13 research outputs found
Brush control and associated botanical changes following tebuthiuron application in Kansas
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Reassortant H9N2 Influenza Viruses Containing H5N1-Like PB1 Genes Isolated from Black-Billed Magpies in Southern China
H9N2 influenza A viruses have become endemic in different types of terrestrial poultry and wild birds in Asia, and are occasionally transmitted to humans and pigs. To evaluate the role of black-billed magpies (Pica pica) in the evolution of influenza A virus, we conducted two epidemic surveys on avian influenza viruses in wild black-billed magpies in Guangxi, China in 2005 and characterized three isolated black-billed magpie H9N2 viruses (BbM viruses). Phylogenetic analysis indicated that three BbM viruses were almost identical with 99.7 to 100% nucleotide homology in their whole genomes, and were reassortants containing BJ94-like (Ck/BJ/1/94) HA, NA, M, and NS genes, SH/F/98-like (Ck/SH/F/98) PB2, PA, and NP genes, and H5N1-like (Ck/YN/1252/03, clade 1) PB1 genes. Genetic analysis showed that BbM viruses were most likely the result of multiple reassortments between co-circulating H9N2-like and H5N1-like viruses, and were genetically different from other H9N2 viruses because of the existence of H5N1-like PB1 genes. Genotypical analysis revealed that BbM viruses evolved from diverse sources and belonged to a novel genotype (B46) discovered in our recent study. Molecular analysis suggested that BbM viruses were likely low pathogenic reassortants. However, results of our pathogenicity study demonstrated that BbM viruses replicated efficiently in chickens and a mammalian mouse model but were not lethal for infected chickens and mice. Antigenic analysis showed that BbM viruses were antigenic heterologous with the H9N2 vaccine strain. Our study is probably the first report to document and characterize H9N2 influenza viruses isolated from black-billed magpies in southern China. Our results suggest that black-billed magpies were susceptible to H9N2 influenza viruses, which raise concerns over possible transmissions of reassortant H9N2 viruses among poultry and wild birds
Phylogenetic Diversity and Genotypical Complexity of H9N2 Influenza A Viruses Revealed by Genomic Sequence Analysis
H9N2 influenza A viruses have become established worldwide in terrestrial poultry and wild birds, and are occasionally transmitted to mammals including humans and pigs. To comprehensively elucidate the genetic and evolutionary characteristics of H9N2 influenza viruses, we performed a large-scale sequence analysis of 571 viral genomes from the NCBI Influenza Virus Resource Database, representing the spectrum of H9N2 influenza viruses isolated from 1966 to 2009. Our study provides a panoramic framework for better understanding the genesis and evolution of H9N2 influenza viruses, and for describing the history of H9N2 viruses circulating in diverse hosts. Panorama phylogenetic analysis of the eight viral gene segments revealed the complexity and diversity of H9N2 influenza viruses. The 571 H9N2 viral genomes were classified into 74 separate lineages, which had marked host and geographical differences in phylogeny. Panorama genotypical analysis also revealed that H9N2 viruses include at least 98 genotypes, which were further divided according to their HA lineages into seven series (A–G). Phylogenetic analysis of the internal genes showed that H9N2 viruses are closely related to H3, H4, H5, H7, H10, and H14 subtype influenza viruses. Our results indicate that H9N2 viruses have undergone extensive reassortments to generate multiple reassortants and genotypes, suggesting that the continued circulation of multiple genotypical H9N2 viruses throughout the world in diverse hosts has the potential to cause future influenza outbreaks in poultry and epidemics in humans. We propose a nomenclature system for identifying and unifying all lineages and genotypes of H9N2 influenza viruses in order to facilitate international communication on the evolution, ecology and epidemiology of H9N2 influenza viruses
New genetic loci link adipose and insulin biology to body fat distribution.
Body fat distribution is a heritable trait and a well-established predictor of adverse metabolic outcomes, independent of overall adiposity. To increase our understanding of the genetic basis of body fat distribution and its molecular links to cardiometabolic traits, here we conduct genome-wide association meta-analyses of traits related to waist and hip circumferences in up to 224,459 individuals. We identify 49 loci (33 new) associated with waist-to-hip ratio adjusted for body mass index (BMI), and an additional 19 loci newly associated with related waist and hip circumference measures (P < 5 × 10(-8)). In total, 20 of the 49 waist-to-hip ratio adjusted for BMI loci show significant sexual dimorphism, 19 of which display a stronger effect in women. The identified loci were enriched for genes expressed in adipose tissue and for putative regulatory elements in adipocytes. Pathway analyses implicated adipogenesis, angiogenesis, transcriptional regulation and insulin resistance as processes affecting fat distribution, providing insight into potential pathophysiological mechanisms
Selection pressure.
<p>Selection pressures on the whole sequence (ω) are calculated for the entire coding regions of the NS1, NS2, PA, NP, PB1, PB2, NA, HA, M1, and M2 genes of the novel swine-origin influenza virus A (H1N1) from April 2009 to May 2010. The number of gene sequences used in this study is shown in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0056201#pone.0056201.s002" target="_blank">Table S1</a>. The ratio ω = <i>dN/dS</i> has become a standard measure of selective pressure; ω≈1 signifies neutral evolution, ω<1 indicates negative selection, ω>1 indicates positive selection, and ω≤0.1 indicates extreme purifying selection. These results indicate that the NS2 gene was under positive selection in April and August 2009 but was under negative selection from May to July 2009 and from September 2009 to May 2010. The remaining eight genes were under negative selection from April 2009 to May 2010.</p
Mutation network for the NS gene of the H1N1 influenza viruses.
<p>A mutation network for Eurasian-“avian-like” swine (Red), classic swine (Orange), human influenza (Blue), triple reassortant swine (Violet), and 2009 H1N1 (Brown). The area of each node is in proportion to the number of sequences the node represents. The ancestral node representing the original sequence type (MV1) is indicated by a black arrow.</p
Worldwide distribution of G1 (A) and G2 (B) type H1N1 viruses.
<p>The G1 genotype was found in early April 2009 throughout North America, Israel, and Portugal. Patients infected in late April and May 2009 with the Mexico type were observed in other countries (e.g., Norway, Thailand, Denmark, the Dominican Republic, Spain, Taiwan, the Netherlands, the United Kingdom, Japan, China, and France). The G2 genotype was also found in the USA, Canada, and Israel, as well as in Taiwan, Malaysia, Singapore, Chile, Russia, Finland, China, Italy, France, and Sweden).</p
Mutation network for the NS gene of the novel influenza virus A (H1N1).
<p>Mutation networks for the NS gene on Apr 2009 (A), Apr to Jun 2009 (B), Apr to Oct 2009 (C), and Apr 2009 to May 2010 (D). The trend of the two prevalent genotypes (G2 and G1 type) remained unchanged from April 2009 to May 2010.</p
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Associations of autozygosity with a broad range of human phenotypes
Abstract: In many species, the offspring of related parents suffer reduced reproductive success, a phenomenon known as inbreeding depression. In humans, the importance of this effect has remained unclear, partly because reproduction between close relatives is both rare and frequently associated with confounding social factors. Here, using genomic inbreeding coefficients (FROH) for >1.4 million individuals, we show that FROH is significantly associated (p < 0.0005) with apparently deleterious changes in 32 out of 100 traits analysed. These changes are associated with runs of homozygosity (ROH), but not with common variant homozygosity, suggesting that genetic variants associated with inbreeding depression are predominantly rare. The effect on fertility is striking: FROH equivalent to the offspring of first cousins is associated with a 55% decrease [95% CI 44–66%] in the odds of having children. Finally, the effects of FROH are confirmed within full-sibling pairs, where the variation in FROH is independent of all environmental confounding