简介：AbstractSFTS virus (SFTSV) is a novel bunyavirus, which was discovered as the etiological agent of severe fever with thrombocytopenia syndrome (SFTS) in China in 2009, and was now prevalent in at least 25 provinces in China. SFTS was subsequently identified in South Korea and Japan in 2012. To explore the molecular evolution and genetic characteristics of this newly identified pathogen, we reported 72 whole genome sequences of SFTSV, and built a dataset of SFTSV genome sequences containing 292 L-segment, 302 M-segment and 502 S-segment. We clearly divided SFTSV into six genotypes, Genotype A-F. It was found that genotype F was the dominant epidemic genotype of Japan, South Korea, and Zhejiang province of China. The coalescent analysis supported that SFTSV originated in the early 18th century from Zhejiang province, and Genotype F was the most primitive one. Henan, Hubei, and Anhui provinces which are located in Dabie Mountain area were mainly epidemic of Genotype A, which emerged relatively late but distributed widely. A total of 37 recombination events were identified, making SFTSV with a high recombination frequency (L segment 5.1%, M segment 3.6%, S segment 0.8%) among negative-strand segmented RNA viruses. It was identified that 19 reassortant strains belonged to 12 reassortment forms of SFTSV genome containing 6 newly identified forms. The reassortment virus and recombination in tick were both found for the first time. We also found many of genotype-specific mutation sites, 7 of which could be considered as potential molecular marker for genotype classification. This study promoted a more comprehensive understanding of the phylogeny and origin, and the genetic diversity of SFTSV, and it could help the studies of other newly discovered tick-borne bunyavirus as reference data and research ideas.

简介：AbstractEbola virus (EBOV) is one of the most pathogenic viruses in humans which can cause a lethal hemorrhagic fever. Understanding the cellular entry mechanisms of EBOV can promote the development of new therapeutic strategies to control virus replication and spread. It has been known that EBOV virions bind to factors expressed at the host cell surface. Subsequently, the virions are internalized by a macropinocytosis-like process, followed by being trafficked through early and late endosomes. Recent researches indicate that the entry of EBOV into cells requires integrated and functional lipid rafts. Whilst lipid rafts have been hypothesized to play a role in virus entry, there is a current lack of supporting data. One major technical hurdle is the lack of effective approaches for observing viral entry. To provide evidence on the involvement of lipid rafts in the entry process of EBOV, we generated the fluorescently labeled Ebola virus like particles (VLPs), and utilized single-particle tracking (SPT) to visualize the entry of fluorescent Ebola VLPs in live cells and the interaction of Ebola VLPs with lipid rafts. In this study, we demonstrate the compartmentalization of Ebola VLPs in lipid rafts during entry process, and inform the essential function of lipid rafts for the entry of Ebola virus. As such, our study provides evidence to show that the raft integrity is critical for Ebola virus pathogenesis and that lipid rafts can serve as potential targets for the development of novel therapeutic strategies.