http://precedings.nature.com/tags/H5N1 Recently posted documents tagged with 'H5N1' Nature Publishing Group en Nature Precedings http://precedings.nature.com/images/header_logo.gif http://precedings.nature.com http://precedings.nature.com/documents/2832/version/1 The dramatic rise of oseltamivir resistance in the H1N1 serotype in the 2007/2008 season and the fixing of H274Y in the 2008/2009 season has raised concerns regarding individuals at risk for seasonal influenza, as well as development of similar resistance in the H5N1 serotype. Previously, oseltamivir resistance produced changes in H1N1 and H3N2 at multiple positions in treated patients. In contrast, the recently reported resistance involved patients who had not recently taken oseltamivir. Moreover, the resistance was limited to the H1N1 which had acquired H274Y. Using phylogenetic analysis I show that the fixing of H274Y was due to hitch hiking on a genetic background that acquired key changes from another circulating sub-clade. H274Y jumped from clade 2C (Hong Kong/2562/2006-like) to clade 1 (New Caledonia/20/1999-like) to clade 2B (Brisbane/59/2007-like) which included multiple introductions. Sub-clades that had acquired key changes on the neuramindase and hemagglutinin genes expanded and fixed of H274Y on H1N1. These changes led to the spread of adamantane resistance on clade 2C outside of Asia, followed by the spread of oseltamivir resistance in 2007/2008 and the fixing of H274Y in 2008/2009. The hemagglutinin change, A193T, was a key component and the coincident polymorphism, S193F, was linked to the fixing of adamantane resistance in H3N2. The aggregation of key polymorphisms onto different genetic backgrounds supports a mechanism of homologous recombination between co-circulating influenza sub-clades, and provides a rationale for the prediction of vaccine targets and emergence of antiviral resistance. http://precedings.nature.com/documents/2832/version/1 Tue, 10 Feb 2009 09:25:49 UTC Emergence and Fixing of Antiviral Resistance in Influenza A Via Recombination and Hitch Hiking hdl:10101/npre.2009.2832.1 2009-02-10 Henry L. Niman Nature Precedings 2009-02-10T09:25:49Z Manuscript Biotechnology Genetics & Genomics Immunology http://creativecommons.org/licenses/by/3.0/ http://precedings.nature.com/documents/459/version/4 Highly pathogenic Influenza A H5N1 was first identified in Guangdong Province in 1996, followed by human cases in Hong Kong in 1997 1,2. The number of confirmed human cases now exceeds 300 and the associated Case Fatality Rate exceeds 60% 3. The genetic diversity of the serotype continues to increase. Four distinct clades or sub-clades have been linked to human cases 4-7. The gradual genetic changes identified in the sub-clades have been attributed to copy errors by viral encoded polymerases that lack an editing function, thereby resulting in antigenic drift 8. We report here the concurrent acquisition of the same polymorphism by multiple, genetically distinct, clade 2.2 sub-clades in Egypt, Russia, Kuwait, and Ghana. These changes are not easily explained by the current theory of “random mutation” through copy error, and are more easily explained by recombination with a common source. The recombination role is further supported by the high fidelity replication in swine influenza 9 and aggregation of single nucleotide polymorphisms in H5N1 clade 2.2 hemagglutinin 10. http://precedings.nature.com/documents/459/version/4 Thu, 08 May 2008 21:53:58 UTC Concurrent Acquisition of a Single Nucleotide Polymorphism in Diverse Influenza H5N1 Clade 2.2 Sub-clades hdl:10101/npre.2008.459.4 2008-05-11 Henry Niman Nature Precedings 2008-05-08T21:53:58Z Manuscript Biotechnology Ecology Genetics & Genomics Microbiology Bioinformatics http://creativecommons.org/licenses/by/3.0/ http://precedings.nature.com/documents/459/version/3 Highly pathogenic Influenza A H5N1 was first identified in Guangdong Province in 1996, followed by human cases in Hong Kong in 1997. The number of confirmed human cases now exceeds 300, and the associated Case Fatality Rate exceeds 60%. The genetic diversity of the serotype continues to increase. Four distinct clades or sub-clades have been linked to human cases. The gradual genetic changes identified in the sub-clades have been attributed to copy errors by viral encoded polymerases that lack an editing function, thereby resulting in antigenic drift. We report here the concurrent acquisition of the same polymorphism by multiple, genetically distinct, clade 2.2 sub-clades in Egypt, Russia, and Ghana. These changes are not easily explained by the current theory of “random mutation” through copy error, and are more easily explained by recombination with a common source. This conclusion is supported by additional polymorphisms shared by clade 2.2 isolates in Egypt and Germany. http://precedings.nature.com/documents/459/version/3 Wed, 12 Sep 2007 10:27:59 UTC Concurrent Acquisition of a Single Nucleotide Polymorphism in Diverse Influenza H5N1 Clade 2.2 Sub-clades hdl:10101/npre.2007.459.3 2007-09-12 Henry L. Niman Nature Precedings 2007-09-12T10:27:59Z Manuscript Biotechnology Chemistry Ecology Genetics & Genomics Immunology Microbiology Bioinformatics http://creativecommons.org/licenses/by/2.5/ http://dx.doi.org/10.1038/npre.2007.553.2 Highly pathogenic Influenza A H5N1 was first identified in Guangdong Province in 1996, followed by human cases in Hong Kong in 1997 1. The number of confirmed human cases now exceeds 300 and the associated Case Fatality Rate exceeds 60% 2. The genetic diversity of the serotype continues to increase. Four distinct clades or sub-clades have been linked to human cases 3.4. The gradual genetic changes identified in the sub-clades have been attributed to copy errors by viral encoded polymerases that lack an editing function, thereby resulting in antigenic drift 5. We traced polymorphism acquisition in Clade 2.2 sequences. We report here the concurrent acquisition of the same polymorphism by multiple, genetically distinct, Clade 2.2 sub-clades in Egypt, Russia and Ghana. These changes are not easily explained by the current theory of “random mutation” through copy error, and are more easily explained by recombination with a common source. This conclusion is supported by additional polymorphisms shared by Clade 2.2 isolates in Egypt, Nigeria and Germany including aggregation of regional polymorphisms from each of these areas into a single Nigerian human hemagglutinin gene. http://dx.doi.org/10.1038/npre.2007.553.2 Tue, 07 Aug 2007 16:18:58 UTC H5N1 Clade 2.2 Polymorphism Tracing Identifies Influenza Recombination and Potential Vaccine Targets doi:10.1038/npre.2007.553.2 2007-08-07 Henry L. Niman Nature Precedings 2007-08-07T16:18:58Z Manuscript Biotechnology Ecology Genetics & Genomics Microbiology Bioinformatics http://creativecommons.org/licenses/by/2.5/ http://dx.doi.org/10.1038/npre.2007.553.1 Highly pathogenic Influenza A H5N1 was first identified in Guangdong Province in 1996, followed by human cases in Hong Kong in 1997 1. The number of confirmed human cases now exceeds 300 and the associated Case Fatality Rate exceeds 60% 2. The genetic diversity of the serotype continues to increase. Four distinct clades or sub-clades have been linked to human cases 3.4. The gradual genetic changes identified in the sub-clades have been attributed to copy errors by viral encoded polymerases that lack an editing function, thereby resulting in antigenic drift 5. We traced polymorphism acquisition in Clade 2.2 sequences. We report here the concurrent acquisition of the same polymorphism by multiple, genetically distinct, Clade 2.2 sub-clades in Egypt, Russia and Ghana. These changes are not easily explained by the current theory of “random mutation” through copy error, and are more easily explained by recombination with a common source. This conclusion is supported by additional polymorphisms shared by Clade 2.2 isolates in Egypt, Nigeria and Germany including aggregation of regional polymorphisms from each of these areas into a single Nigerian human hemagglutinin gene. http://dx.doi.org/10.1038/npre.2007.553.1 Fri, 27 Jul 2007 09:41:02 UTC H5N1 Clade 2.2 Polymorphism Tracing Identifies Influenza Recombination and Potential Vaccine Targets doi:10.1038/npre.2007.553.1 2007-07-27 Henry L. Niman Nature Precedings 2007-07-27T09:41:02Z Manuscript Biotechnology Ecology Genetics & Genomics Microbiology Bioinformatics http://creativecommons.org/licenses/by/2.5/ http://precedings.nature.com/documents/459/version/2 Highly pathogenic Influenza A H5N1 was first identified in Guangdong Province in 1996, followed by human cases in Hong Kong in 1997. The number of confirmed human cases now exceeds 300, and the associated Case Fatality Rate exceeds 60%. The genetic diversity of the serotype continues to increase. Four distinct clades or sub-clades have been linked to human cases. The gradual genetic changes identified in the sub-clades have been attributed to copy errors by viral encoded polymerases that lack an editing function, thereby resulting in antigenic drift. We report here the concurrent acquisition of the same polymorphism by multiple, genetically distinct, clade 2.2 sub-clades in Egypt, Russia, and Ghana. These changes are not easily explained by the current theory of “random mutation” through copy error, and are more easily explained by recombination with a common source. This conclusion is supported by additional polymorphisms shared by clade 2.2 isolates in Egypt and Germany. http://precedings.nature.com/documents/459/version/2 Mon, 23 Jul 2007 13:45:43 UTC Concurrent Acquisition of a Single Nucleotide Polymorphism in Diverse Influenza H5N1 Clade 2.2 Sub-clades hdl:10101/npre.2007.459.2 2007-07-23 Henry L. Niman Nature Precedings 2007-07-23T13:45:43Z Manuscript Biotechnology Ecology Genetics & Genomics Microbiology Bioinformatics http://creativecommons.org/licenses/by/2.5/ http://precedings.nature.com/documents/459/version/1 Highly pathogenic Influenza A H5N1 was first identified in Guangdong Province in 1996, followed by human cases in Hong Kong in 1997 1,2. The number of confirmed human cases now exceeds 300, and the associated Case Fatality Rate exceeds 60% 3. The genetic diversity of the serotype continues to increase. Four distinct clades or sub-clades have been linked to human cases 4-7. The gradual genetic changes identified in the sub-clades have been attributed to copy errors by viral encoded polymerases that lack an editing function, thereby resulting in antigenic drift 8. We report here the concurrent acquisition of the same polymorphism by multiple, genetically distinct, clade 2.2 sub-clades in Egypt, Russia, and Ghana. These changes are not easily explained by the current theory of “random mutation” through copy error, and are more easily explained by recombination with a common source. This conclusion is supported by additional polymorphisms shared by clade 2.2 isolates in Egypt and Germany. http://precedings.nature.com/documents/459/version/1 Mon, 16 Jul 2007 05:09:59 UTC Concurrent Acquisition of a Single Nucleotide Polymorphism in Diverse Influenza H5N1 Clade 2.2 Sub-clades hdl:10101/npre.2007.459.1 2007-07-16 Henry L. Niman Nature Precedings 2007-07-16T05:09:59Z Manuscript Biotechnology Ecology Genetics & Genomics Microbiology Bioinformatics http://creativecommons.org/licenses/by/2.5/ http://precedings.nature.com/documents/385/version/1 The looming influenza pandemic has focused attention1-4 on the rapid evolution of H5N1 and other human and avian serotypes. The basic tenets of influenza genetics5 define gradual changes as drifts caused by point mutations created by a polymerase that lacks a proof reading function. More abrupt changes have been linked to reassortment, which shuffles the eight sub-genomic segments of the influenza genome in dually infected host. The complex evolution of these viruses has created a challenge in vaccine development. Swine influenza isolates from 2003 and 2004 have been identified6 that have acquired a human influenza gene, PB1. My analysis of the eight gene segments found large portions of two genes, PB2 and PA, which were identical matches with 1977 swine isolates7,8. Additional regions were exact matches with 1998 and 2002 isolates,9,10 demonstrating homologous recombination between earlier genomes. The absolute fidelity discounts the role of point mutations in gene drift. Moreover the human PB1 gene represented a reservoir for acquisition of polymorphisms in human seasonal flu. These observations challenge the basic tenets of influenza genetics and provide a method for predicting the changes in seasonal and pandemic influenza, as well as other rapidly evolving genomes. http://precedings.nature.com/documents/385/version/1 Tue, 10 Jul 2007 13:59:11 UTC Swine Influenza A Evolution via Recombination – Genetic Drift Reservoir hdl:10101/npre.2007.385.1 2009-01-09 Henry L. Niman Nature Precedings 2007-07-10T13:59:11Z Manuscript Ecology Genetics & Genomics http://creativecommons.org/licenses/by/2.5/