Host Cell & Pathogen Interactions
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Activation of Innate Immunity Is Required for Efficient Nuclear Reprogramming

Retroviral overexpression of reprogramming factors (Oct4, Sox2, Klf4, c-Myc) generates induced pluripotent stem cells (iPSCs). However, the integration of foreign DNA could induce genomic dysregulation. Cell-permeant proteins (CPPs) could overcome this limitation. To date, this approach has proved exceedingly inefficient. We discovered a striking difference in the pattern of gene expression induced by viral versus CPP-based delivery of the reprogramming factors, suggesting that a signaling pathway required for efficient nuclear reprogramming was activated by the retroviral, but not CPP approach. In gain- and loss-of-function studies, we find that the toll-like receptor 3 (TLR3) pathway enables efficient induction of pluripotency by viral or mmRNA approaches. Stimulation of TLR3 causes rapid and global changes in the expression of epigenetic modifiers to enhance chromatin remodeling and nuclear reprogramming. Activation of inflammatory pathways are required for efficient nuclear reprogramming in the induction of pluripotency.

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Host Cell & Pathogen Interactions
Strategies of Microbial Virulence and Host Defense
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Programmed Cell Death and Inflammation: Winter Is Coming

Programmed Cell Death and Inflammation: Winter Is Coming | Host Cell & Pathogen Interactions | Scoop.it
The life of an organism requires the assistance of an unlikely process: programmed
cell death. Both development and the maintenance of homeostasis result in the production
of superfluous cells that must eventually be disposed of. Furthermore, programmed
cell death can also represent a defense mechanism; for example, by depriving pathogens
of a replication niche. The responsibility of handling these dead cells falls on phagocytes
of the immune system, which surveil their surroundings for dying or dead cells and
efficiently clear them in a quiescent manner.

Via Gilbert C FAURE
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Host and viral traits predict zoonotic spillover from mammals

The majority of human emerging infectious diseases are zoonotic, with viruses that originate in wild mammals of particular concern (for example, HIV, Ebola and SARS). Understanding patterns of viral diversity in wildlife and determinants of successful cross-species transmission, or spillover, are therefore key goals for pandemic surveillance programs. However, few analytical tools exist to identify which host species are likely to harbour the next human virus, or which viruses can cross species boundaries. Here we conduct a comprehensive analysis of mammalian host–virus relationships and show that both the total number of viruses that infect a given species and the proportion likely to be zoonotic are predictable. After controlling for research effort, the proportion of zoonotic viruses per species is predicted by phylogenetic relatedness to humans, host taxonomy and human population within a species range—which may reflect human–wildlife contact. We demonstrate that bats harbour a significantly higher proportion of zoonotic viruses than all other mammalian orders. We also identify the taxa and geographic regions with the largest estimated number of ‘missing viruses’ and ‘missing zoonoses’ and therefore of highest value for future surveillance. We then show that phylogenetic host breadth and other viral traits are significant predictors of zoonotic potential, providing a novel framework to assess if a newly discovered mammalian virus could infect people.

Via Ed Rybicki, Chris Upton + helpers
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ComplexInsight's curator insight, July 7, 5:19 AM
Understanding zoonotic potential will be key to health planning and epidemic prevention in the 21st century.  This paper has key insights such as major hosts (bats) and key geographic zones for observation. If you are involved in health planning or disease modeling - very worthwhile reading.
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Gut bacterial peptides with autoimmunity potential as environmental trigger for late onset complex diseases: In–silico study

Gut bacterial peptides with autoimmunity potential as environmental trigger for late onset complex diseases: In–silico study | Host Cell & Pathogen Interactions | Scoop.it
Recent evidences suggest that human gut microbiota with major component as bacteria can induce immunity. It is also known that gut lining depletes with ageing and that there is increased risk of autoimmune and inflammatory disorders with ageing. It is therefore likely that both may be correlated as depletion of gut lining exposes the gut bacterial antigens to host immune mechanisms, which may induce immunity to certain bacterial proteins, but at the same time such immunity may also be auto-immunogenic to host. This autoimmunity may make a protein molecule nonfunctional and thereby may be involved in late onset metabolic, autoimmune and inflammatory disorders such as, Diabetes, Rheumatoid Arthritis, Hyperlipidemias and Cancer. In this in-silico study we found a large number of peptides identical between human and gut bacteria which were binding to HLA-II alleles, and hence, likely to be auto-immunogenic. Further we observed that such autoimmune candidates were enriched in bacterial species belonging to Firmicutes and Proteobacteria phyla, which lead us to conclude that these phyla may have higher disease impact in genetically predisposed individuals. Functional annotation of human proteins homologous to candidate gut-bacterial peptides showed significant enrichment in metabolic processes and pathways. Cognitive trait, Ageing, Alzheimer, Type 2 diabetes, Chronic Kidney Failure (CKF), Chronic Obstructive Pulmonary Disease (COPD) and various Cancers were the major diseases represented in the dataset. This dataset provides us with gut bacterial autoimmune candidates which can be studied for their clinical significance in late onset diseases.

Via Krishan Maggon , Gilbert C FAURE
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Frontiers | Complement System Part I – Molecular Mechanisms of Activation and Regulation | Immunology

Complement is a complex innate immune surveillance system, playing a key role in defense against pathogens and in host homeostasis. The complement system is initiated by conformational changes in recognition molecular complexes upon sensing danger signals. The subsequent cascade of enzymatic reactions is tightly regulated to assure that complement is activated only at specific locations requiring defense against pathogens, thus avoiding host tissue damage. Here we discuss the recent advances describing the molecular and structural basis of activation and regulation of the complement pathways and their implication on physiology and pathology. This article will review the mechanisms of activation of alternative, classical and lectin pathways, the formation of C3 and C5 convertases, the action of anaphylatoxins and the membrane attack complex. We will also discuss the importance of structure-function relationships using the example of atypical hemolytic uremic syndrome. Lastly we will discuss the development and benefits of therapies using complement inhibitors.

Via Gilbert C FAURE
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Research on male animals prevents women from getting best drugs

Research on male animals prevents women from getting best drugs | Host Cell & Pathogen Interactions | Scoop.it
Male and female mice differ in many ways – a finding that suggests women could be missing out on the best medical treatments, as most are tested on male animals
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A systemic macrophage response is required to contain a peripheral poxvirus infection

A systemic macrophage response is required to contain a peripheral poxvirus infection | Host Cell & Pathogen Interactions | Scoop.it
Author summary Prior to the eradication of variola virus, the orthopoxvirus that causes smallpox, one-third of infected people succumbed to the disease. Despite many complications, smallpox vaccination using vaccinia virus enabled a successful eradication of the disease. Following smallpox eradication, vaccinia (the smallpox vaccine) remains a widely used vaccine vector, so any information about the immune response to the vector can help engineer safer vaccines, or treatment, following complications of immunization. During natural infection, orthopoxviruses spread from a peripheral site of infection to become systemic. This study elucidates the early requirement of innate immune cells to control spread of the smallpox vaccine vector after a peripheral infection. We report that systemic populations of cells, rather than those recruited to the site of infection, are responsible for preventing virus dissemination. The viral control mediated by these cell subsets presents a potential target for therapies and rational vaccine design.

Via Chris Upton + helpers
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Cytokine release syndrome (CRS) and neurotoxicity (NT) after CD19-specific chimeric antigen receptor- (CAR-) modified T cells. | 2017 ASCO Annual Meeting Abstracts

Cytokine release syndrome (CRS) and neurotoxicity (NT) after CD19-specific chimeric antigen receptor- (CAR-) modified T cells. | 2017 ASCO Annual Meeting Abstracts | Host Cell & Pathogen Interactions | Scoop.it
3020 Cytokine release syndrome (CRS) and neurotoxicity (NT) after CD19-specific chimeric antigen receptor- (CAR-) modified T cells. Cameron John Turtle, Kevin Anthony Hay, Juliane Gust, Laila-Aicha Hanafi, Daniel Li, W. Conrad Liles, Mark Wurfel, Susanna Harju-Baker, David Myerson, Luis Gonzalez-Cuyar, Cecilia CS Yeung, Stanley R. Riddell, David G. Maloney; Fred Hutchinson Cancer Research Center, Seattle, WA; Seattle Children's Hospital, Seattle, WA; Juno Therapeutics, Inc., Seattle, WA; University of Washington, Seattle, WA

Via Krishan Maggon , Gilbert C FAURE
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Immunology and Cell Biology - Chromosome choice for initiation of V-(D)-J recombination is not governed by genomic imprinting

Immunology and Cell Biology - Chromosome choice for initiation of V-(D)-J recombination is not governed by genomic imprinting | Host Cell & Pathogen Interactions | Scoop.it
Immunology and Cell Biology focuses on the general functioning of the immune system in its broadest sense, with a particular emphasis on its cell biology. Areas that are covered include but are not limited to: Cellular immunology, Innate and adaptive immunity, Immune responses to pathogens,Tumour immunology,Immunopathology, Immunotherapy, Immunogenetics, Immunological studies in humans and model organisms (including mouse, rat, Drosophila etc)

Via Gilbert C FAURE
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Cutting Edge: A Dual TLR2 and TLR7 Ligand Induces Highly Potent Humoral and Cell-Mediated Immune Responses

Cutting Edge: A Dual TLR2 and TLR7 Ligand Induces Highly Potent Humoral and Cell-Mediated Immune Responses | Host Cell & Pathogen Interactions | Scoop.it
TLR agonists are currently being developed and tested as adjuvants in various formulations to optimize the immunogenicity and efficacy of vaccines. The aim of this study was to evaluate the immunostimulatory properties of a novel compound incorporating covalently linked moieties designed to stimulate both TLR2 and TLR7. This dual TLR2/TLR7 agonist induced the maturation of dendritic cells and primed substantial populations of cytolytic and highly polyfunctional effector CD8+ T cells in vitro, and safely potentiated the immunogenic properties of a nanoparticulate Ag in vivo, eliciting humoral responses with a balanced TH1/TH2 profile in mice. Collectively, these data reveal the potential utility of chimeric adjuvants with synergistic activities mediated via TLRs.

Via Gilbert C FAURE
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IL-6 Signaling Regulates Small Intestinal Crypt Homeostasis

IL-6 Signaling Regulates Small Intestinal Crypt Homeostasis | Host Cell & Pathogen Interactions | Scoop.it
Gut homeostasis is a tightly regulated process requiring finely tuned complex interactions between different cell types, growth factors, or cytokines and their receptors. Previous work has implicated a role for IL-6 and mucosal immune cells in intestinal regeneration following injury and in promoting inflammation and cancer. We hypothesized that IL-6 signaling could also modulate crypt homeostasis. Using mouse in vitro crypt organoid and in vivo models, this study first demonstrated that exogenous IL-6 promoted crypt organoid proliferation and increased stem cell numbers through pSTAT3 activation in Paneth cells. Immunolabeling studies showed that the IL-6 receptor was restricted to the basal membrane of Paneth cells both in vitro and in vivo and that the crypt epithelium also expressed IL-6. Either a blocking Ab to the IL-6 receptor or a neutralizing Ab to IL-6 significantly reduced in vitro basal crypt organoid proliferation and budding, and in vivo significantly reduced the number of nuclei and the number of Lgr5EGFP-positive stem cells per crypt compared with IgG-treated mice, with the number of Paneth cells per crypt also significantly reduced. Functional studies demonstrated that IL-6–induced in vitro crypt organoid proliferation and crypt budding was abrogated by the Wnt inhibitor IWP2. This work demonstrates that autocrine IL-6 signaling in the gut epithelium regulates crypt homeostasis through the Paneth cells and the Wnt signaling pathway.

Via Gilbert C FAURE
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Certain Immune Reactions to Viruses Cause Learning Problems

Certain Immune Reactions to Viruses Cause Learning Problems | Host Cell & Pathogen Interactions | Scoop.it
Neuroscience News has recent neuroscience research articles, brain research news, neurology studies and neuroscience resources for neuroscientists, students, and science fans and is always free to join. Our neuroscience social network has science groups, discussion forums, free books, resources, science videos and more.

Via Bwana Moses
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Host–Pathogen Interactions in Measles Virus Replication and Anti-Viral Immunity

Host–Pathogen Interactions in Measles Virus Replication and Anti-Viral Immunity | Host Cell & Pathogen Interactions | Scoop.it
The measles virus (MeV) is a contagious pathogenic RNA virus of the family Paramyxoviridae, genus Morbillivirus, that can cause serious symptoms and even fetal complications. Here, we summarize current molecular advances in MeV research, and emphasize the connection between host cells and MeV replication. Although measles has reemerged recently, the potential for its eradication is promising with significant progress in our understanding of the molecular mechanisms of its replication and host-pathogen interactions.

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Naked mole-rats turn into plants when oxygen is low

Naked mole-rats turn into plants when oxygen is low | Host Cell & Pathogen Interactions | Scoop.it

Deprived of oxygen, naked mole-rats can survive by metabolizing fructose just as plants do, researchers report this week in the journal Science -- a finding that could lead to treatments for heart attacks and strokes.

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Respiratory syncytial virus–Host interaction in the pathogenesis of bronchiolitis and its impact on respiratory morbidity in later life

Respiratory syncytial virus–Host interaction in the pathogenesis of bronchiolitis and its impact on respiratory morbidity in later life | Host Cell & Pathogen Interactions | Scoop.it
Respiratory syncytial virus (RSV) is the most common agent of severe airway disease in infants and young children. Large epidemiologic studies have demonstrated a clear relationship between RS

Via Gilbert C FAURE
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Recombinant Influenza Vaccine More Effective Than Standard Inactivated Vaccine

Recombinant Influenza Vaccine More Effective Than Standard Inactivated Vaccine | Host Cell & Pathogen Interactions | Scoop.it
From BioPortfolio: A comparison trial conducted during the 2014–2015 flu season found a difference in efficacy.

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Frontiers | Complement System Part II: Role in Immunity | Immunology

The complement system has been considered for a long time as a simple lytic system, aimed to kill bacteria infecting the host organism. Nowadays this vision has changed and it is well accepted that complement is a complex innate immune surveillance system, playing a key role in host homeostasis, inflammation and in the defense against pathogens. This review discusses recent advances in the understanding of the role of complement in physiology and pathology. It starts with a description of complement contribution to the normal physiology (homeostasis) of a healthy organism, including the silent clearance of apoptotic cells and maintenance of cell survival. In pathology, complement can be a friend or a foe. It acts as a friend in the defense against pathogens, by inducing a direct killing by C5b-9 membrane attack complex by triggering inflammatory responses with the anaphylatoxins C3a and C5a and helps the mounting of an adaptive immune response, involving antigen presenting cells, T- and B- lymphocytes. But it can be also an enemy, when pathogens hijack complement regulators to protect themselves from the immune system. Also examples will be discussed, where inadequate complement activation becomes a disease cause, including atypical hemolytic uremic syndrome (aHUS), C3 glomerulopathies (C3G) and systemic lupus erythematosus (SLE). Age related macular degeneration (AMD) and cancer will be described as examples showing that complement contributes to a large variety of diseases, far exceeding the classical examples of diseases associated with complement deficiencies. Finally, we discuss complement as a therapeutic target.

Via Gilbert C FAURE
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Ribosomal DNA Copy Numbers Decrease in Some Cancers

Ribosomal DNA Copy Numbers Decrease in Some Cancers | Host Cell & Pathogen Interactions | Scoop.it

An analysis of human cancer genome projects uncovers a counterintuitive loss of ribosomal gene copies.


Via Integrated DNA Technologies
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Modified viruses deliver death to antibiotic-resistant bacteria

Modified viruses deliver death to antibiotic-resistant bacteria | Host Cell & Pathogen Interactions | Scoop.it
Engineered microbes turn a bacterium's immune response against itself using CRISPR.
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The Types Of Cancer You Can Get From HPV

The Types Of Cancer You Can Get From HPV | Host Cell & Pathogen Interactions | Scoop.it
New study suggests HPV-related genital infection can cause cervical, anal, vulvar, and vaginal cancers.
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Brisbane researchers discover native Australian plant can kill Zika virus

Brisbane researchers discover native Australian plant can kill Zika virus | Host Cell & Pathogen Interactions | Scoop.it
QUT News article
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BACH transcription factors in innate and adaptive immunity

BTB and CNC homology (BACH) proteins are transcriptional repressors of the basic region leucine zipper (bZIP) transcription factor family. Recent studies indicate widespread roles of BACH proteins in controlling the development and function of the innate and adaptive immune systems, including the differentiation of effector and memory cells of the B and T cell lineages, CD4+ regulatory T cells and macrophages. Here, we emphasize similarities at a molecular level in the cell-type-specific activities of BACH factors, proposing that competitive interactions of BACH proteins with transcriptional activators of the bZIP family form a common mechanistic theme underlying their diverse actions. The findings contribute to a general understanding of how transcriptional repressors shape lineage commitment and cell-type-specific functions through repression of alternative lineage programmes.

Via Gilbert C FAURE
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Multi-receptor detection of individual bacterial products by the innate immune system : Nature Reviews Immunology : Nature Research


Via Gilbert C FAURE
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Treating Flu with Skin of Frog

Treating Flu with Skin of Frog | Host Cell & Pathogen Interactions | Scoop.it
Glands in frog skin secrete substances that possess broad antimicrobial function.
Holthausen et al. mined this soup of natural products and discovered a peptide that
destroys diverse human influenza strains (Holthausen et al., 2017). This study points
the way to the discovery of novel anti-influenza molecules targeting conserved elements
on influenza surface proteins.

Via Gilbert C FAURE
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Gilbert C FAURE's curator insight, May 15, 11:20 AM
Witches knew it!
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Interplay between the Hepatitis B Virus and Innate Immunity: From an Understanding to the Development of Therapeutic Concepts

Interplay between the Hepatitis B Virus and Innate Immunity: From an Understanding to the Development of Therapeutic Concepts | Host Cell & Pathogen Interactions | Scoop.it
The hepatitis B virus (HBV) infects hepatocytes, which are the main cell type composing a human liver. However, the liver is enriched with immune cells, particularly innate cells (e.g., myeloid cells, natural killer and natural killer T-cells (NK/NKT), dendritic cells (DCs)), in resting condition. Hence, the study of the interaction between HBV and innate immune cells is instrumental to: (1) better understand the conditions of establishment and maintenance of HBV infections in this secondary lymphoid organ; (2) define the role of these innate immune cells in treatment failure and pathogenesis; and (3) design novel immune-therapeutic concepts based on the activation/restoration of innate cell functions and/or innate effectors. This review will summarize and discuss the current knowledge we have on this interplay between HBV and liver innate immunity.

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PositiveLite.com - The capsid inhibitor—a new class to enter clinical trials

PositiveLite.com- Canada's Online HIV Magazine

Via Bwana Moses
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