International health officials warned Thursday that recent budget cuts have impeded the ability of the World Health Organization to respond to the Ebola outbreak that has killed at least 603 people in Guinea, Liberia and Sierra Leone.
Summary: Codon optimization has been widely used for designing synthetic genes to improve their expression in heterologous host organisms. However, most of the existing codon optimization tools consider a single design criterion and/or implement a rather rigid user interface to yield only one optimal sequence, which may not be the best solution. Hence, we have developed Codon Optimization OnLine (COOL), which is the first web tool that provides the multi-objective codon optimization functionality to aid systematic synthetic gene design. COOL supports a simple and flexible interface for customizing various codon optimization parameters such as codon adaptation index, individual codon usage and codon pairing. In addition, users can visualize and compare the optimal synthetic sequences with respect to various fitness measures. User-defined DNA sequences can also be compared against the COOL optimized sequences to show the extent by which the user’s sequences can be further improved.
The ongoing conflict between viruses and their hosts can drive the co-evolution between host immune genes and viral suppressors of immunity. It has been suggested that an evolutionary ‘arms race’ may occur between rapidly evolving components of the antiviral RNAi pathway ofDrosophila and viral genes that antagonize it. We have recently shown that viral protein 1 (VP1) of Drosophila melanogaster Nora virus (DmelNV) suppresses Argonaute-2 (AGO2)-mediated target RNA cleavage (slicer activity) to antagonize antiviral RNAi. Here we show that viral AGO2 antagonists of divergent Nora-like viruses can have host specific activities. We have identified novel Nora-like viruses in wild-caught populations of D. immigrans (DimmNV) and D. subobscura (DsubNV) that are 36% and 26% divergent from DmelNV at the amino acid level.
Infection with influenza A virus (IAV) is a major cause of worldwide morbidity and mortality. Recent findings indicate that T cell immunity is key to limiting severity of disease arising from IAV infection, particularly in instances where antibody immunity is ineffective. As such, there is a need to understand better the mechanisms that mediate effective IAV-specific cellular immunity, especially given that T cell immunity must form an integral part of any vaccine designed to elicit crossreactive immunity against existing and new strains of influenza virus. Here, we review the current understanding of cellular immunity to IAV, highlighting recent findings that demonstrate important roles for both CD4+ and CD8+ T cell immunity in protection from IAV-mediated disease.
Advances in high-throughput technologies have enabled extensive generation of multi-level omics data. These data are crucial for systems biology research, though they are complex, heterogeneous, highly dynamic, incomplete and distributed among public databases. This leads to difficulties in data accessibility and often results in errors when data are merged and integrated from varied resources. Therefore, integration and management of systems biological data remain very challenging.
We found that 72% of Web sites are still available at the published addresses, only 9% of services are completely unavailable. Older addresses often redirect to new pages. We checked the functionality of all available services: for 33%, we could not test functionality because there was no example data or a related problem; 13% were truly no longer working as expected; we could positively confirm functionality only for 45% of all services.
Robert F. Kennedy Jr. is coming out with a new book that claims thimerosal in vaccines causes autism. This claim has been thoroughly discredited, but RFK Jr. believes that it's all a big conspiracy and that he's right. His crazy anti-vaccine views coupled with his fame make for an especially dangerous combination.
This title should really read “Practical data management takes its show ACROSS the road” because that’s what I’m actually doing. Next week, I’ll be a co-instructor for the second Data Carpentry bootcamp at MSU’s BEACON Center, which is right across the street from me. Who said agricultural ecologists don’t get to travel?
Next generation sequencing (NGS) has revolutionized biomedical research in the last decade and led to a continues stream of developments in bioinformatics addressing the need for fast and space efficient solutions for analyzing NGS data. Often researchers need to analyze a set of genomic sequences which stem from closely related species or are indeed individuals of the same species. Hence the analyzed sequences are very similar. For analyses where local changes in the examined sequence induce only local changes in the results it is obviously desirable to examine identical or similar regions not repeatedly.
Herpes simplex virus 1 (HSV-1) replicates in the nucleus and induces chromosomal DNA damage, including DNA double-strand breaks (DSBs). Host cells repair DSBs by non-homologous end joining (NHEJ) or homologous recombination, but how the cell chooses between these pathways and the impact of this decision on viral replication has been unclear. Karttunen et al. now show that HSV-1 inhibits NHEJ by triggering the Fanconi anaemia pathway. HSV-1 infection induced mono-ubiquitination of the two Fanconi anaemia pathway effectors, FANCI and FANCI-D2, which resulted in their redistribution from sites of DNA damage to viral replication compartments. Furthermore, HSV-1 replication was severely reduced in cells lacking components of the Fanconi anaemia pathway, and inhibition of NHEJ in these cells was sufficient to restore viral growth. These data suggest that HSV-1 manipulates the Fanconi anaemia pathway to suppress NHEJ and promote viral replication.
High-throughput sequencing (HTS) provides the means to analyze clinical specimens at unprecedented molecular detail. While this technology has been successfully applied to virus discovery and other related areas of research, HTS methodology has yet to be exploited for use in a clinical setting for routine diagnostics. Here, a bioinformatics pipeline (ezVIR) was designed to process HTS data from any of the standard platforms and to evaluate the entire spectrum of known human viruses at once, providing results that are easy to interpret and customizable. The pipeline works by identifying the most likely viruses present in the specimen given the sequencing data. Additionally, ezVIR can generate optional reports for strain typing, genome coverage histograms, and can perform cross-contamination analysis for specimens prepared in series. In this pilot study, the pipeline was challenged using HTS data from 20 clinical specimens representative of those most often collected and analyzed in daily practice. The specimens (5 cerebrospinal fluids, 7 bronchoalveolar lavages, 5 plasma, 2 serums and 1 nasopharyngeal aspirate) were originally found to be positive for a diverse range of DNA or RNA viruses by routine molecular diagnostics. The ezVIR pipeline correctly identified 14/14 specimens containing viruses with genomes < 40,000 bp, and 4/6 specimens positive for large genome viruses. Although further validation is needed to evaluate sensitivity and to define detection cut-offs, results obtained in this pilot study indicate that the overall detection success rate, coupled to the ease of interpreting the analysis reports, makes it worth considering using HTS for clinical diagnostics.