Host Cell & Pathogen Interactions
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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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Host Cell & Pathogen Interactions
Strategies of Microbial Virulence and Host Defense
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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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Integration of Human Papillomavirus Genomes in Head and Neck Cancer: Is It Time to Consider a Paradigm Shift?

Integration of Human Papillomavirus Genomes in Head and Neck Cancer: Is It Time to Consider a Paradigm Shift? | Host Cell & Pathogen Interactions | Scoop.it
Human papillomaviruses (HPV) are detected in 70–80% of oropharyngeal cancers in the developed world, the incidence of which has reached epidemic proportions. The current paradigm regarding the status of the viral genome in these cancers is that there are three situations: one where the viral genome remains episomal, one where the viral genome integrates into the host genome and a third where there is a mixture of both integrated and episomal HPV genomes. Our recent work suggests that this third category has been mischaracterized as having integrated HPV genomes; evidence indicates that this category consists of virus–human hybrid episomes. Most of these hybrid episomes are consistent with being maintained by replication from HPV origin. We discuss our evidence to support this new paradigm, how such genomes can arise, and more importantly the implications for the clinical management of HPV positive head and neck cancers following accurate determination of the viral genome status.

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Dengue Infection Impairs Immune Defense Against Zika | The Scientist Magazine®

A memory B cell response to Zika virus in dengue-infected patients produced antibodies that were poorly neutralizing in vitro and instead enhanced infection.
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British Journal of Cancer - HYPE or HOPE: the prognostic value of infiltrating immune cells in cancer

British Journal of Cancer - HYPE or HOPE: the prognostic value of infiltrating immune cells in cancer | Host Cell & Pathogen Interactions | Scoop.it
The BJC is owned by Cancer Research UK, a charity dedicated to understanding the causes, prevention and treatment of cancer and to making sure that the best new treatments reach patients in the clinic as quickly as possible. The journal reflects these aims. It was founded more than fifty years ago and, from the start, its far-sighted mission was to encourage communication of the very best cancer research from laboratories and clinics in all countries. The breadth of its coverage, its editorial independence and it consistent high standards, have made BJC one of the world's premier general cancer journals. Its increasing popularity is reflected by a steadily rising impact factor.

Via Gilbert C FAURE
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Krishan Maggon 's curator insight, August 14, 2:22 AM

British Journal of Cancer (2017) 117, 451–460. doi:10.1038/bjc.2017.220 www.bjcancer.com 
Published online 13 July 2017 

HYPE or HOPE: the prognostic value of infiltrating immune cells in cancer

Tristan A Barnes and Eitan Amir
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Latency, Integration, and Reactivation of Human Herpesvirus-6

Human herpesvirus-6A (HHV-6A) and human herpesvirus-6B (HHV-6B) are two closely related viruses that infect T-cells. Both HHV-6A and HHV-6B possess telomere-like repeats at the terminal regions of their genomes that facilitate latency by integration into the host telomeres, rather than by episome formation. In about 1% of the human population, human herpes virus-6 (HHV-6) integration into germline cells allows the viral genome to be passed down from one generation to the other; this condition is called inherited chromosomally integrated HHV-6 (iciHHV-6). This review will cover the history of HHV-6 and recent works that define the biological differences between HHV-6A and HHV-6B. Additionally, HHV-6 integration and inheritance, the capacity for reactivation and superinfection of iciHHV-6 individuals with a second strain of HHV-6, and the role of hypomethylation of human chromosomes during integration are discussed. Overall, the data suggest that integration of HHV-6 in telomeres represent a unique mechanism of viral latency and offers a novel tool to study not only HHV-6 pathogenesis, but also telomere biology. Paradoxically, the integrated viral genome is often defective especially as seen in iciHHV-6 harboring individuals. Finally, gaps in the field of HHV-6 research are presented and future studies are proposed.

Via Bwana Moses
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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&ndash;2015 flu season found a difference in efficacy.

Via Ed Rybicki
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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.


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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.

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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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A new single-nucleotide polymorphism linked to severe influenza disease

Clear links between human genes and susceptibility to influenza disease are scarce. A recent study uncovers a gene variant coupled to severe influenza, and shows how it hampers the expression of an antiviral gene that is key to immune cell survival.

Via Ed Rybicki, Chris Upton + helpers
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How cells hack their own genes

How cells hack their own genes | Host Cell & Pathogen Interactions | Scoop.it

Researchers at IMBA—Institute of Molecular Biotechnology of the Austrian Academy of Sciences—unveil novel mechanism for gene expression.


Via Integrated DNA Technologies
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Poxviruses Utilize Multiple Strategies to Inhibit Apoptosis

Poxviruses Utilize Multiple Strategies to Inhibit Apoptosis | Host Cell & Pathogen Interactions | Scoop.it
Cells have multiple means to induce apoptosis in response to viral infection. Poxviruses must prevent activation of cellular apoptosis to ensure successful replication. These viruses devote a substantial portion of their genome to immune evasion. Many of these immune evasion products expressed during infection antagonize cellular apoptotic pathways. Poxvirus products target multiple points in both the extrinsic and intrinsic apoptotic pathways, thereby mitigating apoptosis during infection. Interestingly, recent evidence indicates that poxviruses also hijack cellular means of eliminating apoptotic bodies as a means to spread cell to cell through a process called apoptotic mimicry. Poxviruses are the causative agent of many human and veterinary diseases. Further, there is substantial interest in developing these viruses as vectors for a variety of uses including vaccine delivery and as oncolytic viruses to treat certain human cancers. Therefore, an understanding of the molecular mechanisms through which poxviruses regulate the cellular apoptotic pathways remains a top research priority. In this review, we consider anti-apoptotic strategies of poxviruses focusing on three relevant poxvirus genera: Orthopoxvirus, Molluscipoxvirus, and Leporipoxvirus. All three genera express multiple products to inhibit both extrinsic and intrinsic apoptotic pathways with many of these products required for virulence

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Scientists challenge next-generation sequencing dogma: Surprising bacteria study reveals that shotgun sequencing misses major groups of organisms despite producing more data than amplicon sequencing

Scientists challenge next-generation sequencing dogma: Surprising bacteria study reveals that shotgun sequencing misses major groups of organisms despite producing more data than amplicon sequencing | Host Cell & Pathogen Interactions | Scoop.it
Next-generation sequencing -- the ability to sequence millions or billions of small fragments of DNA in parallel -- has revolutionized the biological sciences, playing an essential role in everything from locating mutations that cause human disease to determining how a newly discovered animal fits into the tree of life. But a new study reveals that a favored sequencing method for measuring microbial biodiversity is not as accurate as once thought.

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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.