http://precedings.nature.com/tags/Influenza Recently posted documents tagged with 'Influenza' Nature Publishing Group en Nature Precedings http://precedings.nature.com/images/header_logo.gif http://precedings.nature.com http://precedings.nature.com/documents/3820/version/1 Two important challenges to the use of serological assays for influenza surveillance include the substantial amount of experimental effort involved, and the inherent noisiness of serological data. Here, informed by the observation that log-transformed serological data (obtained from the hemagglutination-inhibition assay) exist in an effectively one-dimensional space, computational methods are developed for accurately and efficiently recovering unmeasured serological data from a sample of measured data, and systematically minimizing noise found in the measured data. Careful application of these methods would enable the collection of better-quality serological data on a greater number of circulating influenza viruses than is currently possible, and improve the ability to identify potential epidemic/pandemic viruses before they become widespread. Although the focus here is on influenza surveillance, the described methods are more widely applicable. http://precedings.nature.com/documents/3820/version/1 Mon, 05 Oct 2009 14:18:48 UTC New methods for analyzing serological data with applications to influenza surveillance hdl:10101/npre.2009.3820.1 2009-10-05 Wilfred Ndifon Nature Precedings 2009-10-05T14:18:48Z Manuscript Immunology Evolutionary Biology http://creativecommons.org/licenses/by/3.0/ http://dx.doi.org/10.1038/npre.2009.3493.1 Through retrospectively analyzing billions of internet search queries, Ginsberg et al. identified a collection of specific searches that track the course of influenza-like illness (ILI) reported by the US Centers for Disease Control and Prevention (CDC). Prospective monitoring during 2007-2008 found high correlation between Google estimates and CDC-reported ILI, with next-day timeliness compared to the 1-2 week delay reported in traditional CDC ILI surveillance. The assertion by Ginsberg et al., however, that internet search term estimates enable public health officials to respond better to seasonal and pandemic influenza does not take into account the current practice of public health, or the state of the art in electronic disease surveillance. http://dx.doi.org/10.1038/npre.2009.3493.1 Wed, 05 Aug 2009 15:06:38 UTC Searching for better flu surveillance? A brief communication arising from Ginsberg et al. Nature 457, 1012-1014 (2009) doi:10.1038/npre.2009.3493.1 2009-08-05 Donald R. Olson Nature Precedings 2009-08-05T15:06:38Z Manuscript Microbiology Bioinformatics http://creativecommons.org/licenses/by/3.0/ 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/743/version/2 The rapid evolution of the H5N1 serotype of avian influenza has been explained by a mechanism involving the selection of single nucleotide polymorphisms generated by copy errors. The recent emergence of H5N1 Clade 2.2 in fifty countries, offered a unique opportunity to view the acquisition of new polymorphism in these evolving genomes. We analyzed the H5N1 hemagglutinin gene from a fatal human case from Nigeria in 2007. The newly emerged polymorphisms were present in diverse H5N1 isolates from the previous year. The aggregation of these polymorphisms from clade 2.2 sub-clades was not supported by recent random mutations, and was most easily explained by recombination between closely related sequences. http://precedings.nature.com/documents/743/version/2 Wed, 12 Sep 2007 11:04:26 UTC Aggregation of Single Nucleotide Polymorphisms in a Human H5N1 Clade 2.2 Hemagglutinin hdl:10101/npre.2007.743.2 2009-03-04 Henry L. Niman Nature Precedings 2007-09-12T11:04:26Z Manuscript Genetics & Genomics Evolutionary Biology http://creativecommons.org/licenses/by/2.5/ 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://precedings.nature.com/documents/743/version/1 The evolution of H5N1 has attracted significant interest 1-4 due to linkages with avian 5,6 and human infections 7,8. The basic tenets of influenza genetics 9 attribute genetic drift to replication errors caused by a polymerase complex that lacks a proof reading function. However, recent analysis 10 of swine influenza genes identifies regions copied with absolute fidelity for more than 25 years. In addition, polymorphism tracing of clade 2.2 H5N1 single nucleotide polymorphisms identify concurrent acquisition 11 of the same polymorphism onto multiple genetic backgrounds in widely dispersed geographical locations. Here we show the aggregation of regional clade 2.2 polymorphisms from Germany, Egypt, and sub-Sahara Africa onto a human Nigerian H5N1 hemagglutinin (HA), implicating recombination in the dispersal and aggregation of single nucleotide polymorphisms from closely related genomes. http://precedings.nature.com/documents/743/version/1 Thu, 16 Aug 2007 15:53:42 UTC Aggregation of Single Nucleotide Polymorphisms in a Human H5N1 Clade 2.2 Hemagglutinin hdl:10101/npre.2007.743.1 2007-08-16 Henry L. Niman Nature Precedings 2007-08-16T15:53:42Z Manuscript Biotechnology 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/