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      Equine infectious anemia virus in China

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          Abstract

          Equine infectious anemia is an equine disease caused by equine infectious anemia virus, which was first reported in 1840. Equine infectious anemia virus research in China started in the 1960s, focusing on etiology, pathology, diagnosis, and immunology. Notably, in 1978 an attenuated vaccine was successfully developed for equine infectious anemia virus, effectively preventing equine infectious anemia virus in China. This article will review equine infectious anemia virus in China, including past and recent research, and commemorate scientists who have made great contributions to equine infectious anemia virus prevention.

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          Bst-2/HM1.24 is a raft-associated apical membrane protein with an unusual topology.

          Sabine Kupzig, Viktor Korolchuk, Ruth Rollason … (2003)
          An expression screen of a rat cDNA library for sequences encoding Golgi-localized integral membrane proteins identified a protein with an apparent novel topology, i.e. with both an N-terminal transmembrane domain and a C-terminal glycosyl-phosphatidylinositol (GPI) anchor. Our data are consistent with this. Thus, the protein would have a topology that, in mammalian cells, is shared only by a minor, but pathologically important, topological isoform of the prion protein (PrP). The human orthologue of this protein has been described previously (BST-2 or HM1.24 antigen) as a cell surface molecule that appears to be involved in early pre-B-cell development and which is present at elevated levels at the surface of myeloma cells. We show that rat BST-2/HM1.24 has both a cell surface and an intracellular (juxtanuclear) location and is efficiently internalized from the cell surface. We also show that the cell surface pool of BST-2/HM1.24 is predominantly present in the apical plasma membrane of polarized cells. The fact that rat BST-2/HM1.24 apparently possesses a GPI anchor led us to speculate that it might exist in cholesterol-rich lipid microdomains (lipid rafts) at the plasma membrane. Data from several experiments are consistent with this localization. We present a model in which BST-2/HM1.24 serves to link adjacent lipid rafts within the plasma membrane.
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            Experimental evolution of parasites.

            Antje D. Ebert (1998)
            Serial passage experiments are a form of experimental evolution that is frequently used in applied sciences; for example, in vaccine development. During these experiments, molecular and phenotypic evolution can be monitored in real time, providing insights into the causes and consequences of parasite evolution. Within-host competition generally drives an increase in a parasite's virulence in a new host, whereas the parasite becomes avirulent to its former host, indicating a trade-off between parasite fitnesses on different hosts. Understanding why parasite virulence seldom escalates similarly in natural populations could help us to manage virulence and deal with emerging diseases.
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              Adenosine deaminases acting on RNA (ADARs) are both antiviral and proviral.

              James E Samuel (2011)
              A-to-I RNA editing, the deamination of adenosine (A) to inosine (I) that occurs in regions of RNA with double-stranded character, is catalyzed by a family of Adenosine Deaminases Acting on RNA (ADARs). In mammals there are three ADAR genes. Two encode proteins that possess demonstrated deaminase activity: ADAR1, which is interferon-inducible, and ADAR2 which is constitutively expressed. ADAR3, by contrast, has not yet been shown to be an active enzyme. The specificity of the ADAR1 and ADAR2 deaminases ranges from highly site-selective to non-selective, dependent on the duplex structure of the substrate RNA. A-to-I editing is a form of nucleotide substitution editing, because I is decoded as guanosine (G) instead of A by ribosomes during translation and by polymerases during RNA-dependent RNA replication. Additionally, A-to-I editing can alter RNA structure stability as I:U mismatches are less stable than A:U base pairs. Both viral and cellular RNAs are edited by ADARs. A-to-I editing is of broad physiologic significance. Among the outcomes of A-to-I editing are biochemical changes that affect how viruses interact with their hosts, changes that can lead to either enhanced or reduced virus growth and persistence depending upon the specific virus. Copyright © 2010 Elsevier Inc. All rights reserved.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Oncotarget
                Journal ID (iso-abbrev): Oncotarget
                Journal ID (publisher-id): Oncotarget
                Journal ID (publisher-id): ImpactJ
                Title: Oncotarget
                Publisher: Impact Journals LLC
                ISSN (Electronic): 1949-2553
                Publication date Collection: 2 January 2018
                Publication date (Electronic): 21 August 2017
                Volume: 9
                Issue: 1
                Pages: 1356-1364
                Affiliations
                1 Department of Veterinary Medicine, College of Animal Sciences, Zhejiang University, Hangzhou, China
                2 School of Animal Husbandry and Medical Engineering, Xinyang Agriculture and Forestry University, Xinyang, China
                3 Guangdong Key Laboratory of Laboratory Animals, Guangdong Laboratory Animals Monitoring Institute, Guangzhou, China
                4 Shanxi Provincial Animal Disease Control Center, Taiyuan, China
                5 The First Affiliated Hospital of Harbin Medical University, Harbin, China
                Author notes
                Correspondence to: Ming-Ming Hu, hmmsdhr@ 123456163.com
                [*]

                These authors contributed equally to this work

                Article
                Publisher ID: 20381
                DOI: 10.18632/oncotarget.20381
                PMC ID: 5787444
                PubMed ID: 29416700
                SO-VID: 0b5623a5-0db8-4d05-900d-ae8dc9b4792a
                Copyright © Copyright: © 2018 Wang et al.
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                Date received : 20 June 2017
                Date accepted : 9 August 2017
                Categories
                Subject: Review

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: equine infectious anemia virus,epidemic,vaccine,virulence,immune response
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: equine infectious anemia virus, epidemic, vaccine, virulence, immune response

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