Summary The 2013-2015 West African epidemic of Ebola virus disease (EVD) reminds us how little is known about biosafety level-4 viruses. Like Ebola virus, Lassa virus (LASV) can cause hemorrhagic fever with high case fatality rates. We generated a genomic catalog of almost 200 LASV sequences from clinical and rodent reservoir samples. We show that whereas the 2013-2015 EVD epidemic is fueled by human-to-human transmissions, LASV infections mainly result from reservoir-to-human infections. We elucidated the spread of LASV across West Africa and show that this migration was accompanied by changes in LASV genome abundance, fatality rates, codon adaptation, and translational efficiency. By investigating intrahost evolution, we found that mutations accumulate in epitopes of viral surface proteins, suggesting selection for immune escape. This catalog will serve as a foundation for the development of vaccines and diagnostics.

International audienceThe degree to which molecular epidemiology reveals informationabout the sources and transmission patterns of an outbreakdepends on the resolution of the technology used and the samplesstudied. Isolates of Escherichia coli O104:H4 from the outbreak centeredin Germany in May–July 2011, and the much smaller outbreakin southwest France in June 2011, were indistinguishable by standardtests. We report a molecular epidemiological analysis usingmultiplatform whole-genome sequencing and analysis of multipleisolates from the German and French outbreaks. Isolates from theGerman outbreak showed remarkably little diversity, with onlytwo single nucleotide polymorphisms (SNPs) found in isolates fromfour individuals. Surprisingly, we found much greater diversity (19SNPs) in isolates from seven individuals infected in the French outbreak.The German isolates form a clade within the more diverseFrench outbreak strains. Moreover, five isolates derived from a singleinfected individual from the French outbreak had extremelylimited diversity. The striking difference in diversity between theGerman and French outbreak samples is consistent with severalhypotheses, including a bottleneck that purged diversity in theGerman isolates, variation in mutation rates in the two E. coli outbreakpopulations, or uneven distribution of diversity in the seedpopulations that led to each outbreak

Venoms have attracted enormous attention because of their potent physiological effects and dynamic evolution, including the convergent recruitment of homologous genes for venom expression. Here we provide novel evidence for the recruitment of genes from the Crustacean Hyperglycemic Hormone (CHH) and arthropod Ion Transport Peptide (ITP) superfamily for venom expression in black widow spiders. We characterized latrodectin peptides from venom gland cDNAs from the Western black widow spider (Latrodectus hesperus), the brown widow (L. geometricus) and cupboard spider (Steatoda grossa). Phylogenetic analyses of these sequences with homologs from other spider, scorpion and wasp venom cDNAs, as well as CHH/ITP neuropeptides, show latrodectins as derived members of the CHH/ITP superfamily. These analyses suggest that CHH/ITP homologs are more widespread in spider venoms, and were recruited for venom expression in two additional arthropod lineages. We also found that the latrodectin 2 gene and nearly all CHH/ITP genes include a phase 2 intron in the same position, supporting latrodectin’s placement within the CHH/ITP superfamily. Evolutionary analyses of latrodectins suggest episodes of positive selection along some sequence lineages, and positive and purifying selection on specific codons, supporting its functional importance in widow venom. We consider how this improved understanding of latrodectin evolution informs functional hypotheses regarding its role in black widow venom as well as its potential convergent recruitment for venom expression across arthropods.

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