quot;:&quot;Eunok Lee&quot;,&quot;sequence&quot;:9},{&quot;name&quot;:&quot;Haelee Ahn&quot;,&quot;sequence&quot;:10},{&quot;name&quot;:&quot;Ansari Shaik&quot;,&quot;sequence&quot;:11},{&quot;name&quot;:&quot;Remi Fromentin&quot;,&quot;sequence&quot;:12},{&quot;name&quot;:&quot;Rebecca Hoh&quot;,&quot;sequence&quot;:13},{&quot;name&quot;:&quot;Charline Bacchus-Souffan&quot;,&quot;sequence&quot;:14},{&quot;name&quot;:&quot;Najla Nasr&quot;,&quot;sequence&quot;:15},{&quot;name&quot;:&quot;Anthony L. Cunningham&quot;,&quot;sequence&quot;:16},{&quot;name&quot;:&quot;Peter W. Hunt&quot;,&quot;sequence&quot;:17},{&quot;name&quot;:&quot;Nicolas Chomont&quot;,&quot;sequence&quot;:18},{&quot;name&quot;:&quot;Stuart G. Turville&quot;,&quot;sequence&quot;:19},{&quot;name&quot;:&quot;Steven G. Deeks&quot;,&quot;sequence&quot;:20},{&quot;name&quot;:&quot;Anthony D. Kelleher&quot;,&quot;sequence&quot;:21},{&quot;name&quot;:&quot;Timothy E. Schlub&quot;,&quot;sequence&quot;:22},{&quot;name&quot;:&quot;Sarah Palmer&quot;,&quot;sequence&quot;:23}]" verified="[]" page="work" ></article-authors> </div> <div class="alert alert-warning mb-0"> <h5 class="mt-0 bg-warning text-dark px-3 rounded d-inline-block"> I am an author on this paper </h5> <div class="font-weight-bold f13"> Click your name to claim this paper and add it to your profile. </div> </div> </div> <div class="f15 panel-box rounded shadow-none border"> <h4 class="mt-0 heading-count">Reviews</h4> <div class="d-flex flex-wrap flex-md-nowrap"> <div class="flex-grow-1"> <h4 class="f16"> Primary Rating <a href="javascript:;" data-toggle="tooltip" data-placement="right" title="The primary rating indicates the level of overall quality for the paper."> <i class="ivu-icon ivu-icon-md-help-circle f18 ml-2"></i> </a> </h4> <div class="d-flex flex-wrap flex-md-nowrap align-items-center alert mb-0"> <div class="d-flex align-items-center justify-content-center"> <Rate disabled allow-half value="4.8" style="font-size: 28px;"></Rate> <strong class="f20 m-3" style="color: #f5a623;">4.8</strong> </div> <div class="text-muted mx-4"> Not enough ratings </div> </div> <h4 class="f16"> Secondary Ratings <a href="javascript:;" data-toggle="tooltip" data-placement="right" title="Secondary ratings independently reflect strengths or weaknesses of the paper."> <i class="ivu-icon ivu-icon-md-help-circle f18 ml-2"></i> </a> </h4> <div class="d-flex flex-wrap flex-md-nowrap alert"> <div class="d-flex flex-shrink-0 align-items-center mr-3"> <h5 class="my-0">Novelty</h5> <strong class="mx-4">-</strong> </div> <div class="d-flex flex-shrink-0 align-items-center mr-3"> <h5 class="my-0">Significance</h5> <strong class="mx-4">-</strong> </div> <div class="d-flex flex-shrink-0 align-items-center mr-3"> <h5 class="my-0">Scientific rigor</h5> <strong class="mx-4">-</strong> </div> </div> </div> <div class="flex-shrink-0"> <div class="border bg-light py-2 px-4"> <h5 class="mb-1">Rate this paper</h5> <Rate class="f24" @on-change="function(value){ location.href='https://www.peeref.com/works/35097577/comments?rating='+value }"></Rate> </div> </div> </div> </div> <div id="collection" class="f15 panel-box rounded shadow-none border"> <h4 class="mt-0 heading-count">Recommended</h4> <div class="my-3"> <ul class="nav nav-pills border-bottom pb-3" style="list-style: none; padding-left: 0;"> <li class="active"> <a href="#articles_from_related" data-toggle="tab" class="mx-0 f15"> <strong>Related</strong> </a> </li> <li class=""> <a href="#articles_from_authors" data-toggle="tab" class="mx-0 f15"> <strong>From Same Authors</strong> </a> </li> <li class=""> <a href="#articles_from_journal" data-toggle="tab" class="mx-0 f15"> <strong>From Same Journal</strong> </a> </li> </ul> <div class="tab-content"> <div id="articles_from_related" class="tab-pane active"> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Article </span> <span class="d-inline-block badge badge-cyan"> Virology </span> </div> <h4> <a href="https://www.peeref.com/works/27665162" class="text-dark hover-underline">A Conserved Acidic Residue in the C-Terminal Flexible Loop of HIV-1 Nef Contributes to the Activity of SERINC5 and CD4 Downregulation</a> </h4> <p class="text-ellipsis-2">Claudia Firrito, Cinzia Bertelli, Annachiara Rosa, Ajit Chande, Swetha Ananth, Hannah van Dijk, Oliver T. Fackler, Charlotte Stoneham, Rajendra Singh, John Guatelli, Massimo Pizzato</p> <div class="d-flex mb-3"> <div class="flex-shrink-0 d-none d-sm-block"> <img src="https://peeref-open.s3.amazonaws.com/storage/images/covers/8207.jpg" alt="" class="border mr-3" width="100"> </div> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> The host protein SERINC5 is incorporated into retrovirus particles and inhibits HIV-1 infectivity. The viral protein Nef counteracts SERINC5 by downregulating it and preventing its incorporation into virions. The ability of Nef to counteract SERINC5 varies between HIV-1 isolates. The study identified a specific Nef allele that is unable to counteract SERINC5 and investigated the molecular determinants responsible for this defect. A specific amino acid substitution was found to restore the ability of the defective Nef to counteract SERINC5 and promote HIV-1 infectivity. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">VIRUSES-BASEL</span> (2023) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/27665162/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Review </span> <span class="d-inline-block badge badge-cyan"> Virology </span> </div> <h4> <a href="https://www.peeref.com/works/82250720" class="text-dark hover-underline">HIV-1 Vpr Functions in Primary CD4+ T Cells</a> </h4> <p class="text-ellipsis-2">Carlos Alberto Vanegas-Torres, Michael Schindler</p> <div class="d-flex mb-3"> <div class="flex-shrink-0 d-none d-sm-block"> <img src="https://peeref-open.s3.amazonaws.com/storage/images/covers/8207.jpg" alt="" class="border mr-3" width="100"> </div> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> HIV-1 encodes four accessory proteins, and Vpr is abundant in virions and exerts various biological effects on host cells, contributing to the establishment of HIV-1 infection. HIV-1 preferentially infects CD4(+)T cells, causing immune dysfunction. Although much is known about the activities of Vpr in host cells, the in vivo relevance of some findings is controversial and requires further validation in physiologically relevant models. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">VIRUSES-BASEL</span> (2024) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/82250720/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Article </span> <span class="d-inline-block badge badge-cyan"> Immunology </span> </div> <h4> <a href="https://www.peeref.com/works/27353998" class="text-dark hover-underline">HIV rapidly targets a diverse pool of CD4+T cells to establish productive and latent infections</a> </h4> <p class="text-ellipsis-2">Pierre Gantner, Supranee Buranapraditkun, Amelie Pagliuzza, Caroline Dufour, Marion Pardons, Julie L. Mitchell, Eugene Kroon, Carlo Sacdalan, Nicha Tulmethakaan, Suteeraporn Pinyakorn, Merlin L. Robb, Nittaya Phanuphak, Jintanat Ananworanich, Denise Hsu, Sandhya Vasan, Lydie Trautmann, Remi Fromentin, Nicolas Chomont</p> <div class="d-flex mb-3"> <div class="flex-shrink-0 d-none d-sm-block"> <img src="https://peeref-open.s3.amazonaws.com/storage/images/covers/3473.jpg" alt="" class="border mr-3" width="100"> </div> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> During early stages of HIV infection, the virus initially targets a small population of proliferating memory CD4+ T cells with high surface expression of CCR5. Productively infected cells exhibit different phenotypes and TCR sequences depending on the stage of infection and location within the body. The TCR repertoire of infected cells is biased towards previously expanded and disseminated clones, suggesting independent infection events. Latent genetically intact proviruses are present early in infection, indicating simultaneous generation of latent infected cells. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">IMMUNITY</span> (2023) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/27353998/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Article </span> <span class="d-inline-block badge badge-cyan"> Biochemistry &amp; Molecular Biology </span> </div> <h4> <a href="https://www.peeref.com/works/84846412" class="text-dark hover-underline">The translational landscape of HIV-1 infected cells reveals key gene regulatory principles</a> </h4> <p class="text-ellipsis-2">Anuja Kibe, Stefan Buck, Anne-Sophie Gribling-Burrer, Orian Gilmer, Patrick Bohn, Tatyana Koch, Chiara Noemi-Marie Mireisz, Andreas Schlosser, Florian Erhard, Redmond P. Smyth, Neva Caliskan</p> <div class="d-flex mb-3"> <div class="flex-shrink-0 d-none d-sm-block"> <img src="https://peeref-open.s3.amazonaws.com/storage/images/covers/6085.jpg" alt="" class="border mr-3" width="100"> </div> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> This study analyzed the transcriptional and translational landscape of HIV-1 infected cells using multiple techniques, and found that HIV-1 mRNA can be efficiently translated. Some open reading frames were also identified, and ribosomal collisions in Gag-Pol were observed, which was related to RNA structural folding. Antisense oligonucleotides could reduce the frameshift efficiency. This study revealed the complexity of HIV-1 gene regulation and provided a new target for antiviral therapy. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">NATURE STRUCTURAL &amp; MOLECULAR BIOLOGY</span> (2025) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/84846412/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Article </span> <span class="d-inline-block badge badge-cyan"> Immunology </span> </div> <h4> <a href="https://www.peeref.com/works/83937579" class="text-dark hover-underline">Differential lipid signaling from CD4+ and CD8+ T cells contributes to type 1 diabetes development</a> </h4> <p class="text-ellipsis-2">Tayleur D. White, Abdulaziz Almutairi, Ying Gai-Tusing, Daniel J. Stephenson, Benjamin D. Stephenson, Charles E. Chalfant, Xiaoyong Lei, Brian Lu, Bruce D. Hammock, Teresa P. Dilorenzo, Sasanka Ramanadham</p> <div class="d-flex mb-3"> <div class="flex-shrink-0 d-none d-sm-block"> <img src="https://peeref-open.s3.amazonaws.com/storage/images/covers/10003.jpg" alt="" class="border mr-3" width="100"> </div> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> This study investigated the role of iPLA(2)β-derived lipids in the pathogenesis of type 1 diabetes and found that differential iDL signaling in CD4+ and CD8+ T cells contributes to the development of T1D, providing new insights for the treatment of T1D. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">FRONTIERS IN IMMUNOLOGY</span> (2024) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/83937579/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Article </span> <span class="d-inline-block badge badge-cyan"> Cell Biology </span> </div> <h4> <a href="https://www.peeref.com/works/27705560" class="text-dark hover-underline">T helper 1 effector memory CD4+T cells protect the skin from poxvirus infection</a> </h4> <p class="text-ellipsis-2">Jake C. Harbour, Mahmoud Abdelbary, John B. Schell, Samantha P. Fancher, Jack J. McLean, Taylen J. Nappi, Susan Liu, Timothy J. Nice, Zheng Xia, Klaus Fruh, Jeffrey C. Nolz</p> <div class="d-flex mb-3"> <div class="flex-shrink-0 d-none d-sm-block"> <img src="https://peeref-open.s3.amazonaws.com/storage/images/covers/8772.jpg" alt="" class="border mr-3" width="100"> </div> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> This study found that Th1 memory CD4+ T cells are crucial for protecting against poxvirus skin infections, while CD8+ T cells are not necessary. Th1 effector memory CD4+ T cells rapidly infiltrate the poxvirus-infected skin microenvironment and produce interferon γ to promote anti-viral immunity. Keratinocytes are the key targets of IFNγ necessary for preventing poxvirus infection of the epidermis. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">CELL REPORTS</span> (2023) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/27705560/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Article </span> <span class="d-inline-block badge badge-cyan"> Gastroenterology &amp; Hepatology </span> </div> <h4> <a href="https://www.peeref.com/works/25012048" class="text-dark hover-underline">Granzyme B+ CD4 T cells accumulate in the colon during chronic HIV-1 infection</a> </h4> <p class="text-ellipsis-2">Stephanie M. Dillon, Kaylee L. Mickens, Tezha A. Thompson, Emily H. Cooper, Sabrina Nesladek, Allison J. Christians, Moriah Castleman, Kejun Guo, Cheyret Wood, Daniel N. Frank, Katerina Kechris, Mario L. Santiago, Cara C. Wilson</p> <div class="d-flex mb-3"> <div class="flex-shrink-0 d-none d-sm-block"> <img src="https://peeref-open.s3.amazonaws.com/storage/images/covers/10591.jpg" alt="" class="border mr-3" width="100"> </div> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> Chronic HIV-1 infection disrupts gut homeostasis, leading to dysbiosis and increased microbial translocation. This study found that GZB(+) CD4 T cells were more prevalent in the colon of chronically infected people with HIV-1 and their frequencies were associated with gut and systemic T cell activation and Prevotella species abundance. In vitro experiments also showed that commensal bacteria upregulated GZB expression more readily in gut CD4 T cells, particularly in inflammatory T helper 17 cells. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">GUT MICROBES</span> (2022) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/25012048/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Article </span> <span class="d-inline-block badge badge-cyan"> Microbiology </span> </div> <h4> <a href="https://www.peeref.com/works/27834452" class="text-dark hover-underline">Exposure to Secreted Bacterial Factors Promotes HIV-1 Replication in CD4+ T Cells</a> </h4> <p class="text-ellipsis-2">M. Znaidia, Y. de Souza-Angelo, S. Letoffe, I. Staropoli, L. Grzelak, J. M. Ghigo, O. Schwartz, N. Casartelli</p> <div class="d-flex mb-3"> <div class="flex-shrink-0 d-none d-sm-block"> <img src="https://peeref-open.s3.amazonaws.com/storage/images/covers/10633.jpg" alt="" class="border mr-3" width="100"> </div> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> Microbial translocation is associated with systemic immune activation in HIV-1 disease. Some bacteria can activate T cells and enhance HIV-1 replication, suggesting a role of bacterial factors in promoting T cell activation and HIV-1 replication. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">MICROBIOLOGY SPECTRUM</span> (2023) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/27834452/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Article </span> <span class="d-inline-block badge badge-cyan"> Cell Biology </span> </div> <h4> <a href="https://www.peeref.com/works/27705962" class="text-dark hover-underline">Identification of aryl hydrocarbon receptor as a barrier to HIV-1 infection and outgrowth in CD4+T cells</a> </h4> <p class="text-ellipsis-2">Debashree Chatterjee, Yuwei Zhang, Christ-Dominique Ngassaki-Yoka, Antoine Dutilleul, Soumia Khalfi, Olivier Hernalsteens, Tomas Raul Wiche Salinas, Jonathan Dias, Huicheng Chen, Yasmine Smail, Jean-Philippe Goulet, Brendan Bell, Jean-Pierre Routy, Carine Van Lint, Petronela Ancuta</p> <div class="d-flex mb-3"> <div class="flex-shrink-0 d-none d-sm-block"> <img src="https://peeref-open.s3.amazonaws.com/storage/images/covers/8772.jpg" alt="" class="border mr-3" width="100"> </div> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> The aryl hydrocarbon receptor (AhR) inhibits HIV-1 replication and outgrowth in TCR-activated CD4+ T cells. AhR blockade improves early/late reverse transcription, integration/translation, and viral outgrowth in CD4+ T cells of people living with HIV-1 receiving antiretroviral therapy. AhR blockade downregulates genes/pathways involved in HIV-1 interaction and gut-homing in CD4+ T cells of ART-treated PLWH, and HIC1 is identified as a direct AhR target. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">CELL REPORTS</span> (2023) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/27705962/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Article </span> <span class="d-inline-block badge badge-cyan"> Multidisciplinary Sciences </span> </div> <h4> <a href="https://www.peeref.com/works/27672614" class="text-dark hover-underline">Phenotypic characterization of single CD4+T cells harboring genetically intact and inducible HIV genomes</a> </h4> <p class="text-ellipsis-2">Caroline Dufour, Corentin Richard, Marion Pardons, Marta Massanella, Antoine Ackaoui, Ben Murrell, Bertrand Routy, Rejean Thomas, Jean-Pierre Routy, Remi Fromentin, Nicolas Chomont</p> <div class="d-flex mb-3"> <div class="flex-shrink-0 d-none d-sm-block"> <img src="https://peeref-open.s3.amazonaws.com/storage/images/covers/8411.jpg" alt="" class="border mr-3" width="100"> </div> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> The phenotypic diversity of HIV-infected cells persisting during antiretroviral therapies (ART) was investigated. CD4+ T cells expressing integrin VLA-4 were found to be enriched in replication-competent HIV. Clonally expanded cells with identical proviruses displayed diverse phenotypes, indicating the role of cellular proliferation in the phenotypic diversification of the HIV reservoir. Genetically intact and inducible viral genomes were associated with higher levels of VLA-4 expression in CD4+ T cells. Replication-competent HIV was highly enriched in memory CD4+ T cells expressing high levels of VLA-4. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">NATURE COMMUNICATIONS</span> (2023) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/27672614/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Article </span> <span class="d-inline-block badge badge-cyan"> Immunology </span> </div> <h4> <a href="https://www.peeref.com/works/28409046" class="text-dark hover-underline">Single-cell epigenetic, transcriptional, and protein profiling of latent and active HIV-1 reservoir revealed that IKZF3 promotes HIV-1 persistence</a> </h4> <p class="text-ellipsis-2">Yulong Wei, Timothy C. Davenport, Jack A. Collora, Haocong Katherine Ma, Delia Pinto-Santini, Javier Lama, Ricardo Alfaro, Ann Durr, Ya-Chi Ho</p> <div class="d-flex mb-3"> <div class="flex-shrink-0 d-none d-sm-block"> <img src="https://peeref-open.s3.amazonaws.com/storage/images/covers/3473.jpg" alt="" class="border mr-3" width="100"> </div> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> Understanding the proliferation and persistence of HIV-1-infected cells is crucial for eradicating HIV-1. By examining the transcription factor accessibility, transcriptome, surface proteins, HIV-1 DNA, and HIV-1 RNA of single CD4+ memory T cells, we identified specific transcription factor accessibility in latent and transcriptionally active HIV-1-infected cells. Additionally, a proliferation program was found to promote the survival of transcriptionally active HIV-1-infected cells. Different epigenetic programs were also involved in driving the heterogeneous cellular states of HIV-1-infected cells, including activation, cytotoxic effector differentiation, migration, and cell death. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">IMMUNITY</span> (2023) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/28409046/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Article </span> <span class="d-inline-block badge badge-cyan"> Microbiology </span> </div> <h4> <a href="https://www.peeref.com/works/28784692" class="text-dark hover-underline">The transcriptome of HTLV-1-infected primary cells following reactivation reveals changes to host gene expression central to the proviral life cycle</a> </h4> <p class="text-ellipsis-2">Aris E. N. R. Aristodemou, David Rueda, Graham R. Taylor, Charles R. M. Bangham, Patrick L. R. Green</p> <div class="d-flex mb-3"> <div class="flex-shrink-0 d-none d-sm-block"> <img src="https://peeref-open.s3.amazonaws.com/storage/images/covers/8957.jpg" alt="" class="border mr-3" width="100"> </div> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> This study analyzed the expression changes of host and viral genes during HTLV-1 reactivation in cells isolated from patients&#039; blood. The study found that changes in viral expression may be related to changes in a group of epigenetic modifiers, which may contribute to the virus returning to a latent state after activation. In addition, the study also identified three deubiquitinases that can promote viral expression. These findings are of great importance for further understanding the lifecycle and infection mechanisms of HTLV-1. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">PLOS PATHOGENS</span> (2023) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/28784692/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Article </span> <span class="d-inline-block badge badge-cyan"> Medicine, General &amp; Internal </span> </div> <h4> <a href="https://www.peeref.com/works/35000332" class="text-dark hover-underline">Activation-induced pyroptosis contributes to the loss of MAIT cells in chronic HIV-1 infected patients</a> </h4> <p class="text-ellipsis-2">Peng Xia, Xu-Dong Xing, Cui-Xian Yang, Xue-Jiao Liao, Fu-Hua Liu, Hui-Huang Huang, Chao Zhang, Jin-Wen Song, Yan-Mei Jiao, Ming Shi, Tian-Jun Jiang, Chun-Bao Zhou, Xi-Cheng Wang, Qing He, Qing-Lei Zeng, Fu-Sheng Wang, Ji-Yuan Zhang</p> <div class="d-flex mb-3"> <div class="flex-shrink-0 d-none d-sm-block"> <img src="https://peeref-open.s3.amazonaws.com/storage/images/covers/11013.jpg" alt="" class="border mr-3" width="100"> </div> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> This study found that activation-induced MAIT cell pyroptosis contributes to the loss of MAIT cells in HIV-1 infected patients, which could potentiate disease progression and poor immune reconstitution. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">MILITARY MEDICAL RESEARCH</span> (2022) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/35000332/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Article </span> <span class="d-inline-block badge badge-cyan"> Biochemical Research Methods </span> </div> <h4> <a href="https://www.peeref.com/works/82842999" class="text-dark hover-underline">HIV-1 Nef Changes the Proteome of T Cells Extracellular Vesicles Depleting IFITMs and Other Antiviral Factors</a> </h4> <p class="text-ellipsis-2">Mara E. da Silva-Januario, Cristina S. da Costa, Lucas A. Tavares, Ana K. Oliveira, Yunan C. Januario, Andreia N. de Carvalho, Murilo H. A. Cassiano, Roger L. Rodrigues, Michael E. Miller, Soledad Palameta, Clarice W. Arns, Eurico Arruda, Adriana F. Paes Leme, Luis L. P. daSilva</p> <div class="d-flex mb-3"> <div class="flex-shrink-0 d-none d-sm-block"> <img src="https://peeref-open.s3.amazonaws.com/storage/images/covers/5931.jpg" alt="" class="border mr-3" width="100"> </div> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> This study characterized the changes in the protein composition of T-cell-derived EVs induced by Nef and identified novel host targets of HIV through quantitative proteomic analysis. The study found that Nef depleted IFITM13 from EVs by excluding it from the plasma membrane and lipid rafts, suggesting that Nef is a modulator of the global protein content of EVs and an HIV factor that antagonizes IFITMs. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">MOLECULAR &amp; CELLULAR PROTEOMICS</span> (2023) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/82842999/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 "> <div> <span class="d-inline-block badge badge-blue"> Article </span> <span class="d-inline-block badge badge-cyan"> Biology </span> </div> <h4> <a href="https://www.peeref.com/works/27877850" class="text-dark hover-underline">Mitochondrial Dysfunction in CD4+T Effector Memory RA plus Cells</a> </h4> <p class="text-ellipsis-2">Marie Strickland, Salanne Lee, Shi Yong Neo, Akhila Balachander, Ivy Low, Seri Mustafah, Wah Ing Goh, Graham D. D. Wright, Anis Larbi, Sylvia L. F. Pender</p> <div class="d-flex mb-3"> <div class="flex-shrink-0 d-none d-sm-block"> <img src="https://peeref-open.s3.amazonaws.com/storage/images/covers/10942.jpg" alt="" class="border mr-3" width="100"> </div> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> The study focuses on investigating the impact of mitochondrial dysfunction on immune responses to infection and vaccination in the elderly population. Specifically, it examines the metabolic responses and mitochondrial dynamics of CD4+ TEMRA cells and other CD4+ memory T cell subtypes. The results show that CD4+ TEMRA cells exhibit altered mitochondrial dynamics, increased glucose uptake, and higher mitochondrial mass, which may contribute to impaired responses to infection and vaccination. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">BIOLOGY-BASEL</span> (2023) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/27877850/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> </div> <div id="articles_from_authors" class="tab-pane "> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Article </span> <span class="d-inline-block badge badge-cyan"> Microbiology </span> </div> <h4> <a href="https://www.peeref.com/works/83105921" class="text-dark hover-underline">Characterising plasmacytoid and myeloid AXL+ SIGLEC-6+ dendritic cell functions and their interactions with HIV</a> </h4> <p class="text-ellipsis-2">Freja A. Warner van Dijk, Orion Tong, Thomas R. O&#039;Neil, Kirstie M. Bertram, Kevin Hu, Heeva Baharlou, Erica E. Vine, Kate Jenns, Martijn P. Gosselink, James W. Toh, Tim Papadopoulos, Laith Barnouti, Gregory J. Jenkins, Gavin Sandercoe, Muzlifah Haniffa, Kerrie J. Sandgren, Andrew N. Harman, Anthony L. Cunningham, Najla Nasr</p> <div class="d-flex mb-3"> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> This study found for the first time that two subsets of the novel myeloid dendritic cell ASDC are present in inflamed human anogenital tissues. These two subsets have significant differences in function, expressing co-stimulatory and maturation markers, and can induce more T cell proliferation and activation, and also polarize naive T cells significantly toward Th2, Th9, Th22, Th17 and Treg. In addition, the study found that within 2 hours after exposure to HIV, CD11c(+) ASDC showed a trend of transferring more viruses to T cells than CD123(+) ASDC and pDC in the first phase of transfer, while in the second phase of transfer, CD123(+) ASDC showed a trend of transferring more HIV than CD11c(+) ASDC, and there was no virus transfer from pDC. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">PLOS PATHOGENS</span> (2024) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/83105921/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Article </span> <span class="d-inline-block badge badge-cyan"> Cell Biology </span> </div> <h4> <a href="https://www.peeref.com/works/81685885" class="text-dark hover-underline">Characterization of the genetic determinants of context-specific DNA methylation in primary monocytes</a> </h4> <p class="text-ellipsis-2">James J. Gilchrist, Hai Fang, Sara Danielli, Marketa Tomkova, Isar Nassiri, Esther Ng, Orion Tong, Chelsea Taylor, Dylan Muldoon, Lea R. Z. Cohen, Hussein Al-Mossawi, Evelyn Lau, Matt Neville, Benjamin Schuster-Boeckler, Julian C. Knight, Benjamin P. Fairfax</p> <div class="d-flex mb-3"> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> This study analyzed 190 samples and found that the sensitivity of monocyte DNAm to LPS is site-dependent, and LPS-induced demethylation occurs after hydroxymethylation. The study also identified 7,359 immune-modulated CpGs and found that demethylated imCpGs are highly enriched in enhancers and colocalize with genes associated with diseases, especially cancer. In addition, DNAm is associated with age, and LPS exposure can increase epigenetic age. Finally, by integrating LPS-induced DNAm changes and genetic variations, the study identified 234 imCpGs under local genetic control and explored the common causal loci between LPS-induced DNAm responses and human disease traits. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">CELL GENOMICS</span> (2024) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/81685885/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Article </span> <span class="d-inline-block badge badge-cyan"> Oncology </span> </div> <h4> <a href="https://www.peeref.com/works/82021901" class="text-dark hover-underline">Severe acute myositis and myocarditis on initiation of 6-weekly pembrolizumab post-COVID-19 mRNA vaccination</a> </h4> <p class="text-ellipsis-2">Robert A. Watson, Weiyu Ye, Chelsea A. Taylor, Elsita Jungkurth, Rosalin Cooper, Orion Tong, Tim James, Brian Shine, Monika Hofer, Damian Jenkins, Robert Pell, Eleni Ieremia, Stephanie Jones, David Maldonado-Perez, Ian S. D. Roberts, Nicholas Coupe, Mark R. Middleton, Miranda J. Payne, Benjamin P. Fairfax</p> <div class="d-flex mb-3"> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> This study describes three cases of severe acute myocarditis with myositis that occurred within 22 days of each other within 1 month after the initial cycle of the anti-PD-1 drug pembrolizumab. All patients had recently received a COVID-19 mRNA booster vaccine prior to treatment and were positive for SARS-CoV2 spike antibody. The study shows that there is a high degree of clonal expansion and public clones between these cases, and some of the T cell clones expanded in the skeletal muscle may recognize viral epitopes. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">JOURNAL FOR IMMUNOTHERAPY OF CANCER</span> (2024) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/82021901/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Article </span> <span class="d-inline-block badge badge-cyan"> Microbiology </span> </div> <h4> <a href="https://www.peeref.com/works/81636208" class="text-dark hover-underline">Herpes simplex virus spreads rapidly in human foreskin, partly driven by chemokine-induced redistribution of Nectin-1 on keratinocytes</a> </h4> <p class="text-ellipsis-2">Hafsa Rana, Naomi R. Truong, Blake Johnson, Heeva Baharlou, Jason J. Herbert, Sasikaran Kandasamy, Robert Goddard, Ralph C. Cohen, Michael Wines, Najla Nasr, Andrew N. Harman, Kirstie M. Bertram, Kerrie J. Sandgren, Anthony L. Cunningham</p> <div class="d-flex mb-3"> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> This study established a human foreskin explant infection model and found that HSV1 enters the epidermis through local microtrauma, then spreads rapidly laterally, and nectin-1 around the infection foci will be redistributed to promote virus spread. These results help to gain an in-depth understanding of the mechanism of HSV1 infection and spread in human genital mucosa. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">PLOS PATHOGENS</span> (2024) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/81636208/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Article </span> <span class="d-inline-block badge badge-cyan"> Infectious Diseases </span> </div> <h4> <a href="https://www.peeref.com/works/84342282" class="text-dark hover-underline">Learning from COVID-19: strengthening Australia&#039;s research capacity through preparedness and collaboration</a> </h4> <p class="text-ellipsis-2">Miranda Z. Smith, Janelle Bowden, Linda Cristine, Anthony L. Cunningham, John Kaldor, Sharon R. Lewin, Andrew Singer, Robyn L. Ward, Tania C. Sorrell</p> <div class="d-flex mb-3"> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> This article discusses the research experiences and lessons learned from Australia&#039;s response to the COVID-19 pandemic, emphasizing the importance of public health platforms and research ecosystems, and proposing research requirements for strengthening pandemic preparedness and response, including developing a research strategy, investing in research partnerships, improving procedures, establishing responsive funding mechanisms, and integrating research outputs into practice and decision-making. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">COMMUNICABLE DISEASES INTELLIGENCE</span> (2024) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/84342282/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Article </span> <span class="d-inline-block badge badge-cyan"> Medicine, Research &amp; Experimental </span> </div> <h4> <a href="https://www.peeref.com/works/84693922" class="text-dark hover-underline">Innate immune cell activation by adjuvant AS01 in human lymph node explants is age independent</a> </h4> <p class="text-ellipsis-2">Vicki V. Stylianou, Kirstie M. Bertram, Van Anh Vo, Elizabeth B. Dunn, Heeva Baharlou, Darcii J. Terre, James Elhindi, Elisabeth Elder, James French, Farid Meybodi, Stephane T. Temmerman, Arnaud M. Didierlaurent, Margherita Coccia, Kerrie J. Sandgren, Anthony L. Cunningham</p> <div class="d-flex mb-3"> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> This study developed an in situ human LN explant model to investigate how vaccine adjuvants initiate immunity. The results showed that AS01 induced DC maturation and a strong proinflammatory cytokine response in intact LN slices, but not in dissociated cell cultures. In addition, the AS01 response in human LNs was independent of age. This model is a valuable tool for studying the mechanism of action of adjuvants in humans and for screening new formulations to streamline vaccine development. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">JOURNAL OF CLINICAL INVESTIGATION</span> (2024) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/84693922/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Review </span> <span class="d-inline-block badge badge-cyan"> Virology </span> </div> <h4> <a href="https://www.peeref.com/works/84709316" class="text-dark hover-underline">Breaching the Barrier: Investigating Initial Herpes Simplex Viral Infection and Spread in Human Skin and Mucosa</a> </h4> <p class="text-ellipsis-2">Hafsa Rana, Naomi R. Truong, Dona R. Sirimanne, Anthony L. Cunningham</p> <div class="d-flex mb-3"> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> This review discusses the initial events and spread of HSV infection, emphasizes the importance of intervention before viral latency, and proposes strategies of vaccine-induced mediators and targeting dermal MNPs. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">VIRUSES-BASEL</span> (2024) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/84709316/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Article </span> <span class="d-inline-block badge badge-cyan"> Cell Biology </span> </div> <h4> <a href="https://www.peeref.com/works/28868062" class="text-dark hover-underline">Effects of Oral Cannabinoids on Systemic Inflammation and Viral Reservoir Markers in People with HIV on Antiretroviral Therapy: Results of the CTN PT028 Pilot Clinical Trial</a> </h4> <p class="text-ellipsis-2">Ralph-Sydney Mboumba Bouassa, Eve Comeau, Yulia Alexandrova, Amelie Pagliuzza, Alexis Yero, Suzanne Samarani, Judy Needham, Joel Singer, Terry Lee, Florian Bobeuf, Claude Vertzagias, Giada Sebastiani, Shari Margolese, Enrico Mandarino, Marina B. Klein, Bertrand Lebouche, Jean-Pierre Routy, Nicolas Chomont, Cecilia T. Costiniuk, Mohammad-Ali Jenabian</p> <div class="d-flex mb-3"> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> Chronic HIV infection is accompanied by persistent inflammation, and this study suggests that cannabinoids may help reduce systemic inflammation in people with HIV. The study found that oral cannabinoids, either in combination with THC and CBD or CBD-only, significantly reduced inflammatory markers and affected immune cell subsets. These findings can guide future large clinical trials investigating the anti-inflammatory properties of cannabinoids. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">CELLS</span> (2023) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/28868062/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Article </span> <span class="d-inline-block badge badge-cyan"> Multidisciplinary Sciences </span> </div> <h4> <a href="https://www.peeref.com/works/28662547" class="text-dark hover-underline">Redefining the human corneal immune compartment using dynamic intravital imaging</a> </h4> <p class="text-ellipsis-2">Laura E. Downie, Xinyuan Zhang, Mengliang Wu, Senuri Karunaratne, Joon Keit Loi, Kirthana Senthil, Sana Arshad, Kirstie Bertram, Anthony L. Cunningham, Nicole Carnt, Scott N. Mueller, Holly R. Chinnery</p> <div class="d-flex mb-3"> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> The healthy human cornea contains immune cells that are commonly presumed to be dendritic cells, but the researchers found that many of these immune cells are actually lymphocytes. These corneal immune cells exhibit rapid, persistent motility and interact with other cells. The behavior of these immune cells can be altered in response to acute and chronic inflammatory stimuli, which can be modulated by therapeutic intervention. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA</span> (2023) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/28662547/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Article </span> <span class="d-inline-block badge badge-cyan"> Microbiology </span> </div> <h4> <a href="https://www.peeref.com/works/28739774" class="text-dark hover-underline">Interferon inhibits the release of herpes simplex virus-1 from the axons of sensory neurons</a> </h4> <p class="text-ellipsis-2">Kevin Danastas, Gerry Guo, Jessica Merjane, Nathan Hong, Ava Larsen, Monica Miranda-Saksena, Anthony L. Cunningham</p> <div class="d-flex mb-3"> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> This study explores the effects of interferons (IFNs) on herpes simplex virus-1 (HSV-1) and reveals that IFNs have the potential to block virus release from nerve endings, thereby preventing transmission into the skin. The study also highlights the potential wider antiviral effects of IFN-γ in neurons, suggesting its role in HSV-1 reactivation. These findings identify new targets for the development of immunotherapies to impede HSV-1 spread from nerves to the skin. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">MBIO</span> (2023) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/28739774/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Article </span> <span class="d-inline-block badge badge-cyan"> Medicine, General &amp; Internal </span> </div> <h4> <a href="https://www.peeref.com/works/27802122" class="text-dark hover-underline">Emergence and antibody evasion of BQ, BA.2.75 and SARS- CoV-2 recombinant sub-lineages in the face of maturing antibody breadth at the population level</a> </h4> <p class="text-ellipsis-2">Anouschka Akerman, Vanessa Milogiannakis, Tyra Jean, Camille Esneau, Mariana Ruiz Silva, Timothy Ison, Christina Fichter, Joseph A. Lopez, Deborah Chandra, Zin Naing, Joanna Caguicla, Daiyang Li, Gregory Walker, Supavadee Amatayakul-Chantler, Nathan Roth, Sandro Manni, Thomas Hauser, Thomas Barnes, Anna Condylios, Malinna Yeang, Maureen Wong, Charles S. P. Foster, Kenta Sato, Sharon Lee, Yang Song, Lijun Mao, Allison Sigmund, Amy Phu, Ann Marie Vande More, Stephanie Hunt, Mark Douglas, Ian Caterson, Warwick Britton, Kerrie Sandgren, Rowena Bull, Andrew Lloyd, Jamie Triccas, Stuart Tangye, Nathan W. Bartlett, David Darley, Gail Matthews, Damien J. Stark, Kathy Petoumenos, William D. Rawlinson, Ben Murrell, Fabienne Brilot, Anthony L. Cunningham, Anthony D. Kelleher, Anupriya Aggarwal, Stuart G. Turville</p> <div class="d-flex mb-3"> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> This study monitored the neutralization potency and breadth of antibodies against Omicron variants over time. The findings show that the antibody response to Omicron variants has been maturing, with increased breadth observed even to variants that were not yet in circulation. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">EBIOMEDICINE</span> (2023) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/27802122/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Letter </span> <span class="d-inline-block badge badge-cyan"> Virology </span> </div> <h4> <a href="https://www.peeref.com/works/27501025" class="text-dark hover-underline">Statement in Support of: Virology under the Microscope-a Call for Rational Discourse</a> </h4> <p class="text-ellipsis-2">Peter Speck, Jason Mackenzie, Rowena A. Bull, Barry Slobedman, Heidi Drummer, Johanna Fraser, Lara Herrero, Karla Helbig, Sarah Londrigan, Gregory Moseley, Natalie Prow, Grant Hansman, Robert Edwards, Chantelle Ahlenstiel, Allison Abendroth, David Tscharke, Jody Hobson-Peters, Robson Kriiger-Loterio, Rhys Parry, Glenn Marsh, Emma Harding, David A. Jacques, Matthew J. Gartner, Wen Shi Lee, Julie McAuley, Paola Vaz, Frank Sainsbury, Michelle D. Tate, Jane Sinclair, Allison Imrie, Stephen Rawlinson, Andrew Harman, Jillian M. Carr, Ebony A. Monson, Merilyn Hibma, Timothy J. Mahony, Thomas Tu, Robert J. Center, Lok Bahadur Shrestha, Robyn Hall, Morgyn Warner, Vernon Ward, Danielle E. Anderson, Nicholas S. Eyre, Natalie E. Netzler, Alison J. Peel, Peter Revill, Michael Beard, Alistair R. Legione, Alexandra J. Spencer, Adi Idris, Jade Forwood, Subir Sarker, Damian F. J. Purcell, Nathan Bartlett, Joshua M. Deerain, Bruce J. Brew, Sassan Asgari, Helen Farrell, Alexander Khromykh, Daniel Enosi Tuipulotu, David Anderson, Sevim Mese, Yaman Tayyar, Kathryn Edenborough, Jasim Muhammad Uddin, Abrar Hussain, Connor J. I. Daymond, Jacinta Agius, Karyn N. Johnson, Paniz Shirmast, Mahdi Abedinzadeshahri, Robin MacDiarmid, Caroline L. Ashley, Jay Laws, Lucy L. Furfaro, Thomas D. Burton, Stephen M. R. Johnson, Zahra Telikani, Mary Petrone, Justin A. Roby, Carolyn Samer, Andreas Suhrbier, April van der Kamp, Anthony Cunningham, Celeste Donato, Jackie Mahar, Wesley D. Black, Subhash Vasudevan, Roman Lenchine, Kirsten Spann, Daniel J. Rawle, Penny Rudd, Jessica Neil, Richard Kingston, Timothy P. Newsome, Ki Wook Kim, Johnson Mak, Kym Lowry, Nathan Bryant, Joanne Meers, Jason A. Roberts, Nigel McMillan, Larisa I. Labzin, Andrii Slonchak, Leon E. Hugo, Bennett Henzeler, Natalee D. Newton, Cassandra T. David, Patrick C. Reading, Camille Esneau, Tatiana Briody, Najla Nasr, Donna McNeale, Brian McSharry, Omid Fakhri, Bethany A. Horsburgh, Grant Logan, Paul Howley, Paul Young</p> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">JOURNAL OF VIROLOGY</span> (2023) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/27501025/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Letter </span> <span class="d-inline-block badge badge-cyan"> Microbiology </span> </div> <h4> <a href="https://www.peeref.com/works/27670140" class="text-dark hover-underline">Statement in Support of: Virology under the Microscope-a Call for Rational Discourse</a> </h4> <p class="text-ellipsis-2">Peter Speck, Jason Mackenzie, Rowena A. Bull, Barry Slobedman, Heidi Drummer, Johanna Fraser, Lara Herrero, Karla Helbig, Sarah Londrigan, Gregory Moseley, Natalie Prow, Grant Hansman, Robert Edwards, Chantelle Ahlenstiel, Allison Abendroth, David Tscharke, Jody Hobson-Peters, Robson Kriiger-Loterio, Rhys Parry, Glenn Marsh, Emma Harding, David A. Jacques, Matthew J. Gartner, Wen Shi Lee, Julie McAuley, Paola Vaz, Frank Sainsbury, Michelle D. Tate, Jane Sinclair, Allison Imrie, Stephen Rawlinson, Andrew Harman, Jillian M. Carr, Ebony A. Monson, Merilyn Hibma, Timothy J. Mahony, Thomas Tu, Robert J. Center, Lok Bahadur Shrestha, Robyn Hall, Morgyn Warner, Vernon Ward, Danielle E. Anderson, Nicholas S. Eyre, Natalie E. Netzler, Alison J. Peel, Peter Revill, Michael Beard, Alistair R. Legione, Alexandra J. Spencer, Adi Idris, Jade Forwood, Subir Sarker, Damian F. J. Purcell, Nathan Bartlett, Joshua M. Deerain, Bruce J. Brew, Sassan Asgari, Helen Farrell, Alexander Khromykh, Daniel Enosi Tuipulotu, David Anderson, Sevim Mese, Yaman Tayyar, Kathryn Edenborough, Jasim Muhammad Uddin, Abrar Hussain, Connor J. Daymond, Jacinta Agius, Karyn N. Johnson, Paniz Shirmast, Mahdi Abedinzadeshahri, Robin MacDiarmid, Caroline L. Ashley, Jay Laws, Lucy L. Furfaro, Thomas D. Burton, Stephen M. R. Johnson, Zahra Telikani, Mary Petrone, Justin A. Roby, Carolyn Samer, Andreas Suhrbier, April van der Kamp, Anthony Cunningham, Celeste Donato, Jackie Mahar, Wesley D. Black, Subhash Vasudevan, Roman Lenchine, Kirsten Spann, Daniel J. Rawle, Penny Rudd, Jessica Neil, Richard Kingston, Timothy P. Newsome, Ki Wook Kim, Johnson Mak, Kym Lowry, Nathan Bryant, Joanne Meers, Jason A. Roberts, Nigel McMillan, Larisa I. Labzin, Andrii Slonchak, Leon E. Hugo, Bennett Henzeler, Natalee D. Newton, Cassandra T. David, Patrick C. Reading, Camille Esneau, Tatiana Briody, Najla Nasr, Donna McNeale, Brian McSharry, Omid Fakhri, Bethany A. Horsburgh, Grant Logan, Paul Howley, Paul Young</p> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">MBIO</span> (2023) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/27670140/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Article </span> <span class="d-inline-block badge badge-cyan"> Medicine, General &amp; Internal </span> </div> <h4> <a href="https://www.peeref.com/works/33496492" class="text-dark hover-underline">Influence of letermovir treatment on gut inflammation in people living with HIV on antiretroviral therapy: protocol of the open-label controlled randomised CIAO study</a> </h4> <p class="text-ellipsis-2">Lena Royston, Stephane Isnard, Carolina A. Berini, Simeng Bu, Peter L. Lakatos, Talat Bessissow, Nicolas Chomont, Marina Klein, Bertrand Lebouche, Alexandra de Pokomandy, Nadine Kronfli, Cecilia T. Costiniuk, Rejean Thomas, Cecile Tremblay, Guy Boivin, Jean-Pierre Routy</p> <div class="d-flex mb-3"> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> This study aims to assess whether letermovir, a novel anti-CMV drug, can inhibit CMV subclinical replication in HIV patients receiving ART, and subsequently reduce CMV-associated gut damage and inflammation. The study will conduct a 14-week open-label, randomized, controlled clinical trial with 60 CMV-seropositive ART-treated HIV patients. The effects of letermovir on gut damage, microbial translocation, inflammation, and HIV reservoir size will be evaluated. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">BMJ OPEN</span> (2023) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/33496492/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 "> <div> <span class="d-inline-block badge badge-blue"> Letter </span> <span class="d-inline-block badge badge-cyan"> Microbiology </span> </div> <h4> <a href="https://www.peeref.com/works/27800447" class="text-dark hover-underline">Statement in Support of: Virology under the Microscope-a Call for Rational Discourse</a> </h4> <p class="text-ellipsis-2">Peter Speck, Jason Mackenzie, Rowena A. Bull, Barry Slobedman, Heidi Drummer, Johanna Fraser, Lara Herrero, Karla Helbig, Sarah Londrigan, Gregory Moseley, Natalie Prow, Grant Hansman, Robert Edwards, Chantelle Ahlenstiel, Allison Abendroth, David Tscharke, Jody Hobson-Peters, Robson Kriiger-Loterio, Rhys Parry, Glenn Marsh, Emma Harding, David A. Jacques, Matthew J. Gartner, Wen Shi Lee, Julie McAuley, Paola Vaz, Frank Sainsbury, Michelle D. Tate, Jane Sinclair, Allison Imrie, Stephen Rawlinson, Andrew Harman, Jillian M. Carr, Ebony A. Monson, Merilyn Hibma, Timothy J. Mahony, Thomas Tu, Robert J. Center, Lok Bahadur Shrestha, Robyn Hall, Morgy Warner, Vernon Ward, Danielle E. Anderson, Nicholas S. Eyre, Natalie E. Netzler, Alison J. Peel, Peter Revill, Michael Beard, Alistair R. Legione, Alexandra J. Spencer, Adi Idris, Jade Forwood, Subir Sarker, Damian F. J. Purcell, Nathan Bartlett, Joshua M. Deerain, Bruce J. Brew, Sassan Asgari, Helen Farrell, Alexander Khromykh, Daniel Enosi Tuipulotu, David Anderson, Sevim Mese, Yaman Tayyar, Kathryn Edenborough, Jasim Muhammad Uddin, Abrar Hussain, Connor J. I. Daymond, Jacinta Agius, Karyn N. Johnson, Paniz Shirmast, Mahdi Abedinzadeshahri, Robin MacDiarmid, Caroline L. Ashley, Jay Laws, Lucy L. Furfaro, Thomas D. Burton, Stephen M. R. Johnson, Zahra Telikani, Mary Petrone, Justin A. Roby, Carolyn Samer, Andreas Suhrbier, April van der Kamp, Anthony Cunningham, Celeste Donato, Jackie Mahar, Wesley D. Black, Subhash Vasudevan, Roman Lenchine, Kirsten Spann, Daniel J. Rawle, Penny Rudd, Jessica Neil, Richard Kingston, Timothy P. Newsome, Ki Wook Kim, Johnson Mak, Kym Lowry, Nathan Bryant, Joanne Meers, Jason A. Roberts, Nigel McMillan, Larisa I. Labzin, Andrii Slonchak, Leon E. Hugo, Bennett Henzeler, Natalee D. Newton, Cassandra T. David, Patrick C. Reading, Camille Esneau, Tatiana Briody, Najla Nasr, Donna McNeale, Brian McSharry, Omid Fakhri, Bethany A. Horsburgh, Grant Logan, Paul Howley, Paul Young</p> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">MSPHERE</span> (2023) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/27800447/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> </div> <div id="articles_from_journal" class="tab-pane "> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Article </span> <span class="d-inline-block badge badge-cyan"> Medicine, Research &amp; Experimental </span> </div> <h4> <a href="https://www.peeref.com/works/83035994" class="text-dark hover-underline">The alanyl-tRNA synthetase AARS1 moonlights as a lactyltransferase to promote YAP signaling in gastric cancer</a> </h4> <p class="text-ellipsis-2">Junyi Ju, Hui Zhang, Moubin Lin, Zifeng Yan, Liwei An, Zhifa Cao, Dandan Geng, Jingwu Yue, Yang Tang, Luyang Tian, Fan Chen, Yi Han, Wenjia Wang, Shimin Zhao, Shi Jiao, Zhaocai Zhou</p> <div class="d-flex mb-3"> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> This study identified a new type of posttranslational modification, lactylation, which occurs widely on lysine residues of histone and nonhistone proteins. The researchers found that AARS1 can directly catalyze protein lactylation using lactate and ATP, and that AARS1 can sense intracellular lactate and translocate to the nucleus to activate the YAP-TEAD complex, promoting gastric cancer cell proliferation. In addition, the expression of AARS1 is associated with the prognosis of gastric cancer patients. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">JOURNAL OF CLINICAL INVESTIGATION</span> (2024) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/83035994/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Article </span> <span class="d-inline-block badge badge-cyan"> Medicine, Research &amp; Experimental </span> </div> <h4> <a href="https://www.peeref.com/works/85035630" class="text-dark hover-underline">Sialylated glycoproteins suppress immune cell killing by binding to Siglec-7 and Siglec-9 in prostate cancer</a> </h4> <p class="text-ellipsis-2">Ru M. Wen, Jessica C. Stark, G. Edward W. Marti, Zenghua Fan, Aram Lyu, Fernando Jose Garcia Marques, Xiangyue Zhang, Nicholas M. Riley, Sarah M. Totten, Abel Bermudez, Rosalie Nolley, Hongjuan Zhao, Lawrence Fong, Edgar G. Engleman, Sharon J. Pitteri, Carolyn R. Bertozzi, James D. Brooks</p> <div class="d-flex mb-3"> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> This study shows that Siglec-7 and Siglec-9 are associated with poor prognosis in patients with prostate cancer, and they are highly expressed in myeloid cells in prostate tumor tissues. Their ligands are also expressed in prostate cancer cells and human prostate tumor tissues. Blocking the interaction between them can inhibit the growth of prostate cancer xenografts and increase immune cell infiltration. In addition, the study also identified CD59 as a candidate Siglec-9 ligand in prostate cancer. These findings provide new targets and strategies for immunotherapy of prostate cancer. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">JOURNAL OF CLINICAL INVESTIGATION</span> (2024) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/85035630/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Article </span> <span class="d-inline-block badge badge-cyan"> Medicine, Research &amp; Experimental </span> </div> <h4> <a href="https://www.peeref.com/works/83004915" class="text-dark hover-underline">ZBP1-mediated apoptosis and inflammation exacerbate steatotic liver ischemia/reperfusion injury</a> </h4> <p class="text-ellipsis-2">Ran Liu, Huan Cao, Shuhua Zhang, Mao Cai, Tianhao Zou, Guoliang Wang, Di Zhang, Xueling Wang, Jianjun Xu, Shenghe Deng, Tongxi Li, Daichao Xu, Jinyang Gu</p> <div class="d-flex mb-3"> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> The study investigated the mechanism underlying the susceptibility of steatotic liver to I/R injury, finding that caspase-8-mediated apoptosis is involved, and RIPK1 kinase induces both apoptosis and inflammation. Inhibiting RIPK1 kinase reduces injury, and ZBP1-mediated RIPK1-driven processes exacerbate it. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">JOURNAL OF CLINICAL INVESTIGATION</span> (2024) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/83004915/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Article </span> <span class="d-inline-block badge badge-cyan"> Medicine, Research &amp; Experimental </span> </div> <h4> <a href="https://www.peeref.com/works/83036005" class="text-dark hover-underline">Excess glucocorticoids inhibit murine bone turnover via modulating the immunometabolism of the skeletal microenvironment</a> </h4> <p class="text-ellipsis-2">Xu Li, Tongzhou Liang, Bingyang Dai, Liang Chang, Yuan Zhang, Shiwen Hu, Jiaxin Guo, Shunxiang Xu, Lizhen Zheng, Hao Yao, Hong Lian, Yu Nie, Ye Li, Xuan He, Zhi Yao, Wenxue Tong, Xinluan Wang, Dick Ho Kiu Chow, Jiankun Xu, Ling Qin</p> <div class="d-flex mb-3"> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> Excessive glucocorticoids can lead to bone loss and delayed fracture healing, which is related to the reduction of bone turnover and the impairment of local nutrient status. Fatty acid oxidation in macrophages can promote osteogenesis. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">JOURNAL OF CLINICAL INVESTIGATION</span> (2024) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/83036005/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Article </span> <span class="d-inline-block badge badge-cyan"> Medicine, Research &amp; Experimental </span> </div> <h4> <a href="https://www.peeref.com/works/84693887" class="text-dark hover-underline">Stimulation of an entorhinal-hippocampal extinction circuit facilitates fear extinction in a post-traumatic stress disorder model</a> </h4> <p class="text-ellipsis-2">Ze-Jie Lin, Xue Gu, Wan-Kun Gong, Mo Wang, Yan-Jiao Wu, Qi Wang, Xin-Rong Wu, Xin-Yu Zhao, Michael X. Zhu, Lu-Yang Wang, Quanying Liu, Ti-Fei Yuan, Wei-Guang Li, Tian-Le Xu</p> <div class="d-flex mb-3"> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> This study unveils a direct pathway through layer 2a fan cells in the lateral entorhinal cortex (LEC) targeting parvalbumin-expressing interneurons (PV-INs) in the vCA1 region to promote low-gamma-band synchronization of LEC-vCA1 activity during extinction learning, which can facilitate fear extinction. Finally, the study shows that it is possible to stimulate the dedicated LEC-vCA1 pathway for therapy to remove traumatic memory traces. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">JOURNAL OF CLINICAL INVESTIGATION</span> (2024) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/84693887/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Review </span> <span class="d-inline-block badge badge-cyan"> Medicine, Research &amp; Experimental </span> </div> <h4> <a href="https://www.peeref.com/works/84720222" class="text-dark hover-underline">Alcohol-associated liver disease</a> </h4> <p class="text-ellipsis-2">Bryan Mackowiak, Yaojie Fu, Luca Maccioni, Bin Gao</p> <div class="d-flex mb-3"> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> Alcohol-related liver disease (ALD) is a major cause of chronic liver disease worldwide, and its pathogenesis is still unclear, and there is currently no FDA-approved treatment. This review discusses new insights into the pathogenesis and therapeutic targets of ALD, as well as the potential translation of these studies into clinical practice and treatment. It also discusses the preclinical models of ALD, the interaction with metabolic dysfunction, alcohol-related liver cancer, the heterogeneity of ALD, and some potential translational research prospects. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">JOURNAL OF CLINICAL INVESTIGATION</span> (2024) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/84720222/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Article </span> <span class="d-inline-block badge badge-cyan"> Medicine, Research &amp; Experimental </span> </div> <h4> <a href="https://www.peeref.com/works/83546172" class="text-dark hover-underline">SLC44A2 regulates vascular smooth muscle cell phenotypic switching and aortic aneurysm</a> </h4> <p class="text-ellipsis-2">Tianyu Song, Shuang Zhao, Shanshan Luo, Chuansheng Chen, Xingeng Liu, Xiaoqi Wu, Zhongxu Sun, Jiawei Cao, Ziyu Wang, Yineng Wang, Bo Yu, Zhiren Zhang, Xiaolong Du, Xiaoqiang Li, Zhijian Han, Hongshan Chen, Feng Chen, Liansheng Wang, Hong Wang, Kangyun Sun, Yi Han, Liping Xie, Yong Ji</p> <div class="d-flex mb-3"> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> This study found that SLC44A2 is a major regulator of VSMC phenotypic switching in aortic aneurysms, which interacts with NRP1 and ITGB3 to activate the TGF-β/SMADβ/SMAD signaling pathway and promote the expression of contractile genes. Elevated SLC44A2 in aortic aneurysms is associated with upregulated RUNX1. Low-dose lenalidomide can suppress the progression of aortic aneurysms by enhancing SLC44A2 expression. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">JOURNAL OF CLINICAL INVESTIGATION</span> (2024) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/83546172/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Article </span> <span class="d-inline-block badge badge-cyan"> Medicine, Research &amp; Experimental </span> </div> <h4> <a href="https://www.peeref.com/works/85007641" class="text-dark hover-underline">TREM2 aggravates sepsis by inhibiting fatty acid oxidation via the SHP1/BTK axis</a> </h4> <p class="text-ellipsis-2">Siqi Ming, Xingyu Li, Qiang Xiao, Siying Qu, Qiaohua Wang, Qiongyan Fang, Pingping Liang, Yating Xu, Jingwen Yang, Yongqiang Yang, Xi Huang, Yongjian Wu</p> <div class="d-flex mb-3"> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> This study found that TREM2 is highly expressed in sepsis and is associated with disease severity. Knockout of TREM2 in mice can improve survival rate and reduce inflammation and organ damage in sepsis. Mechanistically, TREM2 interacts with SHP1 to inhibit FAO. This study reveals that TREM2 is a key regulator of FAO and may provide a promising target for the clinical treatment of sepsis. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">JOURNAL OF CLINICAL INVESTIGATION</span> (2025) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/85007641/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Article </span> <span class="d-inline-block badge badge-cyan"> Medicine, Research &amp; Experimental </span> </div> <h4> <a href="https://www.peeref.com/works/84229610" class="text-dark hover-underline">Single-cell multiomic analysis identifies macrophage subpopulations in promoting cardiac repair</a> </h4> <p class="text-ellipsis-2">Mingzhu Fu, Shengtao Jia, Longhui Xu, Xin Li, Yufang Lv, Yulong Zhong, Shanshan Ai</p> <div class="d-flex mb-3"> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> This study analyzed the spatiotemporal single-cell epigenomic of cardiac MPCs in regenerative and nonregenerative mouse hearts after injury, and discovered the role and mechanism of different types of cardiac MPCs in cardiac injury repair. The study also found that blocking the chemokine CXCR2 can promote wound repair responses, improve cardiac function, and increase the number of Arg1(+) macrophage subsets. These findings provide new insights into the function and fate determination of MPCs during cardiac repair, and offer potential therapeutic targets for myocardial infarction. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">JOURNAL OF CLINICAL INVESTIGATION</span> (2024) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/84229610/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Article </span> <span class="d-inline-block badge badge-cyan"> Medicine, Research &amp; Experimental </span> </div> <h4> <a href="https://www.peeref.com/works/83546177" class="text-dark hover-underline">Myostatin regulates energy homeostasis through autocrine- and paracrine-mediated microenvironment communication</a> </h4> <p class="text-ellipsis-2">Hui Wang, Shanshan Guo, Huanqing Gao, Jiyang Ding, Hongyun Li, Xingyu Kong, Shuang Zhang, Muyang He, Yonghao Feng, Wei Wu, Kexin Xu, Yuxuan Chen, Hanyin Zhang, Tiemin Liu, Xingxing Kong</p> <div class="d-flex mb-3"> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> This study knocked out MSTN from the brown adipose tissue of mice and found that their weight increased and metabolic problems occurred. Further research revealed that MSTN affects metabolism by regulating the expression of KLF4 and FGF21, providing a new target for the treatment of obesity and metabolic diseases. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">JOURNAL OF CLINICAL INVESTIGATION</span> (2024) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/83546177/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Article </span> <span class="d-inline-block badge badge-cyan"> Medicine, Research &amp; Experimental </span> </div> <h4> <a href="https://www.peeref.com/works/84693938" class="text-dark hover-underline">Lactate reprograms glioblastoma immunity through CBX3-regulated histone lactylation</a> </h4> <p class="text-ellipsis-2">Shuai Wang, Tengfei Huang, Qiulian Wu, Huairui Yuan, Xujia Wu, Fanen Yuan, Tingting Duan, Suchet Taori, Yingming Zhao, Nathaniel W. Snyder, Dimitris G. Placantonakis, Jeremy N. Rich</p> <div class="d-flex mb-3"> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> This study reveals the mechanism by which glioblastoma escapes the immune system through lactate-mediated metabolic reprogramming and proposes strategies to enhance the efficacy of immunotherapy by targeting lactate production and CBX3. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">JOURNAL OF CLINICAL INVESTIGATION</span> (2024) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/84693938/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Article </span> <span class="d-inline-block badge badge-cyan"> Medicine, Research &amp; Experimental </span> </div> <h4> <a href="https://www.peeref.com/works/85007559" class="text-dark hover-underline">68Ga-MY6349 PET/CT imaging to assess Trop2 expression in multiple types of cancer</a> </h4> <p class="text-ellipsis-2">Haojun Chen, Liang Zhao, Yizhen Pang, Jiyun Shi, Hannan Gao, Yining Sun, Jianhao Chen, Hao Fu, Jiayu Cai, Lingyu Yu, Ru Zeng, Long Sun, Hua Wu, Zhanxiang Wang, Fan Wang</p> <div class="d-flex mb-3"> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> This study developed a Trop2-specific radiotracer, Ga-68-MY6349, and conducted a clinical trial. The results showed that Ga-68-MY6349 PET/CT can be used to comprehensively assess Trop2 expression in tumors, which is helpful for the diagnosis and staging of cancer and provides a basis for decision-making in Trop2-targeted therapy. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">JOURNAL OF CLINICAL INVESTIGATION</span> (2025) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/85007559/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Article </span> <span class="d-inline-block badge badge-cyan"> Medicine, Research &amp; Experimental </span> </div> <h4> <a href="https://www.peeref.com/works/83987081" class="text-dark hover-underline">A fibroblast-dependent TGF-β1/sFRP2 noncanonical Wnt signaling axis promotes epithelial metaplasia in idiopathic pulmonary fibrosis</a> </h4> <p class="text-ellipsis-2">Max L. Cohen, Alexis N. Brumwell, Tsung Che Ho, Kiana Garakani, Genevieve Montas, Darren Leong, Vivianne W. Ding, Jeffrey A. Golden, Binh N. Trinh, David M. Jablons, Michael A. Matthay, Kirk D. Jones, Paul J. Wolters, Ying Wei, Harold A. Chapman, Claude Jourdan Le Saux</p> <div class="d-flex mb-3"> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> This study investigated the crucial role of reciprocal interactions between alveolar fibroblasts and epithelial cells in lung homeostasis, injury repair, and fibrogenesis. The researchers administered EGCG to ILD patients and conducted single-cell RNA-Seq analysis. The results showed that EGCG downregulated TGF-β1 signaling and several proinflammatory and stress pathways, and reduced sFRP2 expression. Further studies revealed that TGF-β1 signaling promotes a basaloid state in AEC2, and sFRP2 activates a basal cell program. These findings highlight the stage-specific TGF-β1 signaling in ILD and the therapeutic potential of EGCG, and identify the TGF-β1/noncanonical Wnt pathway crosstalk as a mechanism for dysfunctional epithelial signaling in IPF/ILD. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">JOURNAL OF CLINICAL INVESTIGATION</span> (2024) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/83987081/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 border-bottom"> <div> <span class="d-inline-block badge badge-blue"> Article </span> <span class="d-inline-block badge badge-cyan"> Medicine, Research &amp; Experimental </span> </div> <h4> <a href="https://www.peeref.com/works/83546180" class="text-dark hover-underline">CDKL3 is a targetable regulator of cell cycle progression in cancers</a> </h4> <p class="text-ellipsis-2">Haijiao Zhang, Jiahui Lin, Shaoqin Zheng, Lanjing Ma, Zhongqiu Pang, Hongyi Yin, Chengcheng Meng, Yinuo Wang, Qing Han, Xi Zhang, Zexu Li, Liu Cao, Lijun Liu, Teng Fei, Daming Gao, Liang Yang, Xueqiang Peng, Chen Ding, Shixue Wang, Ren Sheng</p> <div class="d-flex mb-3"> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> This study reveals the crucial role of CDKL3 in cancer cell cycle regulation. It drives cell cycle progression and cell growth by associating with specific cyclin and directly phosphorylating Rb. Additionally, CDKL3 prevents the degradation of CDK4, sustaining G1 phase advancement. The researchers designed a CDKL3-specific inhibitor, HZ1, which shows greater potency than CDK4/6 inhibitor in pan-cancer treatment and overcomes acquired resistance to CDK4/6 inhibitor. CDKL3 has significant clinical relevance in colon cancer, and the effectiveness of HZ1 was demonstrated in murine and patient-derived cancer models. This study provides new insights and approaches for cancer treatment. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">JOURNAL OF CLINICAL INVESTIGATION</span> (2024) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/83546180/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> <div class="my-4 "> <div> <span class="d-inline-block badge badge-blue"> Article </span> <span class="d-inline-block badge badge-cyan"> Medicine, Research &amp; Experimental </span> </div> <h4> <a href="https://www.peeref.com/works/84693927" class="text-dark hover-underline">MGA loss-of-function variants cause premature ovarian insufficiency</a> </h4> <p class="text-ellipsis-2">Shuyan Tang, Ting Guo, Chengcheng Song, Lingbo Wang, Jun Zhang, Aleksandar Rajkovic, Xiaoqi Lin, Shiling Chen, Yujun Liu, Weidong Tian, Bangguo Wu, Shixuan Wang, Wenwen Wang, Yunhui Lai, Ao Wang, Shuhua Xu, Li Jin, Hanni Ke, Shidou Zhao, Yan Li, Yingying Qin, Feng Zhang, Zi-Jiang Chen</p> <div class="d-flex mb-3"> <div class="p-3 rounded bg-light-blue"> <strong>Summary:</strong> This study identified heterozygous loss-of-function variants of MGA in POI cases through exome-wide analysis of a discovery cohort from China, and replicated the findings in four additional POI cohorts. The phenotype of Mga+/- female mice mimics that of humans, highlighting the essential role of MGA deficiency in impaired female reproductive ability. </div> </div> <div class="d-flex justify-content-between"> <p class="font-weight-bold"> <span class="text-primary">JOURNAL OF CLINICAL INVESTIGATION</span> (2024) </p> <div class="flex-shrink-0"> <a class="btn btn-outline-primary btn-sm" href="https://www.peeref.com/works/84693927/add-to-collection" target="_blank"> <strong>Add to Collection</strong> </a> </div> </div> </div> </div> </div> </div> </div> </div> </div> <div class="modal fade" id="export-citation" tabindex="-1"> <div class="modal-dialog"> <div class="modal-content"> <div class="modal-header"> <button type="button" class="close" data-dismiss="modal"><span>&times;</span></button> <h4 class="modal-title">Export Citation <b class="text-primary"></b></h4> </div> <div class="modal-body"> <div class="my-3 px-4 f16"> <form action="https://www.peeref.com/works/citation/download" 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