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At least 343 records · Page 19Linked to original sources
bioRxiv2016

Influence of a mono-frequency sound on bacteria can be a function of the sound-level

Chromobacterium violaceum was subjected to sonic stimulation with 300 Hz sound, at five different levels of loudness in the range of 70 - 89.5 dB. Sonic stimulation was found to affect bacterial growth and quorum sensing regulated pigment (violacein) production significantly. Magnitude of this effect was found to be dependent on sound-level. The minimum critical difference required to cause any statistically significant change in bacterial response with respect to sound-level was found to be 13 dB. Growth of C. violaceum was affected more at lower sound intensity, whereas pigment production was affected more at higher sound intensity. Additional experiments with C. violaceum and Serratia marcescens indicated that even a silent speaker emitting no sound can alter bacterial growth and/or pigment production upto a minor extent. Size of the test tube in which bacteria are exposed to sonic stimulation, was not found to affect the results much.

Microbiology↗
bioRxiv2016

Mycobacterium ulcerans low infectious dose and atypical mechanical transmission support insect bites and puncturing injuries in the spread of Buruli ulcer.

Addressing the transmission enigma of the neglected disease Buruli ulcer (BU) is a World Health Organization priority. In Australia, we have observed an association between mosquitoes harboring the causative agent, Mycobacterium ulcerans, and BU. Here we tested a contaminated skin model of BU transmission by dipping the tails from healthy mice in cultures of the causative agent, Mycobacterium ulcerans. Tails were exposed to mosquito (Aedes notoscriptus and Aedes aegypti) blood feeding or punctured with sterile needles. Two of 11 of mice with M. ulcerans contaminated tails exposed to feeding A. notoscriptus mosquitoes developed BU. Eighteen of 20 mice subjected to contaminated tail needle puncture developed BU. Mouse tails coated only in bacteria did not develop disease. We observed a low infectious dose-50 of four colony-forming units and a median incubation time of 12 weeks, consistent with data from human infections. We have uncovered a highly efficient and biologically plausible atypical transmission mode of BU via natural or anthropogenic skin punctures.\n\nAuthor summaryBuruli ulcer is a neglected tropical disease caused by infection with Mycobacterium ulcerans. Unfortunately, how people contract this disease is not well understood. Here we show for the first time using experimental infections in mice that a very low dose of M. ulcerans delivered beneath the skin by a minor injury caused by a blood-feeding insect (mosquito) or a needle puncture is sufficient to cause Buruli ulcer. This research provides important laboratory evidence to advance our understanding of Buruli ulcer disease transmission.

Microbiology↗
bioRxiv2016

Interactions between helicase and primase are crucial for DNA replication in the enteropathogen Clostridium difficile

DNA replication is an essential and conserved process in all domains of life and may serve as a target for the development of new antimicrobials. However, such developments are hindered by a limited understanding of DNA replication in pathogenic micro-organisms. Clostridium difficile is the main cause of health-care associated diarrhea and its DNA replication machinery is virtually uncharacterized. We identified the replicative helicase (CD3657), the helicase loader ATPase (CD3654) and primase (CD1454) of C. difficile and reconstitute helicase and primase activity in vitro. We demonstrate a direct and ATP-dependent interaction between the helicase loader and the helicase. We find that helicase activity is dependent on the presence of primase in vitro. The trinucleotide specificity of primase, which we find to be determined by a single lysine residue, is similar to extreme thermophile Aquifex aeolicus but the presence of helicase allows more efficient de novo synthesis of RNA primers from non-preferred trinucleotides. Thus, helicase-primase interactions constitute a crucial aspect of DNA replication initiation in C. difficile and helicase loading and activation in this organism differs critically from that of the Gram-positive model organism Bacillus subtilis.

Microbiology↗
bioRxiv2016

Individual level predictions of Staphylococcus aureus bacteraemia-associated mortality.

The bacterium Staphylococcus aureus is a major human pathogen, where the emergence of antibiotic resistance is a global public-health concern. Host factors such as age and the presence of co-morbidities have been implicated in a worse outcome for patient. However, this is complicated by the highly complex and multi-faceted nature of bacterial virulence, which has so far prevented a robust mapping between genotype, phenotype and infection outcome. To investigate the role of bacterial and host factors in contributing to S. aureus bacteraemia-associated mortality we sequenced a collection of clinical isolates (of the MLST clonal complex CC22) from patients with bloodstream infections and quantified specific virulence phenotypes. A genome-wide association scan identified several novel virulence-affecting loci, which we validated using a functional genomics approach. Analysing the data comprising bacterial genotype and phenotype as well as clinical meta-data within a machine-learning framework revealed that mortality associated with CC22 bacteraemia is not only influenced by the interactions between host and bacterial factors but can also be predicted at the individual patient-level to a high degree of accuracy. This study clearly demonstrates the potential of using a combined genomics and data analytic approach to enhance our understanding of bacterial pathogenesis. Considering both host and microbial factors, including whole genome sequence and phenotype data, within a predictive framework could thus pave the way towards personalised medicine and infectious disease management.

Microbiology↗
bioRxiv2016

Deep mutational scanning identifies sites in influenza nucleoprotein that affect viral inhibition by MxA

The innate-immune restriction factor MxA inhibits influenza replication by targeting the viral nucleoprotein (NP). Human influenza is more resistant than avian influenza to inhibition by human MxA, and prior work has compared human and avian viral strains to identify amino-acid differences in NP that affect sensitivity to MxA. However, this strategy is limited to identifying sites in NP where mutations that affect MxA sensitivity have fixed during the small number of documented zoonotic transmissions of influenza to humans. Here we use an unbiased deep mutational scanning approach to quantify how all {approx}10,000 amino-acid mutations to NP affect MxA sensitivity. We both identify new sites in NP where mutations affect MxA resistance and re-identify mutations known to have increased MxA resistance during historical adaptations of influenza to humans. Most of the sites where mutations have the greatest effect are almost completely conserved across all influenza A viruses, and the amino acids at these sites confer relatively high resistance to MxA. These sites cluster in regions of NP that appear to be important for its recognition by MxA. Overall, our work systematically identifies the sites in influenza nucleoprotein where mutations affect sensitivity to MxA. We also demonstrate a powerful new strategy for identifying regions of viral proteins that affect interactions with host factors.\n\nAuthor SummaryDuring viral infection, human cells express proteins that can restrict virus replication. However, in many cases it remains unclear what determines the sensitivity of a given viral strain to a particular restriction factor. Here we use a high-throughput approach to measure how all amino-acid mutations to the nucleoprotein of influenza virus affect restriction by the human protein MxA. We find several dozen sites where mutations substantially affect influenzas sensitivity to MxA. While a few of these sites are known to have fixed mutations during past adaptations of influenza to humans, most of the sites are broadly conserved across all influenza strains and have never previously been described as affecting MxA resistance. Our results therefore show that the known historical evolution of influenza has only involved substitutions at a small fraction of the sites where mutations can in principle affect MxA resistance. We suggest that this is because many sites are already broadly fixed at amino acids that confer high resistance.

Microbiology↗
bioRxiv2016

Application of the stochastic labeling methods with random-sequence barcodes for simultaneous quantification and sequencing of environmental 16S rRNA genes

Next-generation sequencing (NGS) is a powerful tool for analyzing environmental DNA and provides the comprehensive molecular view of microbial communities. For obtaining the copy number of particular sequences in the NGS library, however, additional quantitative analysis as quantitative PCR (qPCR) or digital PCR (dPCR) is required. Furthermore, number of sequences in a sequence library does not always reflect the original copy number of a target gene because of biases caused by PCR amplification, making it difficult to convert the proportion of particular sequences in the NGS library to the copy number using the mass of input DNA. To address this issue, we applied stochastic labeling approach with random-tag sequences and developed a NGS-based quantification protocol, which enables simultaneous sequencing and quantification of the targeted DNA. This quantitative sequencing (qSeq) is initiated from single-primer extension (SPE) using a primer with random tag adjacent to the 5 end of target-specific sequence. During SPE, each DNA molecule is stochastically labeled with the random tag. Subsequently, first-round PCR is conducted, specifically targeting the SPE product, followed by second-round PCR to index for NGS. The number of random tags is only determined during the SPE step and is therefore not affected by the two rounds of PCR that may introduce amplification biases. In the case of 16S rRNA genes, after NGS sequencing and taxonomic classification, the absolute number of target phylotypes 16S rRNA gene can be estimated by Poisson statistics by counting random tags incorporated at the end of sequence. To test the feasibility of this approach, the 16S rRNA gene of Sulfolobus tokodaii was subjected to qSeq, which resulted in accurate quantification of 5.0 x 103 to 5.0 x 104 copies of the 16S rRNA gene. Furthermore, qSeq was applied to mock microbial communities and environmental samples, and the results were comparable to those obtained using digital PCR and relative abundance based on a standard sequence library. We demonstrated that the qSeq protocol proposed here is advantageous for providing less-biased absolute copy numbers of each target DNA with NGS sequencing at one time. By this new experiment scheme in microbial ecology, microbial community compositions can be explored in more quantitative manner, thus expanding our knowledge of microbial ecosystems in natural environments.

Microbiology↗
bioRxiv2016

The Transcriptome of the Avian Malaria Parasite Plasmodium ashfordi Displays Host-Specific Gene Expression

Malaria parasites (Plasmodium spp.) include some of the worlds most widespread and virulent pathogens. Our knowledge of the molecular mechanisms these parasites use to invade and exploit hosts other than mice and primates is, however, extremely limited. It is therefore imperative to characterize transcriptome-wide gene expression from non-model malaria parasites and how this varies across host individuals. Here, we used high-throughput Illumina RNA-sequencing on blood from wild-caught Eurasian siskins experimentally infected with a clonal strain of the avian malaria parasite Plasmodium ashfordi (lineage GRW2). By using a multi-step approach to filter out host transcripts, we successfully assembled the blood-stage transcriptome of P. ashfordi. A total of 11 954 expressed transcripts were identified, and 7 860 were annotated with protein information. We quantified gene expression levels of all parasite transcripts across three hosts during two infection stages - peak and decreasing parasitemia. Interestingly, parasites from the same host displayed remarkably similar expression profiles during different infection stages, but showed large differences across hosts, indicating that P. ashfordi may adjust its gene expression to specific host individuals. We further show that the majority of transcripts are most similar to the human parasite Plasmodium falciparum, and a large number of red blood cell invasion genes were discovered, suggesting evolutionary conserved invasion strategies between mammalian and avian Plasmodium. The transcriptome of P. ashfordi and its host-specific gene expression advances our understanding of Plasmodium plasticity and is a valuable resource as it allows for further studies analysing gene evolution and comparisons of parasite gene expression.

Microbiology↗
bioRxiv2016

Deep Annotation of Protein Function across Diverse Bacteria from Mutant Phenotypes

SummaryThe function of nearly half of all protein-coding genes identified in bacterial genomes remains unknown. To systematically explore the functions of these proteins, we generated saturated transposon mutant libraries from 25 diverse bacteria and we assayed mutant phenotypes across hundreds of distinct conditions. From 3,903 genome-wide mutant fitness assays, we obtained 14.9 million gene phenotype measurements and we identified a mutant phenotype for 8,487 proteins with previously unknown functions. The majority of these hypothetical proteins (57%) had phenotypes that were either specific to a few conditions or were similar to that of another gene, thus enabling us to make informed predictions of protein function. For 1,914 of these hypothetical proteins, the functional associations are conserved across related proteins from different bacteria, which confirms that these associations are genuine. This comprehensive catalogue of experimentally-annotated protein functions also enables the targeted exploration of specific biological processes. For example, sensitivity to a DNA-damaging agent revealed 28 known families of DNA repair proteins and 11 putative novel families. Across all sequenced bacteria, 14% of proteins that lack detailed annotations have an ortholog with a functional association in our data set. Our study demonstrates the utility and scalability of high-throughput genetics for large-scale annotation of bacterial proteins and provides a vast compendium of experimentally-determined protein functions across diverse bacteria.

Microbiology↗
bioRxiv2016

A novel ENU-induced ankyrin-1 mutation impairs parasite invasion and increases erythrocyte clearance during malaria infection in mice

Genetic defects in various red blood cell (RBC) cytoskeletal proteins have been long associated with changes in susceptibility towards malaria infection. In particular, while ankyrin (Ank-1) mutations account for approximately 50% of hereditary spherocytosis (HS) cases, an association with malaria is not well-established, and conflicting evidence has been reported. We describe a novel N-ethyl-N-nitrosourea (ENU)-induced ankyrin mutation MRI61689 that gives rise to two different ankyrin transcripts: one with an introduced splice acceptor site resulting a frameshift, the other with a skipped exon. Ank-1(MRI61689/+) mice exhibit an HS-like phenotype including reduction in mean corpuscular volume (MCV), increased osmotic fragility and reduced RBC deformability. They were also found to be resistant to rodent malaria Plasmodium chabaudi infection. Parasites in Ank-1(MRI61689/+) erythrocytes grew normally, but red cells showed resistance to merozoite invasion. Uninfected Ank-1(MRI61689/+) erythrocytes were also more likely to be cleared from circulation during infection; the \"bystander effect\". This increased clearance is a novel resistance mechanism which was not observed in previous ankyrin mouse models. We propose that this bystander effect is due to reduced deformability of Ank-1(MRI61689/+) erythrocytes. This paper highlights the complex roles ankyrin plays in mediating malaria resistance.

Microbiology↗
bioRxiv2016

Quorum sensing modulatory effect of sound stimulation on Serratia marcescens and Pseudomonas aeruginosa

Effect of nine different mono-frequency sound stimuli on two gram-negative bacteria (Pseudomonas aeruginosa and Serratia marcescens) was investigated. Frequency of the test sound ranged from 100 Hz to 2,000 Hz. Both the test bacteria responded differently to sonic stimulation. Sound corresponding to 600 HZ caused a notable reduction in quorum sensing (QS) regulated production of the pigment pyoverdine by P. aeruginosa. 400 Hz sound affected prodigiosin production by S. marcescens the most. 500 Hz sound could enhance prodigiosin production without affecting growth of the producing bacterium, suggesting the effect purely to be QS modulatory. This study has demonstrated the capacity of the sound waves of affecting bacterial growth and quorum sensing regulated metabolite production.

Microbiology↗
bioRxiv2016

Zika virus replication in the mosquito Culex quinquefasciatus in Brazil

Zika virus (ZIKV) is a flavivirus that has recently been associated with increased incidence of neonatal microcephaly and other neurological disorders. The virus is primarily transmitted by mosquito bite, although other routes of infection have been implicated in some cases. The Aedes aegypti mosquito is considered to be the main vector to humans worldwide, but there is evidence of other mosquito species, including Culex quinquefasciatus, playing a role in the Brazilian outbreak. To test this hypothesis, we experimentally compared the vectorial competence of laboratory-reared A. aegypti and C. quinquefasciatus. We found ZIKV in the midgut, salivary glands, and saliva of artificially fed C. quinquefasciatus. Additionally, we collected ZIKV-infected C. quinquefasciatus from urban areas of high microcephaly incidence in Recife, Brazil. Take into account; these findings indicate that there may be a wider range of vectors for ZIKV than anticipated.

Microbiology↗
bioRxiv2016

Investigation of the sexual reproduction strategy of the Perigord black truffle (Tuber melanosporum Vittad.) revealed trioecy

The Perigord black truffle (Tuber melanosporum Vittad.) is a heterothallic ascomycete that establishes ectomycorrhizal symbiosis with trees and shrubs. Small-scale genetic structures of female genotypes in truffle orchards are known, but it has not yet been studied in male genotypes. In this study, our aim was to characterize the small-scale genetic structure of both male and female genotypes over five years in an orchard to better understand the T. melanosporum sexual reproduction strategy, male genotype dynamics, and origins. Two-hundred forty-one ascocarps, 475 ectomycorrhizas, and 20 soil cores were harvested and genotyped using microsatellites and mating type genes. Isolation by distance analysis revealed pronounced small-scale genetic structures for both female and male genotypes. The genotypic diversity was higher for male than female genotypes with numerous small size genotypes suggesting an important turnover due to ascospore recruitment. Larger and perennial female and male genotypes were also detected. Only three genotypes (1.5 %) were found as both female and male genotypes (hermaphrodites) while most were detected only as female or male genotype (dioecy). Our results suggest that germinating ascospores act as male genotypes, but we also proposed that soil mycelium could be a reservoir of male genotypes.

Microbiology↗
bioRxiv2016

A single intracellular protein governs the critical transition from an individual to a coordinated population response during quorum sensing: Origins of primordial language

Quorum sensing (QS) explains a type of bacterial cell-cell communication mediated by exocellular compounds that act as autoinducers (AIs). As such, QS can be considered the most primordial form of language. QS has profound implications for the control of many important traits (e.g. biofilm formation, secretion of virulence factors, etc.). Conceptually, the QS response can be split into its \"listening\" and \"speaking\" components, i.e. the power to sense AI levels vs. the ability to synthesize and release these molecules. By explaining the cell-density dependence of QS behavior as the consequence of the systems arrival to a threshold AI concentration, models of QS have traditionally assumed a salient role for the \"QS speaking\" module during bacterial cell-to-cell communication. In this paper, we have provided evidence that challenges this AI-centered view of QS and establishes LuxR-like activators at the center of QS. Our observation that highly coordinated, cell-density dependent responses can occur in the absence of AI production, implies that the ability to launch such responses is engrained within the \"QS listening\" module. Our data indicates that once a critical threshold of intracellular activator monomers in complex with AI is reached, a highly orchestrated QS response ensues. While displaying a clear cell-density dependence, such response does not strictly require the sensing of population levels by individual cells. We additionally show, both in vivo and in silico, that despite their synchronous nature, QS responses do not require that all the cells in the population participate in the response. Central to our analysis was the discovery that percolation theory (PT) can be used to mathematically describe QS responses. While groundbreaking, our results are in agreement with and integrate the latest conclusions reached in the field. We explain for the first time, the cell-density-dependent synchronicity of QS responses as the function of a single protein, the LuxR-like activator, capable of coordinating the temporal response of a population of cells in the absence of cell-to-cell communication. Being QS the most primordial form of speech, our results have important implications for the evolution of language in its ancient chemical form.\n\nAbbreviations

Microbiology↗
bioRxiv2016

Rapid metagenomic next-generation sequencing during an investigation of hospital-acquired human parainfluenza virus 3 infections

Metagenomic next-generation sequencing (mNGS) is increasingly used for the unbiased detection of viruses, bacteria, fungi, and eukaryotic parasites in clinical samples. Whole genome sequencing (WGS) of clinical bacterial isolates has been shown to inform hospital infection prevention practices, but the use of this technology during potential respiratory virus outbreaks has not been taken advantage of. Here, we report on the use of mNGS to inform the real-time infection prevention response to a cluster of hospital-acquired human parainfluenza 3 virus (HPIV3) infections at a childrens hospital. Isolates from 3 patients with hospital-acquired HPIV3 identified over a 12-day period on a general medical unit and 10 temporally-associated isolates from patients with community-acquired of HPIV3 were analyzed. Our sample-to-sequencer time was <24 hours while our sample-to-answer turn-around time was <60 hours with a hands-on time of approximately 6 hours. Eight (2 case isolates and 6 control isolates) of 13 samples had sufficient sequencing coverage to yield whole genomes for HPIV3, while 10 (2 cases and 8 controls) of 13 samples gave partial genomes and all 13 samples had >1 read to HPIV3. Phylogenetic clustering revealed the presence of identical HPIV3 genomic sequence in the two of the cases with hospital-acquired infection, consistent with the concern for recent transmission within the medical unit. Adequate sequence coverage was not recovered for the third case. This work demonstrates the promise of mNGS to provide actionable information for infection control in addition to microbial detection.

Microbiology↗
bioRxiv2016

A large collection of novel nematode-infecting microsporidia and their diverse interactions with C. elegans and other related nematodes

Microsporidia are fungi-related intracellular pathogens that may infect virtually all animals, but are poorly understood. The nematode Caenorhabditis elegans has recently become a model host for studying microsporidia through the identification of its natural microsporidian pathogen Nematocida parisii. However, it was unclear how widespread and diverse microsporidia infections are in C. elegans or other related nematodes in the wild. Here we describe the isolation and culture of 47 nematodes with microsporidian infections. N. parisii is found to be the most common microsporidia infecting C. elegans in the wild. In addition, we further describe and name six new species in the Nematocida genus. Our sampling and phylogenetic analysis further identify two subclades that are genetically distinct from Nematocida, and we name them Enteropsectra and Pancytospora. Interestingly, unlike Nematocida, these two genera belong to the main clade of microsporidia that includes human pathogens. All of these microsporidia are horizontally transmitted and most specifically infect intestinal cells, except Pancytospora epiphaga that replicates mostly in the epidermis of its Caenorhabditis host. At the subcellular level in the infected host cell, spores of the novel genus Enteropsectra show a characteristic apical distribution and exit via budding off of the plasma membrane, instead of exiting via exocytosis as spores of Nematocida. Host specificity is broad for some microsporidia, narrow for others: indeed, some microsporidia can infect Oscheius tipulae but not its sister species, and conversely. We also show that N. ausubeli fails to strongly induce in C. elegans the transcription of genes that are induced by other Nematocida species, suggesting it has evolved mechanisms to prevent induction of this host response. Altogether, these newly isolated species illustrate the diversity and ubiquity of microsporidian infections in nematodes, and provide a rich resource to investigate host-parasite coevolution in tractable nematode hosts.\n\nAuthor SummaryMicrosporidia are microbial parasites that live inside their host cells and can cause disease in humans and many other animals. The small nematode worm Caenorhabditis elegans has recently become a convenient model host for studying microsporidian infections. In this work, we sample Caenorhabditis and other small nematodes and 47 associated microsporidian strains from the wild. We characterize the parasites for their position in the evolutionary tree of microsporidia and for their lifecycle and morphology. We find several new species and genera, especially some that are distantly related to the previously known Nematocida parisii and instead closely related to human pathogens. We find that some of these species have a narrow host range. We studied two species in detail using electron microscopy and uncover a new likely mode of exit from the host cell, by budding off the host cell plasma membrane rather than by fusion of a vesicle to the plasma membrane as in N. parisii. We also find a new species that infects the epidermis and muscles of Caenorhabditis rather than the host intestinal cells and is closely related to human pathogens. Finally, we find that one Nematocida species fails to elicit the same host response that other Nematocida species do. These new microsporidia open up many windows into microsporidia biology and opportunities to investigate host-parasite coevolution in the C. elegans system.

Microbiology↗
bioRxiv2016

Metatranscriptomics supports mechanism for biocathode electroautotrophy by "Candidatus Tenderia electrophaga"

Biocathodes provide a stable electron source to drive reduction reactions in electrotrophic microbial electrochemical systems. Electroautotrophic biocathode communities may be more robust than monocultures in environmentally relevant settings, but some members are not easily cultivated outside of the electrode environment. We previously used metagenomics and metaproteomics to propose a pathway for coupling extracellular electron transfer (EET) to carbon fixation in \"Candidatus Tenderia electrophaga\", an uncultivated but dominant member of the Biocathode-MCL electroautotrophic community. Here we validate and refine this proposed pathway using differential metatranscriptomics of replicate MCL reactors poised at the growth potential 310 mV and the suboptimal 470 mV (vs. standard hydrogen electrode). At both potentials, transcripts from \"Ca. Tenderia electrophaga\" were more abundant than from any other organism and its relative activity was positively correlated with current. Several genes encoding key components of the proposed \"Ca. Tenderia electrophaga\" EET pathway were more highly expressed at 470 mV, consistent with a need for cells to acquire more electrons to obtain the same amount of energy as at 310 mV. These included cyc2, encoding a homolog of a protein known to be involved in iron oxidation, confirmed to be differentially expressed by droplet digital PCR of independent biological replicates. Average expression of all CO2 fixation related genes is 1.23-fold higher at 310 mV, indicating that reduced energy availability at 470 mV decreased CO2 fixation. Our results substantiate the claim that \"Ca. Tenderia electrophaga\" is the key MCL electroautotroph, which will help guide further development of this community for microbial electrosynthesis.\n\nIMPORTANCEBacteria that directly use electrodes as metabolic electron donors (biocathodes) have been proposed for applications ranging from microbial electrosynthesis to advanced bioelectronics for cellular communication with machines. However, just as we understand very little about oxidation of analogous natural insoluble electron donors, such as iron oxide, the organisms and extracellular electron transfer (EET) pathways underlying the electrode-cell direct electron transfer processes are almost completely unknown. Biocathodes are a stable biofilm cultivation platform to interrogate both the rate and mechanism of EET using electrochemistry and study the electroautotrophic organisms that catalyze these reactions. Here we provide new evidence supporting the hypothesis that the uncultured bacterium \"Candidatus Tenderia electrophaga\" directly couples extracellular electron transfer to CO2 fixation. Our results provide insight into developing biocathode technology, such as microbial electrosynthesis, as well as advancing our understanding of chemolithoautotrophy.

Microbiology↗
bioRxiv2016

Identification of important amino acid replacements in the 2013-2016 Ebola virus outbreak

The phylogenetic relationships of Zaire ebolavirus have been intensively analysed over the course of the 2013-2016 outbreak. However, there has been limited consideration of the functional impact of this variation. Here we describe an analysis of the available sequence data in the context of protein structure and phylogenetic history. Amino acid replacements are rare and predicted to have minor effects on protein stability. Synonymous mutations greatly outnumber nonsynonymous mutations, and most of the latter fall into unstructured intrinsically disordered regions, indicating that purifying selection is the dominant mode of selective pressure. However, one replacement, occurring early in the outbreak in Gueckedou in Guinea on 31st March 2014 (alanine to valine at position 82 in the GP protein), is close to the site where the virus binds to the host receptor NPC1 and is located in the phylogenetic tree at the origin of the major B lineage of the outbreak. The functional and evolutionary evidence indicates this A82V change likely has consequences for EBOV's host specificity and hence adaptation to humans.

Microbiology↗