作者: Morena Pappalardo , Ian G Reddin , Diego Cantoni , Jeremy S Rossman , Martin Michaelis
DOI: 10.1093/BIOINFORMATICS/BTX065
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摘要: Motivation Ebola viruses are not pathogenic but can be adapted to replicate and cause disease in rodents. Here, we used a structural bioinformatics approach analyze the mutations associated with virus adaptation rodents elucidate determinants of host-specific pathogenicity. Results We identified 33 different proteins GP, NP, L, VP24 VP35. Only VP24, GP NP were consistently found mutated rodent-adapted strains. Fewer than five these genes seem required for new species. The role is clear. However, three located protein interface karyopherin α5 may enable inhibit karyopherins subsequently host interferon response. Three further change hydrogen bonding or conformational changes. Hence, there evidence that few including crucial hosts. Since Reston virus, only non-human Ebolavirus species circulates pigs Asia, this raises concerns result novel human Ebolaviruses. Contact m.n.wass@kent.ac.uk , m.michaelis@kent.ac.uk j.s.rossman@kent.ac.uk. Supplementary information data available at Bioinformatics online.