40 research outputs found

    Viral Gastroenteritis Associated with Genogroup II Norovirus among U.S. Military Personnel in Turkey, 2009

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    The present study demonstrates that multiple NoV genotypes belonging to genogroup II contributed to an acute gastroenteritis outbreak at a US military facility in Turkey that was associated with significant negative operational impact. Norovirus (NoV) is an important pathogen associated with acute gastroenteritis among military populations. We describe the genotypes of NoV outbreak occurred at a United States military facility in Turkey. Stool samples were collected from 37 out of 97 patients presenting to the clinic on base with acute gastroenteritis and evaluated for bacterial and viral pathogens. NoV genogroup II (GII) was identified by RT-PCR in 43% (16/37) stool samples. Phylogenetic analysis of a 260 base pair fragment of the NoV capsid gene from ten stool samples indicated the circulation of multiple and rare genotypes of GII NoV during the outbreak. We detected four GII.8 isolates, three GII.15, two GII.9 and a sole GII.10 NoV. Viral sequences could be grouped into four clusters, three of which have not been previously reported in Turkey. The fact that current NoV outbreak was caused by rare genotypes highlights the importance of norovirus strain typing. While NoV genogroup II is recognized as causative agent of outbreak, circulation of current genotypes has been rarely observed in large number of outbreaks

    Evolutionary Dynamics and Emergence of Panzootic H5N1 Influenza Viruses

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    The highly pathogenic avian influenza (HPAI) H5N1 virus lineage has undergone extensive genetic reassortment with viruses from different sources to produce numerous H5N1 genotypes, and also developed into multiple genetically distinct sublineages in China. From there, the virus has spread to over 60 countries. The ecological success of this virus in diverse species of both poultry and wild birds with frequent introduction to humans suggests that it is a likely source of the next human pandemic. Therefore, the evolutionary and ecological characteristics of its emergence from wild birds into poultry are of considerable interest. Here, we apply the latest analytical techniques to infer the early evolutionary dynamics of H5N1 virus in the population from which it emerged (wild birds and domestic poultry). By estimating the time of most recent common ancestors of each gene segment, we show that the H5N1 prototype virus was likely introduced from wild birds into poultry as a non-reassortant low pathogenic avian influenza H5N1 virus and was not generated by reassortment in poultry. In contrast, more recent H5N1 genotypes were generated locally in aquatic poultry after the prototype virus (A/goose/Guangdong/1/96) introduction occurred, i.e., they were not a result of additional emergence from wild birds. We show that the H5N1 virus was introduced into Indonesia and Vietnam 3–6 months prior to detection of the first outbreaks in those countries. Population dynamics analyses revealed a rapid increase in the genetic diversity of A/goose/Guangdong/1/96 lineage viruses from mid-1999 to early 2000. Our results suggest that the transmission of reassortant viruses through the mixed poultry population in farms and markets in China has selected HPAI H5N1 viruses that are well adapted to multiple hosts and reduced the interspecies transmission barrier of those viruses

    Gain and Loss of Phototrophic Genes Revealed by Comparison of Two Citromicrobium Bacterial Genomes

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    Proteobacteria are thought to have diverged from a phototrophic ancestor, according to the scattered distribution of phototrophy throughout the proteobacterial clade, and so the occurrence of numerous closely related phototrophic and chemotrophic microorganisms may be the result of the loss of genes for phototrophy. A widespread form of bacterial phototrophy is based on the photochemical reaction center, encoded by puf and puh operons that typically are in a ‘photosynthesis gene cluster’ (abbreviated as the PGC) with pigment biosynthesis genes. Comparison of two closely related Citromicrobial genomes (98.1% sequence identity of complete 16S rRNA genes), Citromicrobium sp. JL354, which contains two copies of reaction center genes, and Citromicrobium strain JLT1363, which is chemotrophic, revealed evidence for the loss of phototrophic genes. However, evidence of horizontal gene transfer was found in these two bacterial genomes. An incomplete PGC (pufLMC-puhCBA) in strain JL354 was located within an integrating conjugative element, which indicates a potential mechanism for the horizontal transfer of genes for phototrophy

    Emergence and phylodynamics of Citrus tristeza virus in Sicily, Italy

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    [EN] Citrus tristeza virus (CTV) outbreaks were detected in Sicily island, Italy for the first time in 2002. To gain insight into the evolutionary forces driving the emergence and phylogeography of these CTV populations, we determined and analyzed the nucleotide sequences of the p20 gene from 108 CTV isolates collected from 2002 to 2009. Bayesian phylogenetic analysis revealed that mild and severe CTV isolates belonging to five different clades (lineages) were introduced in Sicily in 2002. Phylogeographic analysis showed that four lineages co-circulated in the main citrus growing area located in Eastern Sicily. However, only one lineage (composed of mild isolates) spread to distant areas of Sicily and was detected after 2007. No correlation was found between genetic variation and citrus host, indicating that citrus cultivars did not exert differential selective pressures on the virus. The genetic variation of CTV was not structured according to geographical location or sampling time, likely due to the multiple introduction events and a complex migration pattern with intense co- and recirculation of different lineages in the same area. The phylogenetic structure, statistical tests of neutrality and comparison of synonymous and nonsynonymous substitution rates suggest that weak negative selection and genetic drift following a rapid expansion may be the main causes of the CTV variability observed today in Sicily. Nonetheless, three adjacent amino acids at the p20 N-terminal region were found to be under positive selection, likely resulting from adaptation events.A.W. and S.F.E. were supported by grant BFU2012-30805 from the Spanish Secretaria de Estado de Investigacion, Desarrollo e Innovacion and by a grant 22371 from the John Templeton Foundation. The opinions expressed in this publication are those of the authors and do not necessarily reflect the views of the John Templeton Foundation. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Davino, S.; Willemsen, A.; Panno. Stefano; Davino, M.; Catara, A.; Elena Fito, SF.; Rubio, L. (2013). Emergence and phylodynamics of Citrus tristeza virus in Sicily, Italy. PLoS ONE. 8:66700-66700. doi:10.1371/journal.pone.0066700S66700667008Domingo, E., & Holland, J. J. (1997). RNA VIRUS MUTATIONS AND FITNESS FOR SURVIVAL. Annual Review of Microbiology, 51(1), 151-178. doi:10.1146/annurev.micro.51.1.151Grenfell, B. T. (2004). Unifying the Epidemiological and Evolutionary Dynamics of Pathogens. Science, 303(5656), 327-332. doi:10.1126/science.1090727Moya, A., Holmes, E. C., & González-Candelas, F. (2004). The population genetics and evolutionary epidemiology of RNA viruses. 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PLoS Pathogens, 6(10), e1001166. doi:10.1371/journal.ppat.1001166Vijaykrishna, D., Bahl, J., Riley, S., Duan, L., Zhang, J. X., Chen, H., … Guan, Y. (2008). Evolutionary Dynamics and Emergence of Panzootic H5N1 Influenza Viruses. PLoS Pathogens, 4(9), e1000161. doi:10.1371/journal.ppat.1000161Gómez, P., Sempere, R. N., Aranda, M. A., & Elena, S. F. (2012). Phylodynamics of Pepino mosaic virus in Spain. European Journal of Plant Pathology, 134(3), 445-449. doi:10.1007/s10658-012-0019-0Lefeuvre, P., Martin, D. P., Harkins, G., Lemey, P., Gray, A. J. A., Meredith, S., … Heydarnejad, J. (2010). The Spread of Tomato Yellow Leaf Curl Virus from the Middle East to the World. PLoS Pathogens, 6(10), e1001164. doi:10.1371/journal.ppat.1001164TOMITAKA, Y., & OHSHIMA, K. (2006). A phylogeographical study of the Turnip mosaic virus population in East Asia reveals an ‘emergent’ lineage in Japan. Molecular Ecology, 15(14), 4437-4457. doi:10.1111/j.1365-294x.2006.03094.xWu, B., Blanchard-Letort, A., Liu, Y., Zhou, G., Wang, X., & Elena, S. F. (2011). Dynamics of Molecular Evolution and Phylogeography of Barley yellow dwarf virus-PAV. PLoS ONE, 6(2), e16896. doi:10.1371/journal.pone.0016896MORENO, P., AMBRÓS, S., ALBIACH-MARTÍ, M. R., GUERRI, J., & PEÑA, L. (2008). Citrus tristeza virus: a pathogen that changed the course of the citrus industry. Molecular Plant Pathology, 9(2), 251-268. doi:10.1111/j.1364-3703.2007.00455.xTatineni, S., Robertson, C. J., Garnsey, S. M., & Dawson, W. O. (2011). A plant virus evolved by acquiring multiple nonconserved genes to extend its host range. Proceedings of the National Academy of Sciences, 108(42), 17366-17371. doi:10.1073/pnas.1113227108Folimonova, S. Y. (2012). Superinfection Exclusion Is an Active Virus-Controlled Function That Requires a Specific Viral Protein. Journal of Virology, 86(10), 5554-5561. doi:10.1128/jvi.00310-12Bar-Joseph, M., Marcus, R., & Lee, R. F. (1989). The Continuous Challenge of Citrus Tristeza Virus Control. Annual Review of Phytopathology, 27(1), 291-316. doi:10.1146/annurev.py.27.090189.001451Davino, S., Rubio, L., & Davino, M. (2005). Molecular analysis suggests that recent Citrus tristeza virus outbreaks in Italy were originated by at least two independent introductions. European Journal of Plant Pathology, 111(3), 289-293. doi:10.1007/s10658-003-2815-zAlbiach-Marti, M. R., Mawassi, M., Gowda, S., Satyanarayana, T., Hilf, M. E., Shanker, S., … Dawson, W. O. (2000). Sequences of Citrus Tristeza Virus Separated in Time and Space Are Essentially Identical. Journal of Virology, 74(15), 6856-6865. doi:10.1128/jvi.74.15.6856-6865.2000Rubio, L., Ayllon, M. A., Kong, P., Fernandez, A., Polek, M., Guerri, J., … Falk, B. W. (2001). Genetic Variation of Citrus Tristeza Virus Isolates from California and Spain: Evidence for Mixed Infections and Recombination. Journal of Virology, 75(17), 8054-8062. doi:10.1128/jvi.75.17.8054-8062.2001Silva, G., Marques, N., & Nolasco, G. (2011). The evolutionary rate of citrus tristeza virus ranks among the rates of the slowest RNA viruses. Journal of General Virology, 93(2), 419-429. doi:10.1099/vir.0.036574-0Mawassi, M., Mietkiewska, E., Gofman, R., Yang, G., & Bar-Joseph, M. (1996). Unusual Sequence Relationships Between Two Isolates of Citrus Tristeza Virus. Journal of General Virology, 77(9), 2359-2364. doi:10.1099/0022-1317-77-9-2359Vives, M. C., Dawson, W. O., Flores, R., L√≥pez, C., Albiach-Mart√≠, M. R., Rubio, L., … Moreno, P. (1999). The complete genome sequence of the major component of a mild citrus tristeza virus isolate. Journal of General Virology, 80(3), 811-816. doi:10.1099/0022-1317-80-3-811Martín, S., Elena, S. F., Guerri, J., Moreno, P., Sambade, A., Rubio, L., … Vives, M. C. (2009). Contribution of recombination and selection to molecular evolution of Citrus tristeza virus. Journal of General Virology, 90(6), 1527-1538. doi:10.1099/vir.0.008193-0Vives, M. C., Rubio, L., Sambade, A., Mirkov, T. E., Moreno, P., & Guerri, J. (2005). Evidence of multiple recombination events between two RNA sequence variants within a Citrus tristeza virus isolate. Virology, 331(2), 232-237. doi:10.1016/j.virol.2004.10.037D’Urso, F., Sambade, A., Moya, A., Guerri, J., & Moreno, P. (2003). Variation of haplotype distributions of two genomic regions of Citrus tristeza virus populations from eastern Spain. Molecular Ecology, 12(2), 517-526. doi:10.1046/j.1365-294x.2000.01747.xSambade, A., Rubio, L., Garnsey, S. M., Costa, N., Muller, G. W., Peyrou, M., … Moreno, P. (2002). Comparison of viral RNA populations of pathogenically distinct isolates of Citrus tristeza virus : application to monitoring cross-protection. 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    Reassortment of two tripartite genomes producing a novel reassortant.

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    <p>A) Diagrammatic representation of the emergence of a novel reassortant strain with genes derived from two parents. B) Phylogenetic discordance between segments 1 and 3 (left) and segment 2 (right) for three tripartite strains. Branches in bolder colors represent parental strains, whereas lighter colors represent the acquisition of gene segments from different parents to form a novel reassortant strain.</p

    Dating the emergence of pandemic influenza viruses

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    Pandemic influenza viruses cause significant mortality in humans. In the 20th century, 3 influenza viruses caused major pandemics: the 1918 H1N1 virus, the 1957 H2N2 virus, and the 1968 H3N2 virus. These pandemics were initiated by the introduction and successful adaptation of a novel hemagglutinin subtype to humans from an animal source, resulting in antigenic shift. Despite global concern regarding a new pandemic influenza, the emergence pathway of pandemic strains remains unknown. Here we estimated the evolutionary history and inferred date of introduction to humans of each of the genes for all 20th century pandemic influenza strains. Our results indicate that genetic components of the 1918 H1N1 pandemic virus circulated in mammalian hosts, i.e., swine and humans, as early as 1911 and was not likely to be a recently introduced avian virus. Phylogenetic relationships suggest that the A/Brevig Mission/1/1918 virus (BM/1918) was generated by reassortment between mammalian viruses and a previously circulating human strain, either in swine or, possibly, in humans. Furthermore, seasonal and classic swine H1N1 viruses were not derived directly from BM/1918, but their precursors co-circulated during the pandemic. Mean estimates of the time of most recent common ancestor also suggest that the H2N2 and H3N2 pandemic strains may have been generated through reassortment events in unknown mammalian hosts and involved multiple avian viruses preceding pandemic recognition. The possible generation of pandemic strains through a series of reassortment events in mammals over a period of years before pandemic recognition suggests that appropriate surveillance strategies for detection of precursor viruses may abort future pandemics

    Origins and evolutionary genomics of the 2009 swine-origin H1N1 influenza A epidemic

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    In March and early April 2009, a new swine-origin influenza A (H1N1) virus (S-OIV) emerged in Mexico and the United States. During the first few weeks of surveillance, the virus spread worldwide to 30 countries (as of May 11) by human-to-human transmission, causing the World Health Organisation to raise its pandemic alert to level 5 of 6. This virus has the potential to develop into the first influenza pandemic of the twenty-first century. Here we use evolutionary analysis to estimate the time-scale of the origins and the early development of the S-OIV epidemic. We show that it was derived from several viruses circulating in swine, and that the initial transmission to humans occurred several months before recognition of the outbreak. A phylogenetic estimate of the gaps in genetic surveillance indicates a long period of unsampled ancestry before the S-OIV outbreak, suggesting that the reassortment of swine lineages may have occurred years before human emergence, and that the multiple genetic ancestry of S-OIV is not indicative of an artificial origin. Furthermore, the unsampled history of the epidemic means that the nature and location of the genetically closest swine viruses reveal little about the immediate origin of the epidemic, despite the fact that we included a panel of closely related and previously unpublished swine influenza isolates. Our results highlight the need for systematic surveillance of influenza in swine, and provide evidence that the mixing of new genetic elements in swine can result in the emergence of viruses with pandemic potential in humans
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