Researchers from China and the US describe a mutation in the Zika virus (ZIKV) envelope protein sequence that appears to have sprung up prior to 2013, apparently leading to enhanced neurovirulence, more robust maternal-to-fetal transmission fitness, and increased host viremia. Starting from seven suspicious mutations that arose in ZIKV strains between 2010 and 2013, team relied on phylogenetics, genetic engineering, mouse model experiments, cellular assays, and other approaches to find a key ZIKV envelope substitution, known as E-V473M, and explore its consequences. Together, the results suggest that “just before its 2013 spread in the Americas, Zika virus underwent an envelope protein V473M substitution,” the authors write, noting that E-V473M appeared to be a “critical determinant for enhanced ZIKV virulence, intrauterine transmission during pregnancy, and viremia to facilitate urban transmission.”
A team from Bethlehem University, Tel Aviv University, and the University of Washington describes alterations identified in Palestinian families affected by inherited hearing loss. Based on information from nearly 2,200 individuals from families in Gaza and the West Bank, the researchers suspected that genetic factors were behind some 56 percent of the hearing loss cases in families without a prior history of such conditions. With a combination of panel sequencing, segregation analyses, targeted RNA sequencing, in silico analyses, and other methods, they focused in on possible genetic culprits in 87 percent of those individuals, highlighting more than 100 mutations in one of four dozen different genes in hearing loss-affected individuals from 337 families. Nearly 60 percent of the hearing loss cases involved mutations inherited through consanguineous marriage, the authors note, adding that “inherited hearing loss will likely be much rarer in the next generation” as consanguineous marriages become less common.
Members of the Global Consortium for H5N8 and Related Influenza Viruses retrace the avian origins of reassorted H5 flu strains contributing to an epidemic in Eurasia in 2016 and 2017. The University of Edinburgh-led team did a phylogenetic analysis based on sequences from hundreds of influenza isolates from clinical, domestic bird, and wild bird sources spanning more than two dozen countries, estimating the timing, bird sources, and sites where the highly pathogenic avian influenza virus segments originated. “We found that new genetic material likely came from wild birds across their migratory range and from domestic ducks not only in China but also in central Europe,” the authors report. “This knowledge is important to understand how the virus could adapt to wild birds and become established in wild bird populations.”