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      ICTV Virus Taxonomy Profile: Asfarviridae

      1 , 2 , 3 , 4 , 5 , 1 , ICTV Report Consortium
      Journal of General Virology
      Microbiology Society

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          Abstract

          The family Asfarviridae includes the single species African swine fever virus, isolates of which have linear dsDNA genomes of 170-194 kbp. Virions have an internal core, an internal lipid membrane, an icosahedral capsid and an outer lipid envelope. Infection of domestic pigs and wild boar results in an acute haemorrhagic fever with transmission by contact or ingestion, or by ticks of the genus Ornithodoros. Indigenous pigs act as reservoirs in Africa, where infection is endemic, and from where introductions occur periodically to Europe. This is a summary of the International Committee on Taxonomy of Viruses (ICTV) Report on the taxonomy of the Asfarviridae, which is available at www.ictv.global/report/asfarviridae.

          Most cited references8

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          Is Open Access

          African Swine Fever Virus: A Review

          African swine fever (ASF) is a highly contagious viral disease of swine which causes high mortality, approaching 100%, in domestic pigs. ASF is caused by a large, double stranded DNA virus, ASF virus (ASFV), which replicates predominantly in the cytoplasm of macrophages and is the only member of the Asfarviridae family, genus Asfivirus. The natural hosts of this virus include wild suids and arthropod vectors of the Ornithodoros genus. The infection of ASFV in its reservoir hosts is usually asymptomatic and develops a persistent infection. In contrast, infection of domestic pigs leads to a lethal hemorrhagic fever for which there is no effective vaccine. Identification of ASFV genes involved in virulence and the characterization of mechanisms used by the virus to evade the immune response of the host are recognized as critical steps in the development of a vaccine. Moreover, the interplay of the viral products with host pathways, which are relevant for virus replication, provides the basic information needed for the identification of potential targets for the development of intervention strategies against this disease.
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            Comparison of the genome sequences of non-pathogenic and pathogenic African swine fever virus isolates.

            The genomic coding sequences, apart from the inverted terminal repeats and cross-links, have been determined for two African swine fever virus (ASFV) isolates from the same virus genotype, a non-pathogenic isolate from Portugal, OURT88/3, and a highly pathogenic isolate from West Africa, Benin 97/1. These genome sequences were annotated and compared with that of a tissue culture-adapted isolate, BA71V. The genomes range in length between 170 and 182 kbp and encode between 151 and 157 open reading frames (ORFs). Compared to the Benin 97/1 isolate, the OURT88/3 and BA71V isolates have deletions of 8-10 kbp that encode six copies of the multigene family (MGF) 360 and either one MGF 505/530 copy in the BA71V or two copies in the OURT88/3 isolate. The BA71V isolate has a deletion, close to the right end of the genome, of 3 kbp compared with the other isolates. The five ORFs in this region include an additional copy of an ORF similar to that encoding the p22 virus structural protein. The OURT88/3 isolate has interruptions in ORFs that encode a CD2-like and a C-type lectin protein. Variation between the genomes is observed in the number of copies of five different MGFs. The 109 non-duplicated ORFs conserved in the three genomes encode proteins involved in virus replication, virus assembly and modulation of the host's defences. These results provide information concerning the genetic variability of African swine fever virus isolates that differ in pathogenicity.
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              African swine fever virus morphogenesis.

              This review summarizes recent structural and molecular biology studies related to the morphogenesis of African swine fever virus (ASFV). ASFV possesses icosahedral morphology and is constituted by four concentric layers: the central nucleoid, the core shell, the inner envelope and the icosahedral capsid. The extracellular virus acquires an external envelope by budding through the plasma membrane. The genes coding for 19 of the 54 structural proteins of the ASFV particle are known and the localization within the virion of 18 of these components has been identified. ASFV morphogenesis occurs in specialized areas in the cytoplasm, named viral factories, which are proximal to the microtubule organization center near the nucleus. Investigations of the different steps of morphogenesis by immunocytochemical and electron microscopy techniques, as well as molecular biology and biochemical studies, have shed light on the formation of the different domains of the virus particle, including the recognition of endoplasmic reticulum membranes as the precursors of the virus inner envelope, the progressive formation of the capsid on the convex face of the inner envelope and the simultaneous assembly of the core shell on the concave side of the envelope, with the pivotal contribution of the virus polyproteins and their proteolytic processing by the virus protease for the development of this latter domain. The use of ASFV inducible recombinants as a tool for the study of the individual function of structural and nonstructural proteins has been determinant to understand their role in virus assembly and has provided new insights into the morphogenetic process. Copyright © 2012 Elsevier B.V. All rights reserved.
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                Author and article information

                Journal
                Journal of General Virology
                Microbiology Society
                0022-1317
                1465-2099
                May 01 2018
                May 01 2018
                : 99
                : 5
                : 613-614
                Affiliations
                [1 ] 1​Department of Biotechnology, Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria (INIA), Madrid 28040, Spain
                [2 ] 2​Agricultural Research Service, Plum Island Animal Disease Center, Greenport, NY 11944, USA
                [3 ] 3​The Pirbright Institute, Ash Road, Pirbright, Woking, Surrey GU24 0NF, UK
                [4 ] 4​Centro de Biología Molecular Severo Ochoa (CSIC-UAM), Universidad Autónoma de Madrid, Madrid, Spain
                [5 ] 5​Centre de Recerca en Sanitat Animal, IRTA, (CReSA, IRTA-UAB), Bellaterra, Spain
                Article
                10.1099/jgv.0.001049
                29565243
                78dd5b6d-219d-4ea8-82a8-26dbc1994bb6
                © 2018
                History

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