Researchers discover that individual flu strains elicit an antibody response to multiple different flu strains already experienced by a patient A global team of researchers using a new modelling system have discovered that upon infection, patients...
If you planned to sabotage a factory, a recon trip through the premises would probably be much more useful than just peeping in at the windows. Scientists looking to understand – and potentially thwart – the influenza virus have now gone from a similar window-based view to the full factory tour, thanks to the first complete structure of one of the flu virus’ key machines. The structure, obtained by scientists at the European Molecular Biology Laboratory (EMBL) in Grenoble, France, allows researchers to finally understand how the machine works as a whole. Published today in two papers in Nature, the work could prove instrumental in designing new drugs to treat serious flu infections and combat flu pandemics.
H5N1 highly pathogenic avian influenza virus (HPAIV) of clade 2.3.2 has been circulating in waterfowl in Southern China since 2003. Our previous studies showed that certain H5N1 HPAIV isolates within clade 2.3.2 from Southern China had high pathogenicity in different birds. Guinea pigs have been successfully used as models to evaluate the transmissibility of AIVs and other species of influenza viruses in mammalian hosts. However, few studies have reported pathogenicity and transmissibility of H5N1 HPAIVs of this clade in guinea pigs. In this study, we selected an H5N1 HPAIV isolate, A/duck/Guangdong/357/2008, to investigate the pathogenicity and transmissibility of the virus in guinea pigs. The virus had high pathogenicity in mice; additionally, it only replicated in some tissues of the guinea pigs without production of clinical signs, but was transmissible among guinea pigs. Interestingly, virus isolates from co-caged guinea pigs had the D701N mutation in the PB2 protein. These mutant viruses showed higher pathogenicity in mice and higher replication capability in guinea pigs but did not demonstrate enhanced the transmissibility among guinea pigs. These findings indicate the transmission of the H5N1 virus between mammals could induce virus mutations, and the mutant viruses might have higher pathogenicity in mammals without higher transmissibility. Therefore, the continued evaluation of the pathogenicity and transmissibility of avian influenza virus (AIVs) in mammals is critical to the understanding of the evolutionary characteristics of AIVs and the emergence of potential pandemic strains.
Interaction between the human immune system and influenza virus is predominantly driven by antigenic drift. In this process, ongoing mutation of the virus slowly changes its antigenic signature, eventually allowing the virus to infect people with immunity to earlier versions of the virus. Along with antigenic shifts, through which extreme changes in influenza A lead to pandemics (most often when genes from two or more different strains of influenza reassort to form a new subtype), antigenic drift is the dominant driver of influenza epidemiology. One of the most important results of antigenic drift is the need to periodically reformulate and annually administer influenza vaccine. On page 996 of this issue, Fonville et al. (1) use a technique called “antibody landscapes” to characterize antibody protection from the full spectrum of influenza strains, illuminating the interaction between new influenza exposures and past immunity
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