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inflammation

  • Open Access
    TRAF6 and TAK1 Contribute to SAMHD1-Mediated Negative Regulation of NF-κB Signaling
    Virus-Cell Interactions
    TRAF6 and TAK1 Contribute to SAMHD1-Mediated Negative Regulation of NF-κB Signaling

    Cells respond to pathogen infection by activating a complex innate immune signaling pathway, which culminates in the activation of transcription factors and secretion of a family of functionally and genetically related cytokines. However, excessive immune activation may cause tissue damage and detrimental effects on the host.

    Constanza E. Espada, Corine St. Gelais, Serena Bonifati, Victoria V. Maksimova, Michael P. Cahill, Sun Hee Kim, Li Wu
  • Role of Inflammation in Virus Pathogenesis during Pregnancy
    Minireview
    Role of Inflammation in Virus Pathogenesis during Pregnancy

    Viral infections during pregnancy lead to a spectrum of maternal and fetal outcomes, ranging from asymptomatic disease to more critical conditions presenting with severe maternal morbidity, stillbirth, preterm birth, intrauterine growth restriction, and fetal congenital anomalies, either apparent at birth or later in life. In this article, we review the pathogenesis of several viral infections that are particularly relevant in the...

    Anna Chudnovets, Jin Liu, Harish Narasimhan, Yang Liu, Irina Burd
  • Dengue Virus Targets Nrf2 for NS2B3-Mediated Degradation Leading to Enhanced Oxidative Stress and Viral Replication
    Virus-Cell Interactions
    Dengue Virus Targets Nrf2 for NS2B3-Mediated Degradation Leading to Enhanced Oxidative Stress and Viral Replication

    Dengue virus (DENV) is a mosquito-borne pathogen that threatens 2.5 billion people in more than 100 countries annually. Dengue infection induces a spectrum of clinical symptoms, ranging from classical dengue fever to severe dengue hemorrhagic fever or dengue shock syndrome; however, the complexities of DENV immunopathogenesis remain controversial. Previous studies have reported the importance of the transcription factor Nrf2 in the...

    Matteo Ferrari, Alessandra Zevini, Enrico Palermo, Michela Muscolini, Magdalini Alexandridi, Marilena P. Etna, Eliana M. Coccia, Ana Fernandez-Sesma, Carolyn Coyne, Donna D. Zhang, Ernesto T. A. Marques, David Olagnier, John Hiscott
  • Early Antiretroviral Therapy Prevents Viral Infection of Monocytes and Inflammation in Simian Immunodeficiency Virus-Infected Rhesus Macaques
    Pathogenesis and Immunity
    Early Antiretroviral Therapy Prevents Viral Infection of Monocytes and Inflammation in Simian Immunodeficiency Virus-Infected Rhesus Macaques

    Despite the administration of antiretroviral therapy (ART), HIV persists in treated individuals and ART interruption is associated with viral rebound. Persistent chronic immune activation and inflammation contribute to disease morbidity. Whereas monocytes are infected by HIV/SIV, their role as viral reservoirs (VRs) in visceral tissues has been poorly explored. Our work demonstrates that monocyte cell subsets in the blood, spleen, and...

    Henintsoa Rabezanahary, Julien Clain, Gina Racine, Guadalupe Andreani, Ghita Benmadid-Laktout, Chloé Borde, Fabrizio Mammano, Thibault Mesplèdes, Petronela Ancuta, Ouafa Zghidi-Abouzid, Jérôme Estaquier
  • Selective Interferon Responses of Intestinal Epithelial Cells Minimize Tumor Necrosis Factor Alpha Cytotoxicity
    Pathogenesis and Immunity | Spotlight
    Selective Interferon Responses of Intestinal Epithelial Cells Minimize Tumor Necrosis Factor Alpha Cytotoxicity

    Enteric viral infections are a major cause of gastroenteritis worldwide and have the potential to trigger or exacerbate intestinal inflammatory diseases. Prior studies have identified specialized innate immune responses that are active in the intestinal epithelium following viral infection, but our understanding of the benefits of such an epithelium-specific response is incomplete. Here, we show that the intestinal epithelial antiviral...

    Jacob A. Van Winkle, David A. Constant, Lena Li, Timothy J. Nice
  • Open Access
    Neutrophil-Airway Epithelial Interactions Result in Increased Epithelial Damage and Viral Clearance during Respiratory Syncytial Virus Infection
    Cellular Response to Infection
    Neutrophil-Airway Epithelial Interactions Result in Increased Epithelial Damage and Viral Clearance during Respiratory Syncytial Virus Infection

    This study shows that the RSV-infected human airway drives changes in the behavior of human neutrophils, including increasing activation markers and delaying apoptosis, that result in greater airway damage and viral clearance.

    Yu Deng, Jenny A. Herbert, Elisabeth Robinson, Luo Ren, Rosalind L. Smyth, Claire M. Smith
  • Open Access
    IRF5 Promotes Influenza Virus-Induced Inflammatory Responses in Human Induced Pluripotent Stem Cell-Derived Myeloid Cells and Murine Models
    Pathogenesis and Immunity
    IRF5 Promotes Influenza Virus-Induced Inflammatory Responses in Human Induced Pluripotent Stem Cell-Derived Myeloid Cells and Murine Models

    The inflammatory response to influenza A virus (IAV) participates in infection control but contributes to disease severity. After viral detection, intracellular pathways are activated, initiating cytokine production, but these pathways are incompletely understood. We show that interferon regulatory factor 5 (IRF5) mediates IAV-induced inflammation and, in mice, drives pathology. This was independent of antiviral type 1 IFN and virus...

    Jessica L. Forbester, Mathew Clement, Dannielle Wellington, Amy Yeung, Sandra Dimonte, Morgan Marsden, Lucy Chapman, Eve L. Coomber, Charlotte Tolley, Emily Lees, Christine Hale, Simon Clare, Irina Udalova, Tao Dong, Gordon Dougan, Ian R. Humphreys
  • Attenuation of Equine Lentivirus Alters Mitochondrial Protein Expression Profile from Inflammation to Apoptosis
    Cellular Response to Infection
    Attenuation of Equine Lentivirus Alters Mitochondrial Protein Expression Profile from Inflammation to Apoptosis

    Following viral infection, the working pattern and function of the cell can be transformed through the impact on mitochondria. It still unknown how the mitochondrial response changes in cells infected with viruses in the process of virulence attenuation. EIAVDLV121 is the only effective lentiviral vaccine for large-scale use in the world. EIAVDLV34 is the parent pathogenic strain. Unlike EIAVDLV34-...

    Cheng Du, Yingyi Duan, Xue-Feng Wang, Yuezhi Lin, Lei Na, Xinhui Wang, Kewei Chen, Xiaojun Wang
  • Highly Pathogenic Porcine Reproductive and Respiratory Syndrome Virus Induces Interleukin-17 Production via Activation of the IRAK1-PI3K-p38MAPK-C/EBPβ/CREB Pathways
    Pathogenesis and Immunity
    Highly Pathogenic Porcine Reproductive and Respiratory Syndrome Virus Induces Interleukin-17 Production via Activation of the IRAK1-PI3K-p38MAPK-C/EBPβ/CREB Pathways

    Highly pathogenic porcine reproductive and respiratory syndrome virus (HP-PRRSV) associated with severe pneumonia has been one of the most important viral pathogens in pigs. IL-17 is a proinflammatory cytokine that might be associated with the strong inflammation caused by PRRSV. Therefore, we sought to determine whether PRRSV infection affects IL-17 expression, and if so, determine this might partially explain the underlying mechanisms...

    Honglei Wang, Li Du, Fang Liu, Zeyu Wei, Li Gao, Wen-hai Feng
  • Crimean-Congo Hemorrhagic Fever Mouse Model Recapitulating Human Convalescence
    Pathogenesis and Immunity
    Crimean-Congo Hemorrhagic Fever Mouse Model Recapitulating Human Convalescence

    The role of antibody or virus-specific T-cell responses in control of acute Crimean-Congo hemorrhagic fever virus infection is largely unclear. This is a critical gap in our understanding of CCHF, and investigation of convalescence following severe acute CCHF has been limited by the lack of suitable small animal models. We report here a mouse model of CCHF in which infected mice develop severe disease but ultimately recover. Although...

    David W. Hawman, Kimberly Meade-White, Elaine Haddock, Rumi Habib, Dana Scott, Tina Thomas, Rebecca Rosenke, Heinz Feldmann

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