Host Cell & Pathogen Interactions
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Consequences of flagellin export through the type III secretion system of Pseudomonas syringae reveal a major difference in the innate immune systems of mammals and the model plant Nicotiana bentha...

Consequences of flagellin export through the type III secretion system of Pseudomonas syringae reveal a major difference in the innate immune systems of mammals and the model plant Nicotiana bentha... | Host Cell & Pathogen Interactions | Scoop.it
Summary
Bacterial flagellin is perceived as a microbe (or pathogen)-associated molecular pattern (MAMP or PAMP) by the extracellular pattern recognition receptors, FLS2 and TLR5, of plants and mammals, respectively.

Via IPM Lab, Guogen Yang
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Host Cell & Pathogen Interactions
Strategies of Microbial Virulence and Host Defense
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Microbiota: A high-pressure situation for bacteria

Microbiota: A high-pressure situation for bacteria | Host Cell & Pathogen Interactions | Scoop.it
News and Views

Via Gilbert C FAURE
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Antigen Processing and Presentation | British Society for Immunology

Antigen Processing and Presentation | British Society for Immunology | Host Cell & Pathogen Interactions | Scoop.it
In order to be capable of engaging the key elements of adaptive immunity (specificity, memory, diversity, self/nonself discrimination), antigens have to be processed and presented to immune cells. Antigen presentation is mediated by MHC class I molecules, and the class II molecules found on the surface of antigen-presenting cells (APCs) and certain other cells.

Via Gilbert C FAURE
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The vaccinia virus DNA polymerase structure provides insights into the mode of processivity factor binding. - PubMed - NCBI

The vaccinia virus DNA polymerase structure provides insights into the mode of processivity factor binding. - PubMed - NCBI | Host Cell & Pathogen Interactions | Scoop.it
Nat Commun. 2017 Nov 13;8(1):1455. doi: 10.1038/s41467-017-01542-z.

Via Chris Upton + helpers
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A Next-Generation Sequencing Approach Uncovers Viral Transcripts Incorporated in Poxvirus Virions

A Next-Generation Sequencing Approach Uncovers Viral Transcripts Incorporated in Poxvirus Virions | Host Cell & Pathogen Interactions | Scoop.it
Transcripts are known to be incorporated in particles of DNA viruses belonging to the families of Herpesviridae and Mimiviridae, but the presence of transcripts in other DNA viruses, such as poxviruses, has not been analyzed yet. Therefore, we first established a next-generation-sequencing (NGS)-based protocol, enabling the unbiased identification of transcripts in virus particles. Subsequently, we applied our protocol to analyze RNA in an emerging zoonotic member of the Poxviridae family, namely Cowpox virus. Our results revealed the incorporation of 19 viral transcripts, while host identifications were restricted to ribosomal and mitochondrial RNA. Most viral transcripts had an unknown and immunomodulatory function, suggesting that transcript incorporation may be beneficial for poxvirus immune evasion. Notably, the most abundant transcript originated from the D5L/I1R gene that encodes a viral inhibitor of the host cytoplasmic DNA sensing machinery.

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CAR-T Cell Therapy for Cancer Treatment – An Insight into Side Effects

CAR-T Cell Therapy for Cancer Treatment – An Insight into Side Effects | Host Cell & Pathogen Interactions | Scoop.it
T-Cells are a part of our immune system. Made in the thymus gland of our bodies, they are white blood cells which constantly clean our system by hunting and attacking any abnormal cells or substances. Recently, in August 2017, the U.S. Food and Drug Administration (FDA) approved a genetically engineered T cell therapy called – [...]

Via Krishan Maggon , Gilbert C FAURE
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Gilbert C FAURE's curator insight, November 2, 3:52 AM
efficiency always has side effects
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Evolution of drug-resistant bacteria never exposed to antibiotics

Evolution of drug-resistant bacteria never exposed to antibiotics | Host Cell & Pathogen Interactions | Scoop.it
Antibiotic-resistant microbes are a huge problem in human and global health. One of the microbial characteristics that allows development o
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Gene circuit switches on inside cancer cells, triggers immune attack

Gene circuit switches on inside cancer cells, triggers immune attack | Host Cell & Pathogen Interactions | Scoop.it
Researchers at MIT have developed a synthetic gene circuit that triggers the body’s immune system to attack cancers when it detects signs of the disease.
The circuit, which will only activate a therapeutic response when it detects two specific cancer markers, is described in a paper published today in the journal Cell.
Immunotherapy is widely seen as having considerable potential in the fight against a range of cancers. The approach has been demonstrated successfully in several recent clinical trials, according to Timothy Lu, associate professor of biological engineering and of electrical engineering and computer science at MIT.
“There has been a lot of clinical data recently suggesting that if you can stimulate the immune system in the right way you can get it to recognize cancer,” says Lu, who is head of the Synthetic Biology Group in MIT’s Research Laboratory of Electronics. “Some of the best examples of this are what are called checkpoint inhibitors, where essentially cancers put up stop signs [that prevent] T-cells from killing them. There are antibodies that have been developed now that basically block those inhibitory signals and allow the immune system to act against the cancers.”
However, despite this success, the use of immunotherapy remains limited by the scarcity of tumor-specific antigens — substances that can trigger an immune system response to a particular type of cancer. The toxicity of some therapies, when delivered as a systemic treatment to the whole body, for example, is another obstacle.
What’s more, the treatments are not successful in all cases. Indeed, even in some of the most successful tests, only 30-40 percent of patients will respond to a given therapy, Lu says.
As a result, there is now a push to develop combination therapies, in which different but complementary treatments are used to boost the immune response. So, for example, if one type of immunotherapy is used to knock out an inhibitory signal produced by a cancer, and the tumor responds by upregulating a second signal, an additional therapy could then be used to target this one as well, Lu says.
“Our belief is that there is a need to develop much more specific, targeted immunotherapies that work locally at the tumor site, rather than trying to treat the entire body systemically,” he says. “Secondly, we want to produce multiple immunotherapies from a single package, and therefore be able to stimulate the immune system in multiple different ways.”
To do this, Lu and a team including MIT postdocs Lior Nissim and Ming-Ru Wu, have built a gene circuit encoded in DNA designed to distinguish cancer cells from noncancer cells.
The circuit, which can be customized to respond to different types of tumor, is based on the simple AND gates used in electronics. Such AND gates will only switch on a circuit when two inputs are present.
Cancer cells differ from normal cells in the profile of their gene expression. So the researchers developed synthetic promoters — DNA sequences designed to initiate gene expression but only in cancer cells.
The circuit is delivered to cells in the affected area of the body using a virus. The synthetic promotors are then designed to bind to certain proteins that are active in tumor cells, causing the promoters to turn on.
“Only when two of these cancer promoters are activated, does the circuit itself switch on,” Lu says.
This allows the circuit to target tumors more accurately than existing therapies, as it requires two cancer-specific signals to be present before it will respond.
Once activated, the circuit expresses proteins designed to direct the immune system to target the tumor cells, including surface T cell engagers, which direct T cells to kill the cells. The circuit also expresses a checkpoint inhibitor designed to lift the brakes on T cell activity.
When the researchers tested the circuit in vitro, they found that it was able to detect ovarian cancer cells from amongst other noncancerous ovarian cells and other cell types.
They then tested the circuit in mice implanted with ovarian cancer cells, and demonstrated that it could trigger T cells to seek out and kill the cancer cells without harming other cells around them.
Finally, the researchers showed that the circuit could be readily converted to target other cancer cells.
“We identified other promoters that were selective for breast cancer, and when these were encoded into the circuit, it would target breast cancer cells over other types of cell,” Lu says.
Ultimately, they hope they will also be able to use the system to target other diseases, such as rheumatoid arthritis, inflammatory bowel disease, and other autoimmune diseases.
This advance will open up a new front against cancer, says Martin Fussenegger, a professor of biotechnology and bioengineering at ETH Zurich in Switzerland, who was not involved in the research.
“First author Lior Nissim, who pioneered the very first genetic circuit targeting tumor cells, has now teamed up with Timothy Lu to design RNA-based immunomodulatory gene circuits that take cancer immunotherapy to a new level,” Fussenegger says. “The design of this highly complex tumor-killing gene circuit was made possible by meticulous optimization and integration of several components that target and program tumor cells to become a specific prey for the immune system — this is very smart technology.”
The researchers now plan to test the circuit more fully in a range of cancer models. They are also aiming to develop a delivery system for the circuit, which would be both flexible and simple to manufacture and use.

Via Gerd Moe-Behrens
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Enterococcus faecalis modulates immune activation and slows healing during wound infection | The Journal of Infectious Diseases | Oxford Academic

Enterococcus faecalis  modulates immune activation and slows healing during wound infection | The Journal of Infectious Diseases | Oxford Academic | Host Cell & Pathogen Interactions | Scoop.it
Abstract. Enterococcus faecalis is one of most frequently isolated bacterial species in wounds yet little is known about its pathogenic mechanisms in this sett
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Researchers create molecule that could 'kick and kill' HIV - Scienmag: Latest Science and Health News

Researchers create molecule that could 'kick and kill' HIV - Scienmag: Latest Science and Health News | Host Cell & Pathogen Interactions | Scoop.it
Credit: CDC/A. Harrison and Dr. P. Feorino
In lab animals, a particle developed by UCLA, Stanford, NIH scientists awakens dormant virus cells and then knocks them out
Current anti-AIDS drugs are highly effective at making HIV undetectable and allo..
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A wound-healing program is hijacked to promote cancer metastasis

A wound-healing program is hijacked to promote cancer metastasis | Host Cell & Pathogen Interactions | Scoop.it
In this issue of JEM, Sundaram et al. (<https://doi.org/10.1084/jem.20170354>;) report a mechanism by which the normal epithelial wound healing response is “hijacked” to promote invasion and metastasis in head and neck squamous carcinomas (HNSCCs), a finding that unveils new markers of poor outcomes and potential targets for therapeutic intervention.

Via Gilbert C FAURE
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Synthetic receptors imitate GPCR

Synthetic receptors imitate GPCR | Host Cell & Pathogen Interactions | Scoop.it
[+]Enlarge A synthetic GPCR-like system uses hydroxide first messengers (orange) to deprotonate a receptor end group (blue), causing the receptor to move down into the vesicle membrane. The other end group (pink) binds a zinc cofactor (green) to catalyze a reaction that produces a second...

Via Gerd Moe-Behrens
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HCV-induced autophagosomes are generated via homotypic fusion of phagophores that mediate HCV RNA replication

HCV-induced autophagosomes are generated via homotypic fusion of phagophores that mediate HCV RNA replication | Host Cell & Pathogen Interactions | Scoop.it
Author summary Autophagy is a catabolic process that is important for maintaining cellular homeostasis. During autophagy, crescent membrane structures known as phagophores first appear in the cytoplasm, which then expand to form enclosed double-membrane vesicles known as autophagosomes. It has been shown that hepatitis C virus (HCV) induces autophagy and uses autophagosomal membranes for its RNA replication. In this report, we studied the biogenesis pathway of HCV-induced autophagosomes and demonstrated that phagophores induced by HCV originated from the endoplasmic reticulum and undergo homotypic fusion to generate autophagosomes, and that the HCV RNA replication complex is assembled on phagophores prior to the formation of autophagosomes. These findings provided important information for understanding how an RNA virus controls this important cellular pathway for its replication.

Via Ed Rybicki
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Die Another Day: Inhibition of Cell Death Pathways by Cytomegalovirus

Die Another Day: Inhibition of Cell Death Pathways by Cytomegalovirus | Host Cell & Pathogen Interactions | Scoop.it
Multicellular organisms have evolved multiple genetically programmed cell death pathways that are essential for homeostasis. The finding that many viruses encode cell death inhibitors suggested that cellular suicide also functions as a first line of defence against invading pathogens. This theory was confirmed by studying viral mutants that lack certain cell death inhibitors. Cytomegaloviruses, a family of species-specific viruses, have proved particularly useful in this respect. Cytomegaloviruses are known to encode multiple death inhibitors that are required for efficient viral replication. Here, we outline the mechanisms used by the host cell to detect cytomegalovirus infection and discuss the methods employed by the cytomegalovirus family to prevent death of the host cell. In addition to enhancing our understanding of cytomegalovirus pathogenesis we detail how this research has provided significant insights into the cross-talk that exists between the various cell death pathways.
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Poxviruses: Slipping and sliding through transcription and translation

Poxviruses: Slipping and sliding through transcription and translation | Host Cell & Pathogen Interactions | Scoop.it

Via Chris Upton + helpers
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Quantitative microbiome profiling links gut community variation to microbial load

Quantitative microbiome profiling links gut community variation to microbial load | Host Cell & Pathogen Interactions | Scoop.it
Letter

Via Gilbert C FAURE
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Poxvirus Host Range Genes and Virus–Host Spectrum: A Critical Review

Poxvirus Host Range Genes and Virus–Host Spectrum: A Critical Review | Host Cell & Pathogen Interactions | Scoop.it

The Poxviridae family is comprised of double-stranded DNA viruses belonging to nucleocytoplasmic large DNA viruses (NCLDV). Among the NCLDV, poxviruses exhibit the widest known host range, which is likely observed because this viral family has been more heavily investigated. However, relative to each member of the Poxviridae family, the spectrum of the host is variable, where certain viruses can infect a large range of hosts, while others are restricted to only one host species. It has been suggested that the variability in host spectrum among poxviruses is linked with the presence or absence of some host range genes. Would it be possible to extrapolate the restriction of viral replication in a specific cell lineage to an animal, a far more complex organism? In this study, we compare and discuss the relationship between the host range of poxvirus species and the abundance/diversity of host range genes. We analyzed the sequences of 38 previously identified and putative homologs of poxvirus host range genes, and updated these data with deposited sequences of new poxvirus genomes. Overall, the term host range genes might not be the most appropriate for these genes, since no correlation between them and the viruses’ host spectrum was observed, and a change in nomenclature should be considered. Finally, we analyzed the evolutionary history of these genes, and reaffirmed the occurrence of horizontal gene transfer (HGT) for certain elements, as previously suggested. Considering the data presented in this study, it is not possible to associate the diversity of host range factors with the amount of hosts of known poxviruses, and this traditional nomenclature creates misunderstandings.

 

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Migrating into the Tumor: a Roadmap for T Cells

Migrating into the Tumor: a Roadmap for T Cells | Host Cell & Pathogen Interactions | Scoop.it
Tumors can be divided into ‘hot’ (T cell inflamed) or ‘cold’ (T cell noninflamed)
according to the presence of immune cells. In this review, we discuss variables that
influence T cell migration into the tumor microenvironment. Chemokines can attract
T cells to the tumor site and tumor intrinsic pathways can influence the composition
of local chemokines. Tumor-induced vasculature can hamper T cell migration. Other
immune cells and tumor-derived molecules can block T cell proliferation and survival.

Via Krishan Maggon , Chris Upton + helpers
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Life’s First Molecule Was Protein, Not RNA, New Model Suggests 

Life’s First Molecule Was Protein, Not RNA, New Model Suggests  | Host Cell & Pathogen Interactions | Scoop.it

Which mattered first at the dawn of life: proteins or nucleic acids? Proteins may have had the edge if a theorized process let them grow long enough to become self-replicating catalysts. 


Via Integrated DNA Technologies
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'Assassin' molecules drive cancer cells to self-destruct

'Assassin' molecules drive cancer cells to self-destruct | Host Cell & Pathogen Interactions | Scoop.it

"We think this is how multicellular organisms eliminated cancer before the development of the adaptive immune system, which is about 500 million years old."

 

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Cell Death and Differentiation - MOMP, cell suicide as a BCL-2 family business

Cell Death and Differentiation - MOMP, cell suicide as a BCL-2 family business | Host Cell & Pathogen Interactions | Scoop.it
Cell death and differentiation is a monthly research journal focused on the exciting field of programmed cell death and apoptosis. It provides a single accessible source of information for both scientists and clinicians, keeping them up-to-date with advances in the field. It encompasses programmed cell death, cell death induced by toxic agents, differentiation and the interrelation of these with cell proliferation.

Via Gilbert C FAURE
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The world is running out of antibiotics

The world is running out of antibiotics | Host Cell & Pathogen Interactions | Scoop.it
Bacteria resistant to antibiotic treatments and increased costs are causing depleting effective remedies to cure certain illnesses.
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Ancient Viruses Are Buried in Your DNA

Ancient Viruses Are Buried in Your DNA | Host Cell & Pathogen Interactions | Scoop.it

Endogenous retroviruses wormed into the human genome eons ago. Today viral genes continue to produce a variety of mysterious proteins in the body.


Via Integrated DNA Technologies
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From bacterial killing to immune modulation: Recent insights into the functions of lysozyme

From bacterial killing to immune modulation: Recent insights into the functions of lysozyme | Host Cell & Pathogen Interactions | Scoop.it
Lysozyme is a cornerstone of innate immunity. The canonical mechanism for bacterial killing by lysozyme occurs through the hydrolysis of cell wall peptidoglycan (PG). Conventional type (c-type) lysozymes are also highly cationic and can kill certain bacteria independently of PG hydrolytic activity. Reflecting the ongoing arms race between host and invading microorganisms, both gram-positive and gram-negative bacteria have evolved mechanisms to thwart killing by lysozyme. In addition to its direct antimicrobial role, more recent evidence has shown that lysozyme modulates the host immune response to infection. The degradation and lysis of bacteria by lysozyme enhance the release of bacterial products, including PG, that activate pattern recognition receptors in host cells. Yet paradoxically, lysozyme is important for the resolution of inflammation at mucosal sites. This review will highlight recent advances in our understanding of the diverse mechanisms that bacteria use to protect themselves against lysozyme, the intriguing immunomodulatory function of lysozyme, and the relationship between these features in the context of infection.

Via Gilbert C FAURE
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A novel mechanism of antibody-mediated enhancement of flavivirus infection

A novel mechanism of antibody-mediated enhancement of flavivirus infection | Host Cell & Pathogen Interactions | Scoop.it
Author summary Antibodies are an important component of antiviral host responses and their binding to the surface of virus particles usually leads to neutralization of viral infectivity. In some instances, however, antibodies at sub-neutralizing concentrations can enhance infection of certain cells, because they facilitate the uptake of infectious virus-antibody complexes through interactions with antibody-specific cellular receptors (Fcγ receptors). This mechanism is designated antibody-dependent enhancement of infection and implicated in the pathogenesis of dengue and possibly Zika virus infections, both mosquito-transmitted flaviviruses. Here we describe a novel mechanism of infection enhancement by antibodies that is independent of interactions with Fcγ receptors, using another important human-pathogenic flavivirus, tick-borne encephalitis virus. We demonstrate that binding of a specific antibody to the envelope protein E at the viral surface promotes the exposure of a structural element that interacts with the lipids of the cellular plasma membrane, thus increasing infection. Our study provides new insights into mechanisms that potentially modulate the antiviral effects of antibody populations present in post-infection sera.

Via Ed Rybicki
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Rheostatic Functions of Mast Cells in the Control of Innate and Adaptive Immune Responses

Rheostatic Functions of Mast Cells in the Control of Innate and Adaptive Immune Responses | Host Cell & Pathogen Interactions | Scoop.it
Mast cells are evolutionarily ancient cells, endowed with a unique developmental,
phenotypic, and functional plasticity. They are resident cells that participate in
tissue homeostasis by constantly sampling the microenvironment. As a result of their
large repertoire of receptors, they can respond to multiple stimuli and selectively
release different types and amounts of mediator. Here, we present and discuss the
recent mast cell literature, focusing on studies that demonstrate that mast cells
are more than a switch that is turned ‘off’ when in the resting state and ‘on’ when
in the degranulating state.

Via Krishan Maggon , Gilbert C FAURE
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