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The Legionella Effector RavZ Inhibits Host Autophagy Through Irreversible Atg8 Deconjugation

Eukaryotic cells can use the autophagy pathway to defend against microbes that gain access to the cytosol or reside in pathogen-modified vacuoles.

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Host Cell & Pathogen Interactions
Strategies of Microbial Virulence and Host Defense
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HIV Cure Becomes More Elusive as Disease Rejects Key Drug

HIV Cure Becomes More Elusive as Disease Rejects Key Drug | Host Cell & Pathogen Interactions | Scoop.it

The study suggests that in Sub-Saharan Africa, up to 15 percent* of HIV patients treated with tenofovir-based drug combinations will develop tenofovir resistance in the first year of treatment alone, with this figure rising over time.

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Viral pathogenesis: Stressing out over herpes

Viral pathogenesis: Stressing out over herpes | Host Cell & Pathogen Interactions | Scoop.it
Herpes simplex virus establishes latent infection in peripheral neurons, and neuronal stress is known to reactivate virus production, but the molecular mechanisms underlying reactivation are unclear. Cliffe et al. now show that a neuron-specific Jun N-terminal kinase (JNK) stress pathway activates the expression of latent herpes simplex virus.

 

Herpesvirus graphic courtesy of Russell Kightley Media


Via Ed Rybicki
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RNA chaperones encoded by RNA viruses

RNA chaperones encoded by RNA viruses | Host Cell & Pathogen Interactions | Scoop.it

RNAs are functionally diverse macromolecules whose proper functions rely strictly upon their correct tertiary structures. However, because of their high structural flexibility, correct folding of RNAs is challenging and slow. Therefore, cells and viruses encode a variety of RNA remodeling proteins, including helicases and RNA chaperones. In RNA viruses, these proteins are believed to play pivotal roles in all the processes involving viral RNAs during the life cycle. RNA helicases have been studied extensively for decades, whereas RNA chaperones, particularly virus-encoded RNA chaperones, are often overlooked. This review describes the activities of RNA chaperones encoded by RNA viruses, particularly the ones identified and characterized in recent years, and the functions of these proteins in different steps of viral life cycles, and presents an overview of this unique group of proteins.


Via Ed Rybicki
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Ubiquitin in the activation and attenuation of innate antiviral immunity

Viral infection activates danger signals that are transmitted via the retinoic acid–inducible gene 1–like receptor (RLR), nucleotide-binding oligomerization domain-like receptor (NLR), and Toll-like receptor (TLR) protein signaling...


Via Gilbert Faure au nom de l'ASSIM
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Gilbert Faure au nom de l'ASSIM's curator insight, January 14, 4:47 AM

This places host cells in an antiviral posture by up-regulating antiviral cytokines including type-I interferon (IFN-I). Ubiquitin modifications and cross-talk between proteins within these signaling cascades potentiate IFN-I expression, and inversely, a growing number of viruses are found to weaponize the ubiquitin modification system to suppress IFN-I. Here we review how host- and virus-directed ubiquitin modification of proteins in the RLR, NLR, and TLR antiviral signaling cascades modulate IFN-I expression.

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Interaction of the Clostridium difficile Binary Toxin CDT and its Host Cell Receptor LSR

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STAT-5 Regulates Transcription of the Topoisomerase IIβ-Binding Protein 1 (TopBP1) Gene To Activate the ATR Pathway and Promote Human Papillomavirus Replication

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R-Ras Regulates Murine T Cell Migration and Intercellular Adhesion Molecule-1 Binding

R-Ras Regulates Murine T Cell Migration and Intercellular Adhesion Molecule-1 Binding | Host Cell & Pathogen Interactions | Scoop.it

The trafficking of T-lymphocytes to peripheral draining lymph nodes is crucial for mounting an adaptive immune response. The role of chemokines in the activation of integrins via Ras-related small GTPases has been well established.


Via Gilbert Faure au nom de l'ASSIM
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Gilbert Faure au nom de l'ASSIM's curator insight, December 31, 2015 2:40 AM
Abstract

The trafficking of T-lymphocytes to peripheral draining lymph nodes is crucial for mounting an adaptive immune response. The role of chemokines in the activation of integrins via Ras-related small GTPases has been well established. R-Ras is a member of the Ras-subfamily of small guanosine-5’-triphosphate-binding proteins and its role in T cell trafficking has been investigated in R-Ras null mice (Rras−/−). An examination of the lymphoid organs of Rras−/−mice revealed a 40% reduction in the cellularity of the peripheral lymph nodes. Morphologically, the high endothelial venules of Rras−/− mice were more disorganized and less mature than those of wild-type mice. Furthermore, CD4+ and CD8+ T cells from Rras−/− mice had approximately 42% lower surface expression of L-selectin/CD62L. These aberrant peripheral lymph node phenotypes were associated with proliferative and trafficking defects in Rras−/− T cells. Furthermore, R-Ras could be activated by the chemokine, CCL21. Indeed, Rras−/− T cells had approximately 14.5% attenuation in binding to intercellular adhesion molecule 1 upon CCL21 stimulation. Finally, in a graft-versus host disease model, recipient mice that were transfused with Rras−/− T cells showed a significant reduction in disease severity when compared with mice transplanted with wild-type T cells. These findings implicate a role for R-Ras in T cell trafficking in the high endothelial venules during an effective immune response.

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Evaluation of Intracellular Signaling Downstream Chimeric Antigen Receptors

Evaluation of Intracellular Signaling Downstream Chimeric Antigen Receptors | Host Cell & Pathogen Interactions | Scoop.it

CD19-targeting CAR T cells have shown potency in clinical trials targeting B cell leukemia.


Via Gilbert Faure au nom de l'ASSIM
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A Single-Amino-Acid Substitution in Obg Activates a New Programmed Cell Death Pathway in Escherichia coli

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DNA research offers clues on cell mutation

DNA research offers clues on cell mutation | Host Cell & Pathogen Interactions | Scoop.it

A team of researchers from Colorado State University has been studying DNA damage in living cells to learn more about how genetic abnormalities arise. It has long been known that DNA molecules in every cell get constantly damaged by things from the outside environment, like sunlight, cigarette smoke and radiation. However, more recently researchers have discovered that sources from within the cell itself can sometimes be even more damaging.


Via Integrated DNA Technologies
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Cell Division Enzyme Found to Play Critical Role in Inflammatory Process | GEN News Highlights | GEN

Cell Division Enzyme Found to Play Critical Role in Inflammatory Process | GEN News Highlights | GEN | Host Cell & Pathogen Interactions | Scoop.it
Scientists find that critical mitotic NEK7 enzyme also acts as an on-off switch in the innate immune system.
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Bat immune receptors are one of a kind

In bats, Toll-like receptors, the first-line defense mechanism against invading pathogens, are different from other mammals.

Via Gilbert Faure au nom de l'ASSIM
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Gilbert Faure au nom de l'ASSIM's curator insight, November 27, 2015 5:35 AM

"The changes found in the bat TLRs could reflect the reservoir status described for some bat species carrying specific pathogens," explains Alex Greenwood, head of the Department of Wildlife Diseases at the IZW. Despite the wide acceptance of bats as reservoirs for different pathogens, the genetic variability of the bat immune system underlying such observation has been little investigated. The recent study reveals insights which show that this variability exists and in which direction the genetic basis of parts of the bat immune system deviates from those of other mammals.

 

Marina Escalera-Zamudio, M. Lisandra Zepeda-Mendoza, Elizabeth Loza-Rubio, Edith Rojas-Anaya, Maria L. Méndez-Ojeda, Carlos F. Arias, Alex D. Greenwood. The evolution of bat nucleic acid-sensing Toll-like receptors. Molecular Ecology, 2015; 24 (23): 5899 DOI:10.1111/mec.13431
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Three-dimensional reconstruction. : A mechanism of viral immune evasion revealed by cryo-EM analysis of the TAP transporter : Nature : Nature Publishing Group

Three-dimensional reconstruction. : A mechanism of viral immune evasion revealed by cryo-EM analysis of the TAP transporter : Nature : Nature Publishing Group | Host Cell & Pathogen Interactions | Scoop.it

Cellular immunity against viral infection and tumour cells depends on antigen presentation by major histocompatibility complex class I (MHC I) molecules.


Via Gilbert Faure au nom de l'ASSIM
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Gilbert Faure au nom de l'ASSIM's curator insight, January 21, 5:12 AM

Cellular immunity against viral infection and tumour cells depends on antigen presentation by major histocompatibility complex class I (MHC I) molecules. Intracellular antigenic peptides are transported into the endoplasmic reticulum by the transporter associated with antigen processing (TAP) and then loaded onto the nascent MHC I molecules, which are exported to the cell surface and present peptides to the immune system1. Cytotoxic T lymphocytes recognize non-self peptides and program the infected or malignant cells for apoptosis. Defects in TAP account for immunodeficiency and tumour development. To escape immune surveillance, some viruses have evolved strategies either to downregulate TAP expression or directly inhibit TAP activity. So far, neither the architecture of TAP nor the mechanism of viral inhibition has been elucidated at the structural level. Here we describe the cryo-electron microscopy structure of human TAP in complex with its inhibitor ICP47, a small protein produced by the herpes simplex virus I. Here we show that the 12 transmembrane helices and 2 cytosolic nucleotide-binding domains of the transporter adopt an inward-facing conformation with the two nucleotide-binding domains separated. The viral inhibitor ICP47 forms a long helical hairpin, which plugs the translocation pathway of TAP from the cytoplasmic side. Association of ICP47 precludes substrate binding and prevents nucleotide-binding domain closure necessary for ATP hydrolysis. This work illustrates a striking example of immune evasion by persistent viruses. By blocking viral antigens from entering the endoplasmic reticulum, herpes simplex virus is hidden from cytotoxic T lymphocytes, which may contribute to establishing a lifelong infection in the host.

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Structural Insights into Polymorphic ABO Glycan Binding by Helicobacter pylori: Cell Host & Microbe

Structural Insights into Polymorphic ABO Glycan Binding by Helicobacter pylori: Cell Host & Microbe | Host Cell & Pathogen Interactions | Scoop.it
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New Test Can Evaluate MRSA Superbug DNA In Just Three-Minutes, Pinpoint Best Antibiotic Option

New Test Can Evaluate MRSA Superbug DNA In Just Three-Minutes, Pinpoint Best Antibiotic Option | Host Cell & Pathogen Interactions | Scoop.it
A new MRSA test will revolutionize the way that hospitals handle the treatment of superbugs. The test, which takes only three minutes, evaluate's the superbug's
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Body’s bacteria don’t outnumber human cells so much after all

Body’s bacteria don’t outnumber human cells so much after all | Host Cell & Pathogen Interactions | Scoop.it
New calculations show human cells about equal bacteria in the body.

Via Gilbert Faure au nom de l'ASSIM
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Engineered Antibody Neutralizes All Four Dengue Serotypes

Engineered Antibody Neutralizes All Four Dengue Serotypes | Host Cell & Pathogen Interactions | Scoop.it

Researchers have designed an antibody that targets all four serotypes of dengue, sparking hopes for the first viable dengue therapeutic.


Via Gilbert Faure au nom de l'ASSIM
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Rescooped by Kenzibit from Virology and Bioinformatics from Virology.ca
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Using CRISPR to change "A" to "T" and "C" to "G"

Using CRISPR to change "A" to "T" and "C" to "G" | Host Cell & Pathogen Interactions | Scoop.it
Using CRISPR to change "A" to "T" and "C" to "G"
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SLAM family receptors in normal immunity and immune pathologies

SLAM family receptors in normal immunity and immune pathologies | Host Cell & Pathogen Interactions | Scoop.it

Highlights

 

SLAM family receptors, associated with SAP adaptors, play key roles in immunity.

SLAM receptors can be either activating or inhibitory, depending on the context.

The SLAM family has been implicated in a wide range of human diseases.

One SLAM family receptor, SLAMF7, is a drug target in multiple myeloma.

 

The signaling lymphocytic activation molecule (SLAM) family is a group of six receptors restricted to hematopoietic cells. Most of these receptors are self-ligands, and thus are triggered in the context of interactions between hematopoietic cells. By way of their cytoplasmic domain, SLAM-related receptors associate with the SLAM-associated protein (SAP) family of adaptors, which control the signals and functions of SLAM family receptors. Recent findings have provided new insights into the key roles of SLAM family receptors in normal immunity, their involvement in human diseases and their usefulness as drug targets to treat human malignancies. These data are reviewed herein.


Via Krishan Maggon , Gilbert Faure au nom de l'ASSIM
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Krishan Maggon 's curator insight, December 28, 2015 8:15 AM
Current Opinion in Immunology

Volume 38, February 2016, Pages 45–51

Innate immunity

 
 
SLAM family receptors in normal immunity and immune pathologiesNing Wu1, , André Veillette1, 2, 3, 
 
 
doi:10.1016/j.coi.2015.11.003
Gilbert Faure au nom de l'ASSIM's curator insight, December 28, 2015 8:37 AM

SLAM receptors CD150...

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Interleukin-23-Induced Transcription Factor Blimp-1 Promotes Pathogenicity of T Helper 17 Cells: Immunity

Lastest from current issue of @ImmunityCP #STEM #Immunology Interleukin-23-Induced Transcription Factor Blimp-1... https://t.co/7qE5y3awML


Via Gilbert Faure au nom de l'ASSIM
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Gilbert Faure au nom de l'ASSIM's curator insight, December 31, 2015 2:38 AM
Highlights

 

•IL-23-dependent Blimp-1 enhances Th17 pathogenic factors including GM-CSF and IFN-γ•Distal Lck-Cre-mediated Blimp-1 deletion in peripheral T cells ameliorates EAE•Blimp-1 co-localizes with RORγt and STAT-3 at Il23r, Il17a, and Csf2 enhancer sites•Blimp-1 also represses Il2 and Bcl6, which destabilize the Th17 inflammatory program
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Scientists Have Found A Way To Make Cancer Cells Kill Each Other

Scientists Have Found A Way To Make Cancer Cells Kill Each Other | Host Cell & Pathogen Interactions | Scoop.it
By subjecting cancerous cells to a certain kind of antibody, researchers were able to transform them into natural killer cells — cells that can take out cancer.
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PBL13 Is a Serine/Threonine Protein Kinase That Negatively Regulates Arabidopsis Immune Responses

PBL13 Is a Serine/Threonine Protein Kinase That Negatively Regulates Arabidopsis Immune Responses | Host Cell & Pathogen Interactions | Scoop.it
Receptor-like cytoplasmic kinases (RLCKs) are a subset of plant receptor-like kinases lacking both extracellular and transmembrane domains. Some of the 46 members in the Arabidopsis (Arabidopsis thaliana) RLCK subfamily VII have been linked to plant innate immunity; however, most remain uncharacterized. Thus, multiple subfamily VII members are expected to be involved in plant immune signaling. Here, we investigate the role of AvrPphB SUSCEPTIBLE1-LIKE13 (PBL13), a subfamily VII RLCK with unique domain architecture. Unlike other characterized RLCKs, PBL13 transfer DNA insertion lines exhibit enhanced disease resistance after inoculation with virulent Pseudomonas syringae. The pbl13-2 knockout also exhibits elevated basal-level expression of the PATHOGENESIS-RELATED GENE1 defense marker gene, enhanced reactive oxygen species (ROS) burst in response to perception of bacterial microbial patterns, and accelerated flagellin-induced activation of mitogen-activated protein kinases. Recombinant PBL13 is an active kinase, and its primary autophosphorylated sites map to a 15-amino acid repeat motif unique to PBL13. Complementation of pbl13-2 with PBL13-3xFLAG converts the enhanced resistance and elevated ROS phenotypes back to wild-type levels. In contrast, kinase-dead PBL13K111A-3xFLAG was unable to rescue pbl13-2 disease phenotypes. Consistent with the enhanced ROS burst in the pbl13-2 knockout, PBL13 is able to associate with the nicotinamide adenine dinucleotide phosphate, reduced oxidase RESPIRATORY BURST OXIDASE HOMOLOG PROTEIN D (RBOHD) by split-luciferase complementation assay, and this association is disrupted by flagellin treatment. We conclude that the PBL13 kinase negatively regulates plant innate immunity to pathogenic bacteria and can associate with RBOHD before pathogen perception. These data are consistent with the hypothesis that PBL13 acts to prevent inappropriate activation of defense responses in the absence of pathogen challenge.

Via Christophe Jacquet, Guogen Yang
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Dengue Virus Non-structural Protein 1 Modulates Infectious Particle Production via Interaction with the Structural Proteins

Dengue Virus Non-structural Protein 1 Modulates Infectious Particle Production via Interaction with the Structural Proteins | Host Cell & Pathogen Interactions | Scoop.it

Author Summary Dengue virus (DENV) is a major arthropod-borne human pathogen, infecting more than 400 million individuals annually worldwide; however, neither a therapeutic drug nor a prophylactic vaccine is currently available.


Via Mel Melendrez-Vallard
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Molecular mechanisms of pore formation. : Pore-forming toxins: ancient, but never really out of fashion : Nature Reviews Microbiology : Nature Publishing Group

Molecular mechanisms of pore formation. : Pore-forming toxins: ancient, but never really out of fashion : Nature Reviews Microbiology : Nature Publishing Group | Host Cell & Pathogen Interactions | Scoop.it
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