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      The First Non-LRV RNA Virus in Leishmania

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          Abstract

          In this work, we describe the first Leishmania-infecting leishbunyavirus—the first virus other than Leishmania RNA virus (LRV) found in trypanosomatid parasites. Its host is Leishmania martiniquensis, a human pathogen causing infections with a wide range of manifestations from asymptomatic to severe visceral disease. This virus ( LmarLBV1) possesses many characteristic features of leishbunyaviruses, such as tripartite organization of its RNA genome, with ORFs encoding RNA-dependent RNA polymerase, surface glycoprotein, and nucleoprotein on L, M, and S segments, respectively. Our phylogenetic analyses suggest that LmarLBV1 originated from leishbunyaviruses of monoxenous trypanosomatids and, probably, is a result of genomic re-assortment. The LmarLBV1 facilitates parasites’ infectivity in vitro in primary murine macrophages model. The discovery of a virus in L. martiniquensis poses the question of whether it influences pathogenicity of this parasite in vivo, similarly to the LRV in other Leishmania species.

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          Database resources of the National Center for Biotechnology.

          D Wheeler (2003)
          In addition to maintaining the GenBank(R) nucleic acid sequence database, the National Center for Biotechnology Information (NCBI) provides data analysis and retrieval resources for the data in GenBank and other biological data made available through NCBI's Web site. NCBI resources include Entrez, PubMed, PubMed Central (PMC), LocusLink, the NCBITaxonomy Browser, BLAST, BLAST Link (BLink), Electronic PCR (e-PCR), Open Reading Frame (ORF) Finder, References Sequence (RefSeq), UniGene, HomoloGene, ProtEST, Database of Single Nucleotide Polymorphisms (dbSNP), Human/Mouse Homology Map, Cancer Chromosome Aberration Project (CCAP), Entrez Genomes and related tools, the Map Viewer, Model Maker (MM), Evidence Viewer (EV), Clusters of Orthologous Groups (COGs) database, Retroviral Genotyping Tools, SAGEmap, Gene Expression Omnibus (GEO), Online Mendelian Inheritance in Man (OMIM), the Molecular Modeling Database (MMDB), the Conserved Domain Database (CDD), and the Conserved Domain Architecture Retrieval Tool (CDART). Augmenting many of the Web applications are custom implementations of the BLAST program optimized to search specialized data sets. All of the resources can be accessed through the NCBI home page at: http://www.ncbi.nlm.nih.gov.
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            Leishmania RNA virus controls the severity of mucocutaneous leishmaniasis.

            Mucocutaneous leishmaniasis is caused by infections with intracellular parasites of the Leishmania Viannia subgenus, including Leishmania guyanensis. The pathology develops after parasite dissemination to nasopharyngeal tissues, where destructive metastatic lesions form with chronic inflammation. Currently, the mechanisms involved in lesion development are poorly understood. Here we show that metastasizing parasites have a high Leishmania RNA virus-1 (LRV1) burden that is recognized by the host Toll-like receptor 3 (TLR3) to induce proinflammatory cytokines and chemokines. Paradoxically, these TLR3-mediated immune responses rendered mice more susceptible to infection, and the animals developed an increased footpad swelling and parasitemia. Thus, LRV1 in the metastasizing parasites subverted the host immune response to Leishmania and promoted parasite persistence.
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              Extracellular Vesicles from Trypanosoma brucei Mediate Virulence Factor Transfer and Cause Host Anemia.

              Intercellular communication between parasites and with host cells provides mechanisms for parasite development, immune evasion, and disease pathology. Bloodstream African trypanosomes produce membranous nanotubes that originate from the flagellar membrane and disassociate into free extracellular vesicles (EVs). Trypanosome EVs contain several flagellar proteins that contribute to virulence, and Trypanosoma brucei rhodesiense EVs contain the serum resistance-associated protein (SRA) necessary for human infectivity. T. b. rhodesiense EVs transfer SRA to non-human infectious trypanosomes, allowing evasion of human innate immunity. Trypanosome EVs can also fuse with mammalian erythrocytes, resulting in rapid erythrocyte clearance and anemia. These data indicate that trypanosome EVs are organelles mediating non-hereditary virulence factor transfer and causing host erythrocyte remodeling, inducing anemia.
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                Author and article information

                Journal
                Viruses
                Viruses
                viruses
                Viruses
                MDPI
                1999-4915
                02 February 2020
                February 2020
                : 12
                : 2
                : 168
                Affiliations
                [1 ]Life Science Research Centre, Faculty of Science, University of Ostrava, 71000 Ostrava, Czech Republic; danilaman@ 123456gmail.com (D.G.); diegohqm@ 123456gmail.com (D.H.M.); luzikhina@ 123456gmail.com (N.K.)
                [2 ]Central European Institute of Technology, Masaryk University, 60177 Brno, Czech Republic
                [3 ]Martsinovsky Institute of Medical Parasitology, Sechenov University, Moscow 119435, Russia, alexander_lukashev@ 123456hotmail.com (A.N.L.)
                [4 ]Division of Biomedical and Life Sciences, Faculty of Health and Medicine, Lancaster University, Lancaster LA1 4YE, UK; p.bates@ 123456lancaster.ac.uk
                [5 ]Laboratory of Electron Microscopy, Veterinary Research Institute, 62100 Brno, Czech Republic; kulich@ 123456vri.cz
                [6 ]Department of Parasitology, Faculty of Science, Charles University, 12844 Prague, Czech Republic; Terka.Kratochvilova@ 123456seznam.cz (T.L.); volf@ 123456cesnet.cz (P.V.)
                [7 ]Laboratory of Cellular and Molecular Protistology, Zoological Institute of the Russian Academy of Sciences, St. Petersburg 199034, Russia
                Author notes
                [†]

                These authors contributed equally to this work.

                Author information
                https://orcid.org/0000-0002-5347-8150
                https://orcid.org/0000-0001-9111-5265
                https://orcid.org/0000-0003-1790-1123
                https://orcid.org/0000-0002-1516-437X
                https://orcid.org/0000-0003-4765-3263
                Article
                viruses-12-00168
                10.3390/v12020168
                7077295
                32024293
                dfbfdef0-13b6-46d9-837c-fb4ee7e5be0d
                © 2020 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 06 January 2020
                : 29 January 2020
                Categories
                Article

                Microbiology & Virology
                bunyavirales,leishmania martiniquensis,leishbunyavirus
                Microbiology & Virology
                bunyavirales, leishmania martiniquensis, leishbunyavirus

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