Publications by authors named "Chloe Borde"

Epstein-Barr virus (EBV) is a highly prevalent human herpesvirus that persists for life in more than 95% of the adult population. EBV usually establishes an asymptomatic life-long infection, but it is also associated with malignancies affecting B lymphocytes and epithelial cells mainly. The virus alternates between a latent phase and a lytic phase, both of which contribute to the initiation of the tumor process.

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Energy metabolism reprogramming was recently listed as a hallmark of cancer. In this process, the switch from pyruvate kinase isoenzyme type M1 to pyruvate kinase isoenzyme type M2 (PKM2) is believed to play a crucial role. Interestingly, the activity of the active form of PKM2 can efficiently be inhibited by the high-mobility group box 1 (HMGB1) protein, leading to a rapid blockage of glucose-dependent aerobic respiration and cancer cell death.

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Epstein-Barr virus DNA viral load is used as a surrogate marker to start Rituximab in transplant recipients at risk of developing PTLD. However, an elevated EBV DNAemia does not discriminate lymphoproliferation and replication. We designed a new molecular assay (methyl-qPCR) to distinguish methylated versus unmethylated viral genomes.

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The purine nucleotide adenosine triphosphate (ATP) is known for its fundamental role in cellular bioenergetics. However, in the last decades, different works have described emerging functions for ATP, such as that of a danger signaling molecule acting in the extracellular space on both tumor and stromal compartments. Beside its role in immune cell signaling, several studies have shown that high concentrations of extracellular ATP can directly or indirectly act on cancer cells.

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Microbial natural products are continuing to be a promising platform for future drug lead discover. As a part of our ongoing research program on fungal natural product, herein we report metabolites isolated from the fungus SN15 a pathogen of wheat and related cereals. Its chemical investigation led to the purification of new isoleucinic acid derivatives (-) along with the procuramine ().

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Despite early antiretroviral therapy (ART), treatment interruption is associated with viral rebound, indicating early viral reservoir (VR) seeding and absence of full eradication of human immunodeficiency virus type 1 (HIV-1) that may persist in tissues. Herein, we address the contributing role of monocytes in maintaining VRs under ART, since these cells may represent a source of viral dissemination due to their ability to replenish mucosal tissues in response to injury. To this aim, monocytes with classical (CD14), intermediate (CD14 CD16), and nonclassical (CD16) phenotypes and CD4 T cells were sorted from the blood, spleen, and intestines of untreated and early-ART-treated simian immunodeficiency virus (SIV)-infected rhesus macaques (RMs) before and after ART interruption.

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Autophagy is an essential catabolic process that degrades cytoplasmic components within the lysosome, therefore ensuring cell survival and homeostasis. A growing number of viruses, including members of the Herpesviridae family, have been shown to manipulate autophagy to facilitate their persistence or optimize their replication. Previous works showed that the Epstein-Barr virus (EBV), a human transforming gammaherpesvirus, hijacked autophagy during the lytic phase of its cycle, possibly to favor the formation of viral particles.

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Article Synopsis
  • - High-mobility group box 1 (HMGB1) levels in serum are linked to inflammation and have been proposed as a biomarker for various pathologies.
  • - In a previous study, low levels of autoantibodies against HMGB1 were found to be associated with better survival rates in sepsis patients.
  • - This study examined two sepsis survivors who had high levels of specific HMGB1 antibodies, supporting the idea that these protective antibodies can be produced in response to septic shock.
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Article Synopsis
  • Epstein-Barr virus (EBV) is linked to various cancers, particularly those from lymphoid tissues, and its oncogenic effects are attributed to viral genes active during its latent phase.
  • Research indicates that antiviral treatments targeting the lytic phase of EBV may help prevent cancers like EBV-positive Post-Transplant Lymphoproliferative Diseases.
  • Dipyridamole (DIP), a safe and widely used medication, effectively inhibits EBV reactivation in B-cell lines and could be repurposed, potentially in combination with other antivirals, to treat EBV-related conditions.
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Article Synopsis
  • BALF0/1 is a protein linked to the Epstein-Barr virus (EBV) that affects cell death, but detecting it in infected cells has been challenging due to a lack of specific testing tools.
  • Researchers successfully expressed and purified a shorter version of this protein (tBALF0) in bacteria and used it in an ELISA test to identify antibodies in EBV-infected individuals.
  • The study found low levels of antibodies in patients with recent or past infections but higher levels in one-third of patients with nasopharyngeal carcinoma, indicating a potential link between BALF0/1 and cancer development.
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Follicular T helper (Tfh) cells, a subset of CD4 T lymphocytes, are essential for memory B cell activation, survival, and differentiation and assist B cells in the production of antigen-specific antibodies. Work performed in recent years pointed out the importance of Tfh cells in the context of HIV and SIV infections. The importance of tissue distribution of Tfh is also an important point since their frequency differs between peripheral blood and lymph nodes compared to the spleen, the primary organ for B cell activation, and differentiation.

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A critical role for intracellular TLR9 has been described in recognition and host resistance to Leishmania parasites. As TLR9 requires endolysosomal proteolytic cleavage to achieve signaling functionality, we investigated the contribution of different proteases like asparagine endopeptidase (AEP) or cysteine protease cathepsins B (CatB), L (CatL) and S (CatS) to host resistance during Leishmania major (L. major) infection in C57BL/6 (WT) mice and whether they would impact on TLR9 signaling.

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DNA sequences purified from distinct organisms, e.g. non vertebrate versus vertebrate ones, were shown to differ in their TLR9 signalling properties especially when either mouse bone marrow-derived- or human dendritic cells (DCs) are probed as target cells.

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Highly active antiretroviral therapy is associated with carbohydrate metabolic alterations that may lead to diabetes. One consequence of hyperglycemia is the formation of advanced glycation end products (AGEs) that are involved in diabetes complications. We investigated the impact of AGEs on the infection of monocyte-derived dendritic cells (MDDCs) by HIV-1 and the ability of MDDCs to transmit the virus to T cells.

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Objective: HMGB1 concentration is currently regarded as an important biological marker in many inflammation-related conditions. Although ELISA has been proposed as a convenient way to quantify HMGB1 in biological fluids, various molecules have been shown to complex with HMGB1 and may interfere with HMGB1 detection by this technique. We describe here a simple technical improvement that dissociates HMGB1 containing complexes and therefore increases ELISA sensitivity.

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Purpose: To assess the prevalence and predictive value of natural autoantibodies to high-mobility group box 1 (HMGB1) during sepsis.

Methods: Anti-HMGB1 and anti-human serum albumin (HSA) autoantibodies were detected by ELISA in 178 plasma samples longitudinally collected from 40 critically ill patients with septic shock. One hundred thirty-two plasma samples from healthy donors were used as control.

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Background: High mobility group box 1 protein (HMGB1) is a major endogenous danger signal that triggers inflammation and immunity during septic and aseptic stresses. HMGB1 recently emerged as a key soluble factor in the pathogenesis of various infectious diseases, but nothing is known of its behaviour during herpesvirus infection. We therefore investigated the dynamics and biological effects of HMGB1 during HSV-2 infection of epithelial HEC-1 cells.

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HMGB1 (High Mobility group box 1) protein was originally identified as a DNA-binding protein that functions as a structural co-factor. Recent works demonstrated that HMGB1 can be released outside the cell, upon immune activation or primary cell necrosis. In the extracellular space, HMGB1 acts as a potent soluble factor that coordinates cellular events that are crucial for the amplification of inflammation, establishment of early immune responses and tissue repair.

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The existence of infectious agents smaller than bacteria was demonstrated already near the close of the 19th century by Martinus Beijerinck. After this discovery it took more than 60 years before a resilient definition of viruses could be given and an introduction to modern virology was established. Indeed, the major challenge was to conceive living submicrospic agents exclusively defined in opposition to the bacteriological criteria (non-observable, non-cultivable,).

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Background: Protein HMGB1, an abundant nuclear non-histone protein that interacts with DNA and has an architectural function in chromatin, was strikingly shown some years ago to also possess an extracellular function as an alarmin and a mediator of inflammation. This extracellular function has since been actively studied, both from a fundamental point of view and in relation to the involvement of HMGB1 in inflammatory diseases. A prerequisite for such studies is the ability to detect HMGB1 in blood or other biological fluids and to accurately measure its concentration.

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