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Single Amino Acid Substitutions Confer the Antiviral Activity of the TRAF3 Adaptor Protein onto TRAF5 -- Zhang et al. 5 (250): ra81 -- Science Signaling

The TRAF [tumor necrosis factor receptor–associated factor] family of cytoplasmic adaptor proteins link cell-surface receptors to intracellular signaling pathways that regulate innate and adaptive immune responses. In response to activation of RIG-I (retinoic acid–inducible gene I), a component of a pattern recognition receptor that detects viruses, TRAF3 binds to the adaptor protein Cardif [caspase activation and recruitment domain (CARD) adaptor–inducing interferon-β (IFN-β)], leading to induction of type I IFNs. We report the crystal structures of the TRAF domain of TRAF5 and that of TRAF3 bound to a peptide from the TRAF-interacting motif of Cardif. By comparing these structures, we identified two residues located near the Cardif binding pocket in TRAF3 (Tyr440 and Phe473) that potentially contributed to Cardif recognition. In vitro and cellular experiments showed that forms of TRAF5 with mutation of the corresponding residues to those of TRAF3 had TRAF3-like antiviral activity. Our results provide a structural basis for the critical role of TRAF3 in activating RIG-I–mediated IFN production.

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How ZMapp antibodies bind to Ebola virus

How ZMapp antibodies bind to Ebola virus | Host Cell & Pathogen Interactions | Scoop.it
The structure of the antibodies in ZMapp bound to the Ebola virus glycoprotein reveal how they inhibit infection and how ZMapp might be improved.
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Scripps Research Institute Scientists Reveal Weak Spots in Ebola’s Defenses

Scripps Research Institute Scientists Reveal Weak Spots in Ebola’s Defenses | Host Cell & Pathogen Interactions | Scoop.it
News Release
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What Makes Ebola So Deadly? [VIDEO]

What Makes Ebola So Deadly? [VIDEO] | Host Cell & Pathogen Interactions | Scoop.it
The Ebola virus is able to kill its victim so quickly because of its effective warfare against a body's immune system.
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Alfonso Barrios Sanz's curator insight, November 11, 7:29 AM

The strain currently affecting is the most severe. This strain produces a strong hemorrhagic fever. Also it is a very contagious virus, so we have to take high security methods. 

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Coronavirus Cell Entry Occurs through the Endo-/Lysosomal Pathway in a Proteolysis-Dependent Manner

Coronavirus Cell Entry Occurs through the Endo-/Lysosomal Pathway in a Proteolysis-Dependent Manner | Host Cell & Pathogen Interactions | Scoop.it
From molecules to physiology
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First detailed picture of a cancer-related cell enzyme in action on a chromosome

First detailed picture of a cancer-related cell enzyme in action on a chromosome | Host Cell & Pathogen Interactions | Scoop.it

A landmark study published in the Oct. 30, print edition of the Nature provides new insight into the function of an enzyme related to the BRCA1 breast cancer protein. The study by a team at Penn State University is the first to produce a detailed working image of an enzyme in the Polycomb Repressive Complex 1 (PRC1) -- a group that regulates cell development and is associated with many types of cancer.


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Innate immunity summit

Innate immunity summit | Host Cell & Pathogen Interactions | Scoop.it
The Innate Immunity Summit, London, 10-12 Nov 2014 http://t.co/xS4azgK2yn

Via Gilbert Faure au nom de l'ASSIM
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Research shows viral DNA infects cells by changing from solid to fluid-like state

Research shows viral DNA infects cells by changing from solid to fluid-like state | Host Cell & Pathogen Interactions | Scoop.it
Many double-stranded DNA viruses infect cells by ejecting their genetic information into a host cell. But how does the usually rigid DNA packaged inside a virus' shell flow from the virus to the cell?
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GEN | News Highlights:With Cas9 Built-In, Mouse Is CRISPR-Ready

GEN | News Highlights:With Cas9 Built-In, Mouse Is CRISPR-Ready | Host Cell & Pathogen Interactions | Scoop.it
Broad Institute and MIT researchers engineer Cas9 animal models to study disease, inform drug discovery.
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Fesquet didier's curator insight, September 27, 11:06 AM

un autre outils pour customiser les genomes in vivo!

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The TIR-Domain Containing Adaptor TRAM Is Required for TLR7 Mediated RANTES Production

The TIR-Domain Containing Adaptor TRAM Is Required for TLR7 Mediated RANTES Production | Host Cell & Pathogen Interactions | Scoop.it
by Enda Shevlin, Sinéad M. Miggin Toll-like receptor 7 (TLR7) plays a vital role in the immune response to ssRNA viruses such as human rhinovirus (HRV) and Influenza, against which there are currently no treatments or vaccines with long term...

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Ebola Protein Discovery Could Clear Path For Treatment - YouTube

Researchers found Ebola's VP24 protein interferes with the body's immune response system. It's a finding that could lead to future treatment. Follow Jay Stru...
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The Role of Host and Microbial Factors in the Pathogenesis of Pneumococcal Bacteraemia Arising from a Single Bacterial Cell Bottleneck

The Role of Host and Microbial Factors in the Pathogenesis of Pneumococcal Bacteraemia Arising from a Single Bacterial Cell Bottleneck | Host Cell & Pathogen Interactions | Scoop.it
From molecules to physiology
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Mouse Cytomegalovirus infection overrules T regulatory cell suppression on natural killer cells

Cytomegalovirus establishes lifelong persistency in the host and leads to life threatening situations in immunocompromised patients. FoxP3+ T regulatory cells (Tregs) critically control and suppress innate and adaptive immune responses. However, their specific role during MCMV infection, especially pertaining to their interaction with NK cells, remains incompletely defined.
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Small Things Considered: Why CRISPR Doesn't Work in E. coli

Small Things Considered: Why CRISPR Doesn't Work in E. coli | Host Cell & Pathogen Interactions | Scoop.it
by Elio | We received this query: »I enjoyed the article on your blog 'Six Questions About CRISPRs' by Merry Youle. I am an ex-lambdologist, having quit phage lambda in the early 70s and moved to GM-plants. There is one thing about CRISPR that I do not understand: Why did lambdologists not find CRISPR?
They found phage...
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Rescooped by Ken Yaw Agyeman-Badu from immunology
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Atypical MHC class II-expressing antigen-presenting cells: can anything replace a dendritic cell?

Atypical MHC class II-expressing antigen-presenting cells: can anything replace a dendritic cell? | Host Cell & Pathogen Interactions | Scoop.it

Dendritic cells, macrophages and B cells are regarded as the classical antigen-presenting cells of the immune system. However, in recent years, there has been a rapid increase in the number of cell types that are suggested to present antigens on MHC class II molecules to CD4+ T cells. In this Review, we describe the key characteristics that define an antigen-presenting cell by examining the functions of dendritic cells. We then examine the functions of the haematopoietic cells and non-haematopoietic cells that can express MHC class II molecules and that have been suggested to represent 'atypical' antigen-presenting cells. We consider whether any of these cell populations can prime naive CD4+ T cells and, if not, question the effects that they do have on the development of immune responses.


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Krishan Maggon 's curator insight, November 15, 9:22 AM
Atypical MHC class II-expressing antigen-presenting cells: can anything replace a dendritic cell?Taku Kambayashi& Terri M. LauferAffiliationsCorresponding authorNature Reviews Immunology 14, 719–730 (2014) doi:10.1038/nri3754Published online 17 October 2014
Gilbert Faure au nom de l'ASSIM's curator insight, November 16, 1:09 PM

and epithelial cells in autoimmunity

Rescooped by Ken Yaw Agyeman-Badu from Virology and Bioinformatics from Virology.ca
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Host-Specific Parvovirus Evolution in Nature Is Recapitulated by In Vitro Adaptation to Different Carnivore Species

Host-Specific Parvovirus Evolution in Nature Is Recapitulated by In Vitro Adaptation to Different Carnivore Species | Host Cell & Pathogen Interactions | Scoop.it
From molecules to physiology
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Rescooped by Ken Yaw Agyeman-Badu from Influenza
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Influenza A virus uses the aggresome processing machinery for host cell entry

During cell entry, capsids of incoming influenza A viruses (IAVs) must be uncoated before viral ribonucleoproteins (vRNPs) can enter the nucleus for replication. After hemagglutinin-mediated membrane fusion in late endocytic vacuoles, the vRNPs and the matrix proteins dissociate from each other and disperse within the cytosol. Here, we found that for capsid disassembly, IAV takes advantage of the host cell’s aggresome formation and disassembly machinery. The capsids mimicked misfolded protein aggregates by carrying unanchored ubiquitin chains that activated a histone deacetylase 6 (HDAC6)–dependent pathway. The ubiquitin-binding domain was essential for recruitment of HDAC6 to viral fusion sites and for efficient uncoating and infection. That other components of the aggresome processing machinery, including dynein, dynactin, and myosin II, were also required suggested that physical forces generated by microtubule- and actin-associated motors are essential for IAV entry.


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The role of TGF-ß signaling and apoptosis in innate and adaptive im... - PubMed - NCBI

BMC Syst Biol. 2014 Oct 24;8(1):116. [Epub ahead of print]
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Inhibition of cytoplasmic mRNA stress gran... [Cell Host Microbe. 2007] - PubMed - NCBI

PubMed comprises more than 23 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
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Rescooped by Ken Yaw Agyeman-Badu from SynBioFromLeukipposInstitute
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Thesis: Controlling gene expression in enterobacteriaceae: studies on sRNAs and strategies for synthetic biology


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Socrates Logos's curator insight, September 30, 3:55 PM

Dissertation presented to obtain the Master Degree in Molecular, Genetics and Biomedicine


by

Apura, Patrícia de Faria Pais


Transcriptional and post-transcriptional control of gene expression dictate the levels of proteins in the cell. Therefore the modulation of gene expression can have important consequences for biotechnological and/or pharmaceutical purposes. Among the types of cellular RNAs, small RNAs (sRNAs) have been an emerging class of bacterial gene expression regulators, which mostly act by base-pairing with one or more mRNA target(s) affecting their translation and/or their stability. Here, we focus on the study of SraL sRNA, more specifically in the validation of putative targets for this sRNA obtained in a previous transcriptomic analysis. Until now SraL was only shown to regulate the mRNA levels of Trigger Factor, an important protein chaperone. The information here reported give strong evidence for SraL involvement in the cysteine biosynthetic pathway, which requires further investigation. Nevertheless, our results could not provide a validation of those putative targets previously obtained by transcriptomic analyses. Optimization of protein expression requires not only an increase of the stability of mRNA transcripts but also an optimal behavior of function-encoding DNA segments, which are often context-dependent. Building on the work of others, we have designed a set of combinatorial promoters and 5’UTRs and evaluated their effects/outcomes using Superfolder GFP as reporter. Our data shows a clear variability of protein levels within our set of constructs. The highest levels of protein were associated with the implementation of an insulation sequence flanking the promoter region and the introduction of 5’ stabilizing structures at the mRNA level. Further investigation concerning the alteration of the rate of the mRNA decay by depletion of the function of participating nucleases, might constitute an advantageous approach. The knowledge collected will be extremely important to design robust modules which substantially increase protein production. This field is rapidly growing and much remains to be discovered about these important regulatory processes.

 


http://bit.ly/1qSyrSW

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Bacterial 'communication system' could be used to stop, kill cancer cells, study finds

Bacterial 'communication system' could be used to stop, kill cancer cells, study finds | Host Cell & Pathogen Interactions | Scoop.it
A molecule used as a communication system by bacteria can be manipulated to prevent cancer cells from spreading, a study has demonstrated. "During an infection, bacteria release molecules which allow them to 'talk' to each other," said the lead author of the study. "Depending on the type of molecule released, the signal will tell other bacteria to multiply, escape the immune system or even stop spreading."
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Filoviruses Require Endosomal Cysteine Proteases for Entry but Exhibit Distinct Protease Preferences

Ken Yaw Agyeman-Badu's insight:

Filoviruses are enveloped viruses that cause sporadic outbreaks of severe hemorrhagic fever [CDC, MMWR Morb. Mortal. Wkly. Rep. 50:73–77, 2001; Colebunders and Borchert, J. Infect. 40:16–20, 2000; Colebunders et al., J. Infect. Dis. 196(Suppl. 2):S148–S153, 2007; Geisbert and Jahrling, Nat. Med. 10:S110-S121, 2004]. Previous studies revealed that endosomal cysteine proteases are host factors for ebolavirus Zaire (Chandran et al., Science 308:1643–1645, 2005; Schornberg et al., J. Virol. 80:4174–4178, 2006). In this report, we show that infection mediated by glycoproteins from other phylogenetically diverse filoviruses are also dependent on these proteases and provide additional evidence indicating that they cleave GP1 and expose the binding domain for the critical host factor Niemann-Pick C1. Using selective inhibitors and knockout-derived cell lines, we show that the ebolaviruses Zaire and Cote d'Ivoire are strongly dependent on cathepsin B, while the ebolaviruses Sudan and Reston and Marburg virus are not. Taking advantage of previous studies of cathepsin B inhibitor-resistant viruses (Wong et al., J. Virol. 84:163–175, 2010), we found that virus-specific differences in the requirement for cathepsin B are correlated with sequence polymorphisms at residues 47 in GP1 and 584 in GP2. We applied these findings to the analysis of additional ebolavirus isolates and correctly predicted that the newly identified ebolavirus species Bundibugyo, containing D47 and I584, is cathepsin B dependent and that ebolavirus Zaire-1995, the single known isolate of ebolavirus Zaire that lacks D47, is not. We also obtained evidence for virus-specific differences in the role of cathepsin L, including cooperation with cathepsin B. These studies strongly suggest that the use of endosomal cysteine proteases as host factors for entry is a general property of members of the family Filoviridae.

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Ken Yaw Agyeman-Badu's curator insight, September 14, 11:23 PM

Filoviruses are enveloped viruses that cause sporadic outbreaks of severe hemorrhagic fever [CDC, MMWR Morb. Mortal. Wkly. Rep. 50:73–77, 2001; Colebunders and Borchert, J. Infect. 40:16–20, 2000; Colebunders et al., J. Infect. Dis. 196(Suppl. 2):S148–S153, 2007; Geisbert and Jahrling, Nat. Med. 10:S110-S121, 2004]. Previous studies revealed that endosomal cysteine proteases are host factors for ebolavirus Zaire (Chandran et al., Science 308:1643–1645, 2005; Schornberg et al., J. Virol. 80:4174–4178, 2006). In this report, we show that infection mediated by glycoproteins from other phylogenetically diverse filoviruses are also dependent on these proteases and provide additional evidence indicating that they cleave GP1 and expose the binding domain for the critical host factor Niemann-Pick C1. Using selective inhibitors and knockout-derived cell lines, we show that the ebolaviruses Zaire and Cote d'Ivoire are strongly dependent on cathepsin B, while the ebolaviruses Sudan and Reston and Marburg virus are not. Taking advantage of previous studies of cathepsin B inhibitor-resistant viruses (Wong et al., J. Virol. 84:163–175, 2010), we found that virus-specific differences in the requirement for cathepsin B are correlated with sequence polymorphisms at residues 47 in GP1 and 584 in GP2. We applied these findings to the analysis of additional ebolavirus isolates and correctly predicted that the newly identified ebolavirus species Bundibugyo, containing D47 and I584, is cathepsin B dependent and that ebolavirus Zaire-1995, the single known isolate of ebolavirus Zaire that lacks D47, is not. We also obtained evidence for virus-specific differences in the role of cathepsin L, including cooperation with cathepsin B. These studies strongly suggest that the use of endosomal cysteine proteases as host factors for entry is a general property of members of the family Filoviridae.

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5 Viruses That Are Scarier Than Ebola

5 Viruses That Are Scarier Than Ebola | Host Cell & Pathogen Interactions | Scoop.it
By Elizabeth Palermo, Staff Writer
Published: 08/15/2014 01:58 PM EDT on LiveScience

The Ebola virus has now killed more than 1,000 people in West Africa. Although the mortality rate of the most recent outbreak isn't as high as in previous eve...
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Quantitative Temporal Viromics: An Approach to Investigate Host-Pathogen Interaction

Quantitative Temporal Viromics: An Approach to Investigate Host-Pathogen Interaction | Host Cell & Pathogen Interactions | Scoop.it

A systematic quantitative analysis of temporal changes in host and viral proteins throughout the course of a productive infection could provide dynamic insights into virus-host interaction. We developed a proteomic technique called “quantitative temporal viromics” (QTV), which employs multiplexed tandem-mass-tag-based mass spectrometry. Human cytomegalovirus (HCMV) is not only an important pathogen but a paradigm of viral immune evasion. QTV detailed how HCMV orchestrates the expression of >8,000 cellular proteins, including 1,200 cell-surface proteins to manipulate signaling pathways and counterintrinsic, innate, and adaptive immune defenses. QTV predicted natural killer and T cell ligands, as well as 29 viral proteins present at the cell surface, potential therapeutic targets. Temporal profiles of >80% of HCMV canonical genes and 14 noncanonical HCMV open reading frames were defined. QTV is a powerful method that can yield important insights into viral infection and is applicable to any virus with a robust in vitro model.


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Why HIV Virions Have Low Numbers of Envelope Spikes: Implications for Vaccine Development

Why HIV Virions Have Low Numbers of Envelope Spikes: Implications for Vaccine Development | Host Cell & Pathogen Interactions | Scoop.it
From molecules to physiology
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