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Reassortment events in the evolution of hantaviruses

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Virus Genes

Springer US

Hantavirus, Reassortment, Evolution

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      Abstract

      Hantaviruses (order Bunyavirales, family Hantaviridae), known as important zoonotic human pathogens, possess the capacity to exchange genome segments via genetic reassortment due to their tri-segmented genome. Although not as frequent as in the arthropod-borne bunyaviruses, reports indicating reassortment events in the evolution of hantaviruses have been recently accumulating. The intra- and inter-lineage reassortment between closely related variants has been repeatedly reported for several hantaviruses including the rodent-borne human pathogens such as Sin Nombre virus, Puumala virus, Dobrava-Belgrade virus, or Hantaan virus as well as for the more recently recognized shrew-borne hantaviruses, Imjin and Seewis. Reassortment between more distantly related viruses was rarely found but seems to play a beneficial role in the process of crossing the host species barriers. Besides the findings based on phylogenetic studies of naturally occurring strains, hantavirus reassortants were generated also in in vitro studies. Interestingly, only reassortants with exchanged M segments could be generated suggesting that a high degree of genetic compatibility is required for the S and L segments while the exchange of M segment is better tolerated or is particularly beneficial. Altogether, the numerous reports on hantavirus reassortment, summarized in this review, clearly demonstrate that reassortment events play a significant role in hantavirus evolution and contributed to the currently recognized hantavirus diversity.

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      Complete genome analysis of 33 ecologically and biologically diverse Rift Valley fever virus strains reveals widespread virus movement and low genetic diversity due to recent common ancestry.

      Rift Valley fever (RVF) virus is a mosquito-borne RNA virus responsible for large explosive outbreaks of acute febrile disease in humans and livestock in Africa with significant mortality and economic impact. The successful high-throughput generation of the complete genome sequence was achieved for 33 diverse RVF virus strains collected from throughout Africa and Saudi Arabia from 1944 to 2000, including strains differing in pathogenicity in disease models. While several distinct virus genetic lineages were determined, which approximately correlate with geographic origin, multiple exceptions indicative of long-distance virus movement have been found. Virus strains isolated within an epidemic (e.g., Mauritania, 1987, or Egypt, 1977 to 1978) exhibit little diversity, while those in enzootic settings (e.g., 1970s Zimbabwe) can be highly diverse. In addition, the large Saudi Arabian RVF outbreak in 2000 appears to have involved virus introduction from East Africa, based on the close ancestral relationship of a 1998 East African virus. Virus genetic diversity was low (approximately 5%) and primarily involved accumulation of mutations at an average of 2.9 x 10(-4) substitutions/site/year, although some evidence of RNA segment reassortment was found. Bayesian analysis of current RVF virus genetic diversity places the most recent common ancestor of these viruses in the late 1800s, the colonial period in Africa, a time of dramatic changes in agricultural practices and introduction of nonindigenous livestock breeds. In addition to insights into the evolution and ecology of RVF virus, these genomic data also provide a foundation for the design of molecular detection assays and prototype vaccines useful in combating this important disease.
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          Pathogenic and nonpathogenic hantaviruses differentially regulate endothelial cell responses.

          Hantaviruses cause two human diseases: hemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS). Hantaviruses infect human endothelial cells but cause little or no damage to the infected endothelium. We analyzed with Affymetrix DNA Arrays (Santa Clara, CA) the endothelial cell transcriptional responses directed by hantaviruses associated with HPS [New York-1 virus (NY-1V)], HFRS [Hantaan virus (HTNV)], or by a hantavirus not associated with human disease [Prospect Hill virus (PHV)]. Hantavirus infections induced 117 cellular genes and repressed 25 genes by >3-fold, 4 days postinfection (p.i.). Although >80% of cells were infected by each virus 1 day p.i., PHV induced or repressed 67 genes at this early time compared with three genes altered by HTNV or NY-1V. The early high-level induction of 24 IFN-stimulated genes by PHV (4- to 229-fold) represents a fundamental difference in the temporal regulation of cellular responses by pathogenic and nonpathogenic hantaviruses. Because all hantaviruses induced >23 IFN-stimulated genes at late times p.i., pathogenic hantaviruses appear to suppress early cellular IFN responses that are activated by nonpathogenic hantaviruses. At late times p.i., 13 genes were commonly induced by HTNV and NY-1V that were not induced by PHV. In contrast to NY-1V, HTNV uniquely induced a variety of chemokines and cell adhesion molecules (i.e., IL-8, IL-6, GRO-beta, ICAM), as well as two complement cascade-associated factors that may contribute to immune components of HFRS disease. NY-1V failed to induce most cellular chemokines directed by HTNV (3/14) or genes primarily activated by NF-kappaB. However, NY-1V uniquely induced beta3 integrin-linked potassium channels, which could play a role in HPS-associated vascular permeability. These studies provide a basic understanding of hantavirus-directed cellular responses that are likely to differentiate pathogenic and nonpathogenic hantaviruses, contribute to HFRS and HPS pathogenesis, and provide insight into disease mechanisms and potential therapeutic interventions.
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            Author and article information

            Affiliations
            [1 ]ISNI 0000 0001 2180 9405, GRID grid.419303.c, Biomedical Research Center, Institute of Virology, , Slovak Academy of Sciences, ; Bratislava, Slovakia
            [2 ]ISNI 0000 0001 2218 4662, GRID grid.6363.0, Institute of Virology, , Charité University Hospital, ; Helmut-Ruska-Haus, Berlin, Germany
            Author notes

            Edited by Detlev H. Kruger.

            Contributors
            ORCID: http://orcid.org/0000-0002-6931-1224, +421-2-59302465 , boris.klempa@savba.sk
            Journal
            Virus Genes
            Virus Genes
            Virus Genes
            Springer US (New York )
            0920-8569
            1572-994X
            25 July 2018
            25 July 2018
            2018
            : 54
            : 5
            : 638-646
            30047031
            6153690
            1590
            10.1007/s11262-018-1590-z
            © The Author(s) 2018

            Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

            Funding
            Funded by: FundRef http://dx.doi.org/10.13039/501100001659, Deutsche Forschungsgemeinschaft;
            Award ID: KR1293/15-1
            Award Recipient :
            Funded by: FundRef http://dx.doi.org/10.13039/100010666, H2020 Research Infrastructures;
            Award ID: 653316
            Award Recipient :
            Funded by: FundRef http://dx.doi.org/10.13039/501100005357, Agentúra na Podporu Výskumu a Vývoja;
            Award ID: APVV-15-0232
            Award Recipient :
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            Article
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            © Springer Science+Business Media, LLC, part of Springer Nature 2018

            Microbiology & Virology

            evolution, reassortment, hantavirus

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