Genetic mutations may allow bird flu to spread to humans
Scientists from the Scripps Research Institute in California have identified genetic mutations that may occur in the avian influenza A (H7N9) virus genome which may allow the avian influenza strain to spread between humans. H7N9 is a strain of influenza virus that normally infects birds, but has spread to at least 779 humans in a number of outbreaks related to poultry markets. The virus is not currently capable of spreading sustainably from human to human, but scientists are concerned that it may potentially mutate into a form that can. The Scripps team focused on a gene that codes for the H7 haemagglutinin, a protein found on the surface of influenza viruses. This protein allows influenza viruses to latch onto host cells. Flu strains that circulate in avian viruses have different subtypes of haemagglutinin, called H1–H16. So far only three subtypes have been found in human influenza viruses (H1, H2 and H3). As other avian influenza viruses, H7N9 is specific for receptors on bird cells, but not receptors on human cells. However, a transition to human specificity may enable H7N9 to circulate among humans. Using molecular modelling and knowledge of the haemagglutinin’s structure, the Scripps researchers identified mutations that may change the protein’s amino acid sequence and cause a switch to human specificity. They produced the haemagglutinin with different combinations of these mutations in an experimental cell line. The scientists harvested the mutant haemagglutinin proteins from the cells and tested how strongly they bound to human-type and bird-type receptors. Several forms with mutations in three amino acids bound far more strongly to human receptors; they had switched specificity from bird to human. These triple-mutant H7 haemagglutinins also successfully latched onto cells in samples of human trachea tissue. Safety regulations prohibit introducing these mutations to actual H7N9 viruses, limiting scientists’ ability to test their effects in animals. Nonetheless, the research team suggests that keeping an eye out for the development of these mutations in humans infected with H7N9 may help trigger a timely response to prevent potential spread. The findings were published in PLOS Pathogens.
New technique may identify potential malaria drug targets
University of Melbourne researchers have developed a new technique for investigating the effects of gene deletion at later stages in the life cycle of a parasite that causes malaria in rodents. The study was published in PLOS Pathogens. New treatments are needed for malaria because of increasing drug resistance in the single-celled Plasmodium parasites that cause it. Metabolic processes in Plasmodium that are essential for its development may serve as potential new drug targets. However, the Plasmodium life cycle, which occurs in both mosquitos and host animals, makes it difficult to identify and study such processes. The Australian researchers showed their novel technique by focusing on an important metabolic process in Plasmodium berghei, which causes malaria in rodents and is commonly used in mouse studies of malaria. This metabolic process requires a gene known as the ferrochelatase (FC) gene, and it allows P. berghei to produce a chemical compound known as heme. Heme synthesis is known to be essential for P. berghei development in mosquitos that transmit the parasite between rodent hosts, but it is not essential during a later stage in the host bloodstream. However, between these two stages, P. berghei undergoes a developmental phase in the host liver, and it has been unclear whether heme synthesis is essential at this stage. The researchers produced P. berghei parasites that are capable of expressing the FC gene and developing properly in mosquitos, but produce a mix of FC-expressing and FC-deficient parasites once they infect mouse liver cells. The scientists genetically engineered the parasites so that FC-deficient individuals would express fluorescent markers, allowing for easy identification. They found that FC-deficient parasites were unable to complete their liver development phase, suggesting that disrupting the heme synthesis pathway may be an effective way to target Plasmodium parasites in the liver. Such an approach would be prophylactic, since symptoms aren’t apparent until the parasite leaves the liver and begins its bloodstream phase. This same novel approach involving fluorescent markers may be adapted for other genes, allowing scientists to identify additional metabolic processes that are essential for Plasmodium development in host animals.
Students with ADHD not reaching minimum education standards
Murdoch Children’s Research Institute researchers have found that a high number of Australian children with attention deficit hyperactivity disorder (ADHD) are struggling academically, with 40% of students failing to meet the literacy and numeracy (NAPLAN) national minimum standards in at least one academic area. In Australia, 6–7% of students entering high school have ADHD. The study, published in the Journal of Developmental and Behavioral Pediatrics, showed that in Year 7, 73% of students with ADHD had a particular problem with writing, and almost 25% were below the minimum standard. In Year 9, 54% of students had difficulties, and 37.5% did not reach the minimum standard. Difficulty with writing was much higher for boys than girls. While some students with ADHD are performing well, most are performing academically below grade-level averages and are placed in the lowest two NAPLAN performance bands. Lead researcher, Nardia Zendarski said that the study showed just how large the gap was between high-achieving students and students with ADHD. “The gap is the same difference as other ‘at-risk’ cohorts.” Teens with ADHD experience a range of other problems, with some struggling in terms of academic outcomes; this can also affect their mental health, their ability to make friends and how they engage with the school community. In addition to academic support, interventions targeting factors that the study found were associated with poor academic outcomes may improve academic achievement across this critical period. These factors included inattention, bullying and low supervision and monitoring of the adolescent by their parents. “We should stop focusing on the argument around whether these kids should be medicated or not and start focusing on providing the services and support that they need to reach their full potential. These programs could be used to support all kids with learning difficulties,” Ms Zendarski said.
Can drones improve outcomes for out-of-hospital cardiac arrests?
Swedish researchers have found that drones carrying an automated external defibrillator (AED) arrived in less time than emergency medical services (EMS), with a reduction in response time of about 16 minutes. Published in JAMA, the study involved simulated out-of-hospital cardiac arrests (OHCAs). A drone was developed and certified by the Swedish Transportation Agency and was equipped with an AED weighing 770 g and placed at a fire station in a municipality north of Stockholm. The drone was equipped with a global positioning system and a high-definition camera and integrated with an autopilot software system. It was dispatched for out-of-sight flights in October 2016 to locations where OHCAs within a 10 km radius from the fire station had occurred between 2006 and 2014. Eighteen remotely operated flights were performed with a median flight distance of about 3.2 km. The median time from call to dispatch of EMS was 3:00 minutes. The median time from dispatch to drone launch was 3 seconds. The median time from dispatch to arrival of the drone was 5:21 minutes versus 22:00 minutes for EMS. The drone arrived more quickly than EMS in all cases, with a median reduction in response time of 16:39 minutes. Limitations of the study include the small number of flights over short distances in good weather.
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