St.Jude Children’s Research Hospital scientists report that avian H2N2 influenza A viruses related to 1957-1958 pandemic infect human cells and spread among ferrets; may aid identification of emerging threats...
Viruses are no fun to get. It may come as a surprise then that a new form of cancer treatment actually infects patients with viruses to help them. How does this treatment work? Which specific age group is it aimed at to help?
Papillomaviruses have a remarkable infection cycle that depends on the development of a stratified epithelium. The virus infects the lower, dividing layers of the epithelium and viral genomes replicate at low copy number, and are maintained in these cells, for long periods of time. As infected cells differentiate and move to the surface of the epithelium, they switch on high level viral DNA replication, synthesize capsid proteins and form new viral particles. Viral replication takes place in nuclear foci and is dependent on the E1 and E2 replication proteins. Brd4 is a cellular chromatin binding protein that interacts with E2 and is important for transcriptional regulation of papillomaviruses. In this study we examine the role of Brd4 at different stages in the formation of viral replication foci. In the absence of viral DNA replication, Brd4 links the viral proteins to host chromatin. However, when viral genomes begin to amplify to high levels, Brd4 is displaced from nuclear foci and is not required for replication.
Scientists have found cases of Middle East Respiratory Syndrome (MERS) in camels in Qatar, health officials said on Thursday, fuelling speculation that camels might be the animal reservoir that allowed the virus to infect and kill humans.
The sobemoviruses have one of the smallest of all known RNA virus genomes. ORF1 encodes P1 which plays a role in suppression of silencing and virus movement, ORFs 2a and 2b encode the replicational polyproteins P2a and P2ab, and ORF3 encodes the coat protein. Translation of ORF2a from the genomic RNA is dependent on a leaky scanning mechanism. We report the presence of an additional ORF (ORFx), conserved in all sobemoviruses. ORFx overlaps the 5′ end of ORF2a in the +2 reading frame and also extends some distance upstream of ORF2a. ORFx lacks an AUG initiation codon and its expression is predicted to depend on low level initiation at near-cognate non-AUG codons, such as CUG, by a proportion of the ribosomes that are scanning the region between the ORF1 and ORF2a initiation codons. Mutations that disrupt translation of ORFx in turnip rosette virus prevent the establishment of infection."
[Their] pipeline has... uncovered conservation patterns, putative effectors and motifs of fungal pathogens that would have been overlooked by existing approaches that identify effectors as small, secreted, cysteine-rich peptides. It can be applied to any pathogenic proteome data, such as microbial pathogen data of plants and other organisms.
Scientists at The Scripps Research Institute have determined the most detailed picture yet of a crucial part of the hepatitis C virus, which the virus uses to infect liver cells. The new data reveal unexpected structural features of this protein.
By tracing ancient human DNA, scientists are learning that prehistoric humans may have immigrated and diversified earlier and more frequently -- and there were a lot more of them -- than we previously realized. An analysis of the oldest known human genetic material found that a new collection of 400,000-year-old hominins -- ancient humans -- may be a common ancestor to Neanderthals and Denisovans. The findings were published in the journal Nature this week and they give us new clues about the origins of modern humans.
Hopes of a total cure for HIV have been dealt a blow, after researchers in the US discovered that the "reservoir" of inactive viruses in a patient's body may be up to 60 times larger than previously thought.
Although modern drug treatments have proved hugely effective at controlling the HIV virus, enabling patients to live long and full lives and reducing infection rates, they do not kill all the viruses in an infected individual.
These viruses remain a threat because they can become active again if a patient stops taking their antiretroviral drugs. The findings, published in the journal Cell following a study at the Howard Hughes Medical Institute (HHMI) in Maryland, were "discouraging" experts said, but should re-focus efforts to make sure HIV positive people are getting the treatment they need.
"The findings suggest that there are a lot more of these proviruses that we have to worry about than we thought," said Robert Siliciano, an HHMI investigator at The Johns Hopkins University, who led the new study. "It doesn't mean that it's hopeless, but it does mean we need to focus on getting an even clearer idea of the scope of the problem."
In HIV positive patients the virus targets the immune system's T cells, and becomes integrated into the cell's genes, making the cell reproduce the virus. Antiretroviral drugs target these active forms of the virus, but in some cells, the virus remains inactive. It is this type of virus that researchers now believe is far more numerous than previously thought. As of yet, researchers have no way of eradicating inactive HIV viruses.
E. coli showing evolution? Yes! Researchers at Michigan State University have been growing Escherichia coli for 25 years, which is over 58,000 generations, in a project called the Long-Term Experimental Evolution project. And during this time, through studying 12 populations of E. coli, they have found that the bacteria continues to adapt to its environment, with no upper limit in sight- even in the 40,00-50,000 generation range, E. coli‘s “fitness” (a measure of how the organism has adapted to its environment) increased by 3-4% per generation!
Achieving the goal of malaria elimination will depend on targeting Plasmodium pathways essential across all life stages. Here we identify a lipid kinase, phosphatidylinositol-4-OH kinase (PI(4)K), as the target of imidazopyrazines, a new antimalarial compound class that inhibits the intracellular development of multiple Plasmodium species at each stage of infection in the vertebrate host. Imidazopyrazines demonstrate potent preventive, therapeutic, and transmission-blocking activity in rodent malaria models, are active against blood-stage field isolates of the major human pathogens P. falciparum and P. vivax, and inhibit liver-stage hypnozoites in the simian parasite P. cynomolgi. We show that imidazopyrazines exert their effect through inhibitory interaction with the ATP-binding pocket of PI(4)K, altering the intracellular distribution of phosphatidylinositol-4-phosphate. Collectively, our data define PI(4)K as a key Plasmodium vulnerability, opening up new avenues of target-based discovery to identify drugs with an ideal activity profile for the prevention, treatment and elimination of malaria.
Assessing the mortality impact of the 2009 influenza A H1N1 virus (H1N1pdm09) is essential for optimizing public health responses to future pandemics. The World Health Organization reported 18,631 laboratory-confirmed pandemic deaths, but the total pandemic mortality burden was substantially higher. Between 123,000 and 203,000 pandemic respiratory deaths were estimated globally for the last 9 mo of 2009.
Objectives: There are very few data from men on the risk of HIV acquisition associated with penile human papillomavirus (HPV) infection and no data on the potential modifying effect of male circumcision.
"The influence of CD25+CD4+ regulatory T cells (Treg) on acute and chronic viral infection of the central nervous system (CNS) was examined using a glial tropic murine coronavirus. Treg in the CNS were highest during initial T cell mediated virus control, decreased and then remained relatively stable during persistence. Anti-CD25 treatment did not affect CNS recruitment of inflammatory cells. Viral control was initially delayed; however, neither the kinetics of viral control nor viral persistence were affected. By contrast, the absence of Treg during the acute phase resulted in increased demyelination during viral persistence. These data suggest that CNS inflammation, progression of viral control and viral persistence are relatively independent of CD25+CD4+ Treg. However, their absence during acute infection alters the ability of the host to limit tissue damage."
This is a guide for anyone who needs to share data with a statistician. The target audiences I have in mind are:
Scientific collaborators who need statisticians to analyze data for themStudents or postdocs in scientific disciplines looking for consulting adviceJunior statistics students whose job it is to collate/clean data sets
The goals of this guide are to provide some instruction on the best way to share data to avoid the most common pitfalls and sources of delay in the transition from data collection to data analysis. The Leek group works with a large number of collaborators and the number one source of variation in the speed to results is the status of the data when they arrive at the Leek group. Based on my conversations with other statisticians this is true nearly universally.
My strong feeling is that statisticians should be able to handle the data in whatever state they arrive. It is important to see the raw data, understand the steps in the processing pipeline, and be able to incorporate hidden sources of variability in one's data analysis. On the other hand, for many data types, the processing steps are well documented and standardized. So the work of converting the data from raw form to directly analyzable form can be performed before calling on a statistician. This can dramatically speed the turnaround time, since the statistician doesn't have to work through all the pre-processing steps first.