BackgroundPeste des petits ruminants (PPR) is a contagious disease listed by the World Organisation for Animal health (OIE) as being a specific hazard. It affects sheep, goats, and wild ungulates, and is prevalent throughout the developing world particularly Asia, the Middle East, and Africa. PPR has been targeted for eradication by 2030 by the Food and Agriculture Organization of the United Nations (FAO) and the OIE, after the successful eradication of the related disease, rinderpest in cattle. PPR was first reported in 1942 in the Ivory Coast in Western Africa and has since extended its range in Asia, the Middle East, and Africa posing an immediate threat of incursion into Europe, South East Asia and South Africa. Although robust vaccines are available, the use of these vaccines in a systematic and rational manner is not widespread, resulting in this devastating disease becoming an important neglected tropical disease in the developing world.MethodologyWe isolated and characterized the PPR virus from an outbreak in Cheraga, northern Algeria, during October 2015 by analyzing the partial N-gene sequence in comparison with other viruses from the Maghreb region. As well as sequencing the full length viral genome and performing real-time RT-PCR on clinical samples. Maximum-likelihood and Bayesian temporal and phylogeographic analyses were performed to assess the persistence and spread of PPRV circulation from Eastern Africa in the Maghreb region of North Africa.ConclusionsRecent PPR outbreaks in Cheraga, in the northern part of Algiers (October 2015) and North-West Morocco (June, 2015) highlight that PPRV has spread to the northern border of North Africa and may pose a threat of introduction to Europe. Phylogeographic analysis suggests that lineage IV PPRV has spread from Eastern Africa, most likely from the Sudan 2000 outbreak, into Northern Africa resulting in the 2008 Moroccan outbreak. Maximum-likelihood and Bayesian analysis shows that these North African viruses cluster closely together suggesting the existence of continual regional circulation. Considering the same virus is circulating in Algeria, Morocco and Tunisia, implementation of a common Maghreb PPR eradication strategy would be beneficial for the region.
Peste-des-petits ruminants (PPR) is one of the most important infectious diseases of domesticated small ruminants. From the initial identification in 1942 in West Africa, PPR virus (PPRV) has spread throughout much of the developing world. PPRV is now considered endemic throughout Africa, with the notable exception of South Africa, the Middle-East and Israel, as well as South-, East-, and Central Asia. Despite this widespread dispersal, the evolution and transmission of PPRV in endemic populations is not well understood. This understanding will be critical in the planning of rational measures to eradicate PPRV by the planned time as defined by the FAO and OIE. To further advance the understanding of the evolution of PPRV the full genome sequence of 18 viruses isolated from Israel from consecutive years between 1997–2014 were generated. This data set is unique and crucial for the understanding of the evolution of PPRV, as it represents the first set of full-length sequence data available from consecutive years from a single geographic location. Analysis of these full genome sequences shows 96.2–99.9% nucleotide conservation across the Israel isolates and further demonstrates the strong purifying selection pressures on PPRV within Israel and globally. Four amino acid substitutions indicative of putative positive selection were additionally identified within the Israel isolates. The mean substitution rate per site per year was estimated to be 9.22 x 10−4 (95% HPD 6.206 x 10−4–1.26 x 10−3). Using Bayesian and phylogenetic analyses we further demonstrate that the PPRV isolates from Israel belongs to linage IV and form a single strong regional cluster within all other lineage IV viruses circulating worldwide implying a single incursion into Israel.
Background Extracellular vesicles (EVs) are small membrane vesicles secreted by the cells that mediate intercellular transfer of molecules and contribute to transduction of various signals. Viral infection and action of pro-inflammatory cytokines has been shown to alter molecular composition of EV content. Transfer of antiviral proteins by EVs is thought to contribute to the development of inflammation and antiviral state. Altered incorporation of selected host RNAs into EVs in response to infection has also been demonstrated for several viruses, but not for WNV. Considering the medical significance of flaviviruses and the importance of deeper knowledge about the mechanisms of flavivirus-host interactions we assessed the ability of West Nile virus (WNV) and type I interferon (IFN), the main cytokine regulating antiviral response to WNV, to alter the composition of EV RNA cargo. Results We employed next generation sequencing to perform transcriptome-wide profiling of RNA cargo in EVs produced by cells infected with WNV or exposed to IFN-alpha. RNA profile of EVs secreted by uninfected cells was also determined and used as a reference. We found that WNV infection significantly changed the levels of certain host microRNAs (miRNAs), small noncoding RNAs (sncRNAs) and mRNAs incorporated into EVs. Treatment with IFN-alpha also altered miRNA and mRNA profiles in EV but had less profound effect on sncRNAs. Functional classification of RNAs differentially incorporated into EVs upon infection and in response to IFN-alpha treatment demonstrated association of enriched in EVs mRNAs and miRNAs with viral processes and pro-inflammatory pathways. Further analysis revealed that WNV infection and IFN-alpha treatment changed the levels of common and unique mRNAs and miRNAs in EVs and that IFN-dependent and IFN-independent processes are involved in regulation of RNA sorting into EVs during infection. Conclusions WNV infection and IFN-alpha treatment alter the spectrum and the levels of mRNAs, miRNAs and sncRNAs in EVs. Differentially incorporated mRNAs and miRNAs in EVs produced in response to WNV infection and to IFN-alpha treatment are associated with viral processes and host response to infection. WNV infection affects composition of RNA cargo in EVs via IFN-dependent and IFN-independent mechanisms. Electronic supplementary material The online version of this article (10.1186/s12864-019-5835-6) contains supplementary material, which is available to authorized users.
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