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Genomic Variation in Seven Khoe-San Groups Reveals Adaptation and Complex African History

"The history of click-speaking Khoe-San, and African populations in general, remains poorly understood. We genotyped ∼2.3 million SNPs in 220 southern Africans and found that the Khoe-San diverged from other populations ≥100,000 years ago, but structure within the Khoe-San dated back to about 35,000 years ago. Genetic variation in various sub-Saharan populations did not localize the origin of modern humans to a single geographic region within Africa; instead, it indicated a history of admixture and stratification. We found evidence of adaptation targeting muscle function and immune response, potential adaptive introgression of UV-light protection, and selection predating modern human diversification involving skeletal and neurological development. These new findings illustrate the importance of African genomic diversity in understanding human evolutionary history."

 

Ex Africa, semper aliquid novi...or old, in this case!

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Virology and Bioinformatics from Virology.ca
Virus and bioinformatics articles with some microbiology and immunology thrown in for good measure
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It's a group effort - the curators:

It's a group effort - the curators: | Virology and Bioinformatics from Virology.ca | Scoop.it

get in touch if you want to help curate this topic

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Code sharing - Nature

Papers in Nature journals should make computer code accessible where possible.
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Global rise in human infectious disease outbreaks

Global rise in human infectious disease outbreaks | Virology and Bioinformatics from Virology.ca | Scoop.it

To characterize the change in frequency of infectious disease outbreaks over time worldwide, we encoded and analysed a novel 33-year dataset (1980–2013) of 12 102 outbreaks of 215 human infectious diseases, comprising more than 44 million cases occuring in 219 nations. We merged these records with ecological characteristics of the causal pathogens to examine global temporal trends in the total number of outbreaks, disease richness (number of unique diseases), disease diversity (richness and outbreak evenness) and per capitacases. Bacteria, viruses, zoonotic diseases (originating in animals) and those caused by pathogens transmitted by vector hosts were responsible for the majority of outbreaks in our dataset. After controlling for disease surveillance, communications, geography and host availability, we find the total number and diversity of outbreaks, and richness of causal diseases increased significantly since 1980 (p < 0.0001). When we incorporate Internet usage into the model to control for biased reporting of outbreaks (starting 1990), the overall number of outbreaks and disease richness still increase significantly with time (p < 0.0001), but per capita cases decrease significantly (p = 0.005). Temporal trends in outbreaks differ based on the causal pathogen's taxonomy, host requirements and transmission mode. We discuss our preliminary findings in the context of global disease emergence and surveillance.

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Paper Behind The Green Coffee Bean Diet Craze Retracted

Paper Behind The Green Coffee Bean Diet Craze Retracted | Virology and Bioinformatics from Virology.ca | Scoop.it
The "scientific" paper that helped ignite the green coffee bean diet craze has been retracted. The details of the retraction and the full background of the story were fully reported by Ivan Oransky on Retraction Watch. The paper, published in Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy, purported to report the substantial weight loss findings [...]
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Chris Upton + helpers's curator insight, October 27, 1:06 PM

Typical nonsense nonscience!

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Ten Simple Rules for Writing a PLOS Ten Simple Rules Article

Ten Simple Rules for Writing a PLOS Ten Simple Rules Article | Virology and Bioinformatics from Virology.ca | Scoop.it
PLOS Computational Biology is an open-access
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Identification of an env-defective HIV-1 mutant capable of spontaneous reversion to a wild-type phenotype in certain T-cell lines

Attempts to eradicate HIV from cellular reservoirs are vital but depend on a clear understanding of how viral variants are transmitted and survive in the different cell types that constitute such reservoirs. Mutations in the env gene of HIV may be able to exert a differential influence on viral transmission ability in regard to cell-free and cell-associated viral forms.

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Honeysuckle-encoded atypical microRNA2911 directly targets influenza A viruses - Cell Research

Honeysuckle-encoded atypical microRNA2911 directly targets influenza A viruses - Cell Research | Virology and Bioinformatics from Virology.ca | Scoop.it

Influenza A viruses (IAVs), particularly H1N1, H5N1 and H7N9, pose a substantial threat to public health worldwide. Here, we report that MIR2911, a honeysuckle (HS)-encoded atypical microRNA, directly targets IAVs with a broad spectrum. MIR2911 is highly stable in HS decoction, and continuous drinking or gavage feeding of HS decoction leads to a significant elevation of the MIR2911 level in mouse peripheral blood and lung. Bioinformatics prediction and a luciferase reporter assay showed that MIR2911 could target various IAVs, including H1N1, H5N1 and H7N9. Synthetic MIR2911 significantly inhibited H1N1-encoded PB2 and NS1protein expression, but did not affect mutants in which the MIR2911-binding nucleotide sequences were altered. Synthetic MIR2911, extracted RNA from HS decoction and HS decoction all significantly inhibited H1N1 viral replication and rescued viral infection-induced mouse weight loss, but did not affect infection with a mutant virus in which the MIR2911-binding nucleotide sequences of PB2 and NS1 were altered. Importantly, the inhibitory effect of HS decoction on viral replication was abolished by an anti-MIR2911 antagomir, indicating that the physiological concentration of MIR2911 in HS decoction could directly and sufficiently suppress H1N1 viral replication. MIR2911 also inhibited H5N1 and H7N9 viral replication in vitroand in vivo. Strikingly, administration of MIR2911 or HS decoction dramatically reduced mouse mortality caused by H5N1 infection. Our results demonstrate that MIR2911 is the first active component identified in Traditional Chinese Medicine to directly target various IAVs and may represent a novel type of natural product that effectively suppresses viral infection.

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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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Ebola In The United States: Fears vs. Facts

Ebola In The United States: Fears vs. Facts | Virology and Bioinformatics from Virology.ca | Scoop.it
Stop panicking about a major Ebola outbreak in the United States – you’re in very good hands.
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A Loop Region in the N-Terminal Domain of Ebola Virus VP40 Is Important in Viral Assembly, Budding, and Egress

A Loop Region in the N-Terminal Domain of Ebola Virus VP40 Is Important in Viral Assembly, Budding, and Egress | Virology and Bioinformatics from Virology.ca | Scoop.it
Ebola virus (EBOV) causes viral hemorrhagic fever in humans and can have clinical fatality rates of ~60%. The EBOV genome consists of negative sense RNA that encodes seven proteins including viral protein 40 (VP40). VP40 is the major Ebola virus matrix protein and regulates assembly and egress of infectious Ebola virus particles. It is well established that VP40 assembles on the inner leaflet of the plasma membrane of human cells to regulate viral budding where VP40 can produce virus like particles (VLPs) without other Ebola virus proteins present. The mechanistic details, however, of VP40 lipid-interactions and protein-protein interactions that are important for viral release remain to be elucidated. Here, we mutated a loop region in the N-terminal domain of VP40 (Lys127, Thr129, and Asn130) and find that mutations (K127A, T129A, and N130A) in this loop region reduce plasma membrane localization of VP40. Additionally, using total internal reflection fluorescence microscopy and number and brightness analysis we demonstrate these mutations greatly reduce VP40 oligomerization. Lastly, VLP assays demonstrate these mutations significantly reduce VLP release from cells. Taken together, these studies identify an important loop region in VP40 that may be essential to viral egress.
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De novo assembly of soybean wild relatives for pan-genome analysis of diversity and agronomic traits

De novo assembly of soybean wild relatives for pan-genome analysis of diversity and agronomic traits | Virology and Bioinformatics from Virology.ca | Scoop.it
Approximately 80% of the pan-genome was present in all seven accessions (core), whereas the rest was dispensable and exhibited greater variation than the core genome, perhaps reflecting a role in adaptation to diverse environments.
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This Is What The Ebola Virus Really Looks Like -- And How It Works

This Is What The Ebola Virus Really Looks Like -- And How It Works | Virology and Bioinformatics from Virology.ca | Scoop.it
We're guessing that by now, you're pretty familiar with this little squiggle. But if you want to know what Ebola really looks like -- and how it hijacks cells to wreak havoc inside the human body -- you need a detailed diagram of an Ebola virus parti...
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Genomic and Functional Characteristics of Human Cytomegalovirus Revealed by Next-Generation Sequencing

Genomic and Functional Characteristics of Human Cytomegalovirus Revealed by Next-Generation Sequencing | Virology and Bioinformatics from Virology.ca | Scoop.it
The complete genome of human cytomegalovirus (HCMV) was elucidated almost 25 years ago using a traditional cloning and Sanger sequencing approach. Analysis of the genetic content of additional laboratory and clinical isolates has lead to a better, albeit still incomplete, definition of the coding potential and diversity of wild-type HCMV strains. The introduction of a new generation of massively parallel sequencing technologies, collectively called next-generation sequencing, has profoundly increased the throughput and resolution of the genomics field. These increased possibilities are already leading to a better understanding of the circulating diversity of HCMV clinical isolates. The higher resolution of next-generation sequencing provides new opportunities in the study of intrahost viral population structures. Furthermore, deep sequencing enables novel diagnostic applications for sensitive drug resistance mutation detection. RNA-seq applications have changed the picture of the HCMV transcriptome, which resulted in proof of a vast amount of splicing events and alternative transcripts. This review discusses the application of next-generation sequencing technologies, which has provided a clearer picture of the intricate nature of the HCMV genome. The continuing development and application of novel sequencing technologies will further augment our understanding of this ubiquitous, but elusive, herpesvirus.
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Regulation of Influenza A Virus Nucleoprotein Oligomerisation by Phosphorylation

In the influenza virus ribonucleoprotein complex the oligomerisation of the nucleoprotein is mediated by an interaction between the tail-loop of one molecule and the groove of the neighbouring molecule. In this study we show that phosphorylation of a serine residue (S165) within the groove of influenza A virus nucleoprotein inhibits oligomerisation and, consequently, ribonucleoprotein activity and viral growth. We propose that nucleoprotein oligomerisation in infected cells is regulated by reversible phosphorylation.

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Ewan's Blog: bioinformatician at large: RNA is now a first class bioinformatics molecule.

core function of ribosomes – makin

Via Wei Shen
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Algal virus found in humans, slows brain activity

Algal virus found in humans, slows brain activity | Virology and Bioinformatics from Virology.ca | Scoop.it
Potential pathogen present in nearly half of healthy people surveyed
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Theory and Empiricism in Virulence Evolution

Theory and Empiricism in Virulence Evolution | Virology and Bioinformatics from Virology.ca | Scoop.it

Dobzhansky famously wrote, “Nothing in biology makes sense except in the light of evolution.” Given the importance of viral evolution to disease emergence, pathogenesis, drug resistance, and vaccine efficacy, it has been well studied by theoreticians and experimentalists. Indeed, as the highly theoretical concepts of quasispecies and error catastrophe gained mainstream attention over the last thirty years, notions of viral populations and viral evolution became almost inseparable for many virologists. In contrast, a large body of theoretical work on the evolution of virulence has yet to gain traction in the virology community. Our purpose here is to offer a brief introduction to virulence theory, explain some of its strengths and weaknesses, and suggest how theory might be united with empiric data. While we focus our discussion on viruses, many of the concepts presented are similarly applicable to other prokaryotic and eukaryotic pathogens.

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Developing Skills in Second Year Biological Science Undergraduates: Bioscience Education: Volume 22, Issue 1 (Higher Education Academy)

Developing Skills in Second Year Biological Science Undergraduates: Bioscience Education: Volume 22, Issue 1 (Higher Education Academy) | Virology and Bioinformatics from Virology.ca | Scoop.it
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FastMG: a simple, fast, and accurate maximum likelihood procedure to estimate amino acid replacement rate matrices from large data sets

Amino acid replacement rate matrices are a crucial component of many protein analysis systems such as sequence similarity search, sequence alignment, and phylogenetic inference. Ideally, the rate matrix reflects the mutational behavior of the actual data under study; however, estimating amino acid replacement rate matrices requires large protein alignments and is computationally expensive and complex. As a compromise, sub-optimal pre-calculated generic matrices are typically used for protein-based phylogeny. Sequence availability has now grown to a point where problem-specific rate matrices can often be calculated if the computational cost can be controlled.
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The hemagglutinin of the influenza A(H1N1)pdm09 is mutating towards stability

The last influenza A pandemic provided an excellent opportunity to study the adaptation of the influenza A(H1N1)pdm09 virus to the human host. Particularly, due to the availability of sequences taken from isolates since the beginning of the pandemic until date, we could monitor amino acid changes that occurred in the hemagglutinin (HA) as the virus spread worldwide and became the dominant H1N1 strain. HA is crucial to viral infection because it binds to sialidated cell-receptors and mediates fusion of cell and viral membranes; because antibodies that bind to HA may block virus entry to the cell, this protein is subjected to high selective pressure. Multiple alignment analysis of sequences of the HA from isolates taken since 2009 to date allowed us to find amino acid changes that were positively selected as the pandemic progressed. We found nine changes that became prevalent: HA1 subunits D104N, K166Q, S188T, S206T, A259T, and K285E; and HA2 subunits E47K, S124N, and E172K. Most of these changes were located in areas involved in inter- and intrachain interactions, while only two (K166Q and S188T) were located in known antigenic sites. We conclude that selective pressure on HA was aimed to improve its functionality and hence virus fitness, rather than at avoidance of immune recognition.

 

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Could Reston virus be a vaccine for Ebola virus?

Could Reston virus be a vaccine for Ebola virus? | Virology and Bioinformatics from Virology.ca | Scoop.it
I have received many questions about whether immunizing with Reston virus could protect against infection with Ebola virus. The answer is no.
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The Ebola Number You Haven't Heard: 80% Of U.S. Ebola Patients Have Survived

The Ebola Number You Haven't Heard: 80% Of U.S. Ebola Patients Have Survived | Virology and Bioinformatics from Virology.ca | Scoop.it
Ebola's a death sentence — or at least, that's the popular wisdom. And in the current West Africa outbreak, that's not far from the truth. The Ebola survival rate in Guinea might be somewhere around 30%.

Via Technical Dr. Inc., Mel Melendrez-Vallard
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Omics Find Chinks in Ebola Armor for Vaccine and Drug Development

Omics Find Chinks in Ebola Armor for Vaccine and Drug Development | Virology and Bioinformatics from Virology.ca | Scoop.it

On October 12, the Ebola crisis hit home in a new way, as the first case of person-to-person transmission of the virus was reported in Texas. A nurse who helped treat the Liberian man who died from the virus has tested positive for the disease, despite wearing a gown, gloves, mask, and other protective gear while in contact with the victim.

Ebola (EBOV), a single-stranded RNA filovirus, causes infections characterized by immune suppression and a systemic inflammatory response. This results in impairment of the vascular, coagulation, and immune systems, leading to multiorgan failure and shock (in some ways resembling septic shock).

But while overwhelming challenges in controlling and treating this disease remain, the availability of genomic and proteomic data accumulated and shared by researchers since the virus’ discovery in 1976 has already translated into invaluable knowledge about the deadly RNA virus, pinpointing potential targets for diagnostics, vaccines, and therapeutics.

Ed Rybicki's insight:

Of COURSE 'omics will solve the problem.  It can solve EVERYTHING B-)

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Hepatitis A virus and the origins of picornaviruses

Hepatitis A virus and the origins of picornaviruses | Virology and Bioinformatics from Virology.ca | Scoop.it
Hepatitis A virus (HAV) remains enigmatic, despite 1.4 million cases worldwide annually. It differs radically from other picornaviruses, existing in an enveloped form and being unusually stable, both genetically and physically, but has proved difficult to study. Here we report high-resolution X-ray structures for the mature virus and the empty particle. The structures of the two particles are indistinguishable, apart from some disorder on the inside of the empty particle. The full virus contains the small viral protein VP4, whereas the empty particle harbours only the uncleaved precursor, VP0. The smooth particle surface is devoid of depressions that might correspond to receptor-binding sites. Peptide scanning data extend the previously reported VP3 antigenic site, while structure-based predictions suggest further epitopes. HAV contains no pocket factor and can withstand remarkably high temperature and low pH, and empty particles are even more robust than full particles. The virus probably uncoats via a novel mechanism, being assembled differently to other picornaviruses. It utilizes a VP2 /`domain swap/' characteristic of insect picorna-like viruses, and structure-based phylogenetic analysis places HAV between typical picornaviruses and the insect viruses. The enigmatic properties of HAV may reflect its position as a link between /`modern/' picornaviruses and the more /`primitive/' precursor insect viruses; for instance, HAV retains the ability to move from cell-to-cell by transcytosis.
Ed Rybicki's insight:

Cool...B-)

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We Have Nothing: The Human Cost Of Ebola

We Have Nothing: The Human Cost Of Ebola | Virology and Bioinformatics from Virology.ca | Scoop.it
Harrowing personal stories reveal the catastrophic impact of the deadly virus on one of the world's poorest regions.
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Footage From 1976 Documents Discovery of Ebola Virus

Footage From 1976 Documents Discovery of Ebola Virus | Virology and Bioinformatics from Virology.ca | Scoop.it
In 1976, a group of health workers took a pair of film cameras to what was then known as Zaire and documented their discovery of a new, deadly virus. Today we know that virus as Ebola.
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