Publications by authors named "Marc Wagner"

Background: Infection of astrocytes by Human Immunodeficiency Virus (HIV-1) remains a topic of debate, with conflicting data, yet instances of astrocytes containing viral DNA have been observed . In this study, we aimed to elucidate potential routes through which astrocytes could be infected and their ability to produce infectious particles using primary human astrocytes.

Methods: We infected primary astrocytes derived from either neuroprogenitor cells (NPCs) or induced pluripotent stem cells (iPSCs) that express both C-X-C chemokine receptor type 4 (CXCR4) and the C-C chemokine receptor type 5 (CCR5) coreceptors, using either cell-free HIV-1 virus directly or cell-associated virus indirectly through infected macrophages and microglia.

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The development of 3D-organoid models has revolutionized the way diseases are studied. Recently, our brain organoid model has been shown to recapitulate in in vitro the human brain cytoarchitecture originally encountered in HIV-1 neuropathogenesis, allowing downstream applications. Infected monocytes, macrophages, and microglia are critically important immune cells for infection and dissemination of HIV-1 throughout brain during acute and chronic phase of the disease.

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We present the first determination of the energy dependence of the B-D[over ¯] and B^{*}-D[over ¯] isospin-0, S-wave scattering amplitudes both below and above the thresholds using lattice QCD, which allows us to investigate rigorously whether mixed bottom-charm b[over ¯]c[over ¯]ud tetraquarks exist as bound states or resonances. The scattering phase shifts are obtained using Lüscher's method from the energy spectra in two different volumes. To ensure that no relevant energy level is missed, we use large, symmetric 7×7 and 8×8 correlation matrices that include, at both source and sink, B^{(*)}-D[over ¯] scattering operators with the lowest three or four possible back-to-back momenta in addition to local b[over ¯]c[over ¯]ud operators.

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Neuroinflammation and synaptodendritic damage represent the pathological hallmarks of HIV-1 associated cognitive disorders (HAND). The post-synaptic protein neurogranin (Nrgn) is significantly reduced in the frontal cortex of postmortem brains from people with HIV (PWH) and it is associated with inflammatory factors released by infected microglia/macrophages. However, the mechanism involved in synaptic loss have yet to be elucidated.

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Neuroinflammation and synaptodendritic damage represent the pathological hallmarks of HIV-1 associated cognitive disorders (HAND). The post-synaptic protein neurogranin (Nrgn) is significantly reduced in the frontal cortex of postmortem brains from people with HIV (PWH) and it is associated with inflammatory factors released by infected microglia/macrophages. However, the mechanism involved in synaptic loss have yet to be elucidated.

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Objectives: This study describes prevention behavior and psychosocial health among people living with HIV (PLHIV) and HIV-negative people during the early wave of the coronavirus disease 2019 (COVID-19) pandemic in the United States. We assessed differences by HIV status and associations between social disruption and psychosocial health.

Design: A cross-sectional telephone/videoconference administered survey of 3411 PLHIV and HIV-negative participants in the Multicenter AIDS Cohort Study/WIHS Combined Cohort Study (MWCCS).

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This case highlights the rare entity, salivary duct carcinoma (SDC), which is difficult to diagnose and manage. It is the first published case of a metastatic, HER2-positive parotid SDC successfully treated by a dual anti-HER2 treatment associated to a chemotherapy.

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HIV-1 associated neurocognitive disorder (HAND) is characterized by neuroinflammation and glial activation that, together with the release of viral proteins, trigger a pathogenic cascade resulting in synaptodendritic damage and neurodegeneration that lead to cognitive impairment. However, the molecular events underlying HIV neuropathogenesis remain elusive, mainly due to lack of brain-representative experimental systems to study HIV-CNS pathology. To fill this gap, we developed a three-dimensional (3D) human brain organoid (hBORG) model containing major cell types important for HIV-1 neuropathogenesis; neurons and astrocytes along with incorporation of HIV-infected microglia.

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DNA methylation is involved in many different biological processes in the development and well-being of crop plants such as transposon activation, heterosis, environment-dependent transcriptome plasticity, aging, and many diseases. Whole-genome bisulfite sequencing is an excellent technology for detecting and quantifying DNA methylation patterns in a wide variety of species, but optimized data analysis pipelines exist only for a small number of species and are missing for many important crop plants. This is especially important as most existing benchmark studies have been performed on mammals with hardly any repetitive elements and without CHG and CHH methylation.

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Background: Paraneoplastic limbic encephalitis (PLE) is a rare autoimmune neurological syndrome observed in cancer patients. PLE is difficult to diagnose and presents a variable response to treatment, depending on the characteristics of the tumor and neuronal autoantibodies.

Case Presentation: A 64-year-old, Caucasian, non-smoker man presented with a rapidly developing cognitive impairment, personality change, spatial disorientation, and short-term memory loss associated with anorexia and cervical and inguinal lymph nodes.

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Article Synopsis
  • HAND is a common neurocognitive disorder in HIV-1-infected individuals, linked to synaptic damage, with neurogranin (Ng) playing an unclear role in this context.* -
  • The study found that Ng levels were significantly lower in the frontal cortex of HAND-positive patients compared to uninfected individuals, and while calmodulin (CaM) levels remained unchanged, the interaction between Ng and CaM was diminished.* -
  • This reduced interaction was associated with lower levels of CaMKII and synaptic markers, suggesting that inflammatory factors like interleukin-1β and interleukin-8 may play a role in the loss of Ng during HIV-1 infection.*
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High glucose transporter 1 (Glut1) surface expression is associated with increased glycolytic activity in activated CD4+ T cells. Phosphatidylinositide 3-kinases (PI3K) activation measured by p-Akt and OX40 is elevated in CD4+Glut1+ T cells from HIV+ subjects. TCR engagement of CD4+Glut1+ T cells from HIV+ subjects demonstrates hyperresponsive PI3K-mammalian target of rapamycin signaling.

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Extracellular adenosine triphosphate (eATP) is a potent molecule that has the capacity to modulate various aspects of cell functions including gene expression. This element of modulation is essential to the role of ATP as a therapeutic agent. The hypothesis presented is that ATP can have an important impact on the treatment of HIV infection.

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HIV-1 Vpr has been shown to transactivate LTR-directed expression through its interaction with several proteins of cellular origin including the glucocorticoid receptor (GR). Upon activation, steroid receptors bind to proteins containing the signature motif LxxLL, translocate into the nucleus, bind to their response element, and activate transcription. The presence of such motifs in HIV-1 Vpr has prompted us to undertake the analysis of the role of specific leucine residue(s) involved in Vpr-GR interaction, subcellular localization and its effect on Vpr-GR-mediated transactivation.

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HIV-1 Vpr is a protein with multiple functions. It has been suggested that such pleiotropic effects by a viral protein may be mediated by its association with viral and cellular proteins or through modulation of expression of specific cellular genes. To address this, we used cDNA microarray techniques to analyze the regulation of a panel of host cellular genes by HIV-1 Vpr using isogenic HIV-1 either with or without Vpr expression.

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