5 results on '"Wiman, Asa"'
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2. Low 2018/19 vaccine effectiveness against influenza A(H3N2) among 15–64-year-olds in Europe: exploration by birth cohort
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Kissling, Esther, Pozo, Francisco, Buda, Silke, Vilcu, Ana-Maria, Gherasim, Alin, Brytting, Mia, Domegan, Lisa, Gomez, Veronica, Meijer, Adam, Lazar, Mihaela, Vucina, Vesna Visekruna, Duerrwald, Ralf, van der Werf, Sylvie, Larrauri, Amparo, Enkirch, Theresa, O'Donnell, Joan, Guiomar, Raquel, Hooiveld, Mariette, Petrovic, Goranka, Stoian, Elena, Penttinen, Pasi, Valenciano, Marta, Preuss, Ute, Tolksdorf, Kristin, Biere, Barbara, Smallfield, Maria, Wedde, Marianne, Falchi, Alessandra, Masse, Shirley, Villechenaud, Natacha, Souty, Cecile, Blanchon, Thierry, Launay, Titouan, Enouf, Vincent, Behillil, Sylvie, Lina, Bruno, Valette, Martine, Mazagatos, Clara, Casas, Inmaculada, Garcia Comas, Luis, Insua Marisquerena, Maria Esther, Carlos Galan, Juan, Castilla, Jesus, Garcia Cenoz, Manuel, Navascues, Ana, Quinones Rubio, Carmen, Ibanez Perez, Ana Carmen, Martinez Ochoa, Eva, Blasco, Miriam, Gimenez Duran, Jaume, Maria Vanrell, Juana, Reina, Jordi, Castrillejo, Daniel, Wiman, Asa, Hunt, Meadhbh, Joyce, Michael, Levis, Olga, Collins, Claire, Dunford, Linda, Bennett, Charlene, Moran, Joanne, Tuite, Grainne, Connell, Jeff, de Gascun, Cillian, Rodrigues, Ana Paula, Machado, Ausenda, Nunes, Baltazar, Kislaya, Irina, Costa, Ines, Conde, Patricia, Cristovao, Paula, Pechirra, Pedro, Borges, Vitor, Bagheri, Mariam, van den Brink, Sharon, Dijkstra, Frederika, Goderski, Gabriel, van der Hoek, Wim, de Lange, Marit, Marzec, Ton, Overduin, Pieter, Reukers, Daphne, Teirlinck, Anne, Wijsman, Lisa, Donker, Ge, Mihai, Maria Elena, Cherciu, Carmen Maria, Alexandrescu, Viorel, Kaic, Bernard, Filipovic, Sanja Kurecic, Novosel, Iva Pem, Makaric, Zvjezdana Lovric, Zajec, Martina, Drazenovic, Vladimir, Moren, Alain, I-MOVE Primary Care Study Team, EpiConcept [Paris], Instituto de Salud Carlos III [Madrid] (ISC), Robert Koch Institute [Berlin] (RKI), Institut Pierre Louis d'Epidémiologie et de Santé Publique (iPLESP), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), CIBER de Epidemiología y Salud Pública (CIBERESP), Public Health Agency of Sweden, Health Protection Surveillance Centre (HPSC), Instituto Nacional de Saùde Dr Ricardo Jorge [Portugal] (INSA), National Institute for Public Health and the Environment [Bilthoven] (RIVM), Cantacuzino Institute [Romania], Réseau International des Instituts Pasteur (RIIP), Génétique Moléculaire des Virus à ARN - Molecular Genetics of RNA Viruses (GMV-ARN (UMR_3569 / U-Pasteur_2)), Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité), Centre National de Référence des virus des infections respiratoires (dont la grippe) - National Reference Center Virus Influenzae [Paris] (CNR - laboratoire coordonnateur), Institut Pasteur [Paris] (IP), and Netherlands Institute for Health Services Research [Utrecht] (NIVEL)
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vacunas de la gripe ,Male ,0301 basic medicine ,potencia vacunal ,Epidemiology ,[SDV]Life Sciences [q-bio] ,humanos ,Gripe ,adolescente ,Hemagglutinin Glycoproteins, Influenza Virus ,virus de la influenza A ,0302 clinical medicine ,infecciones del tracto respiratorio ,memoria inmunológica ,vigilancia centinela ,Determinantes de Saúde e Doença ,Medicine ,030212 general & internal medicine ,Respiratory Tract Infections ,mediana edad ,Vaccine effectiveness ,anciano ,birth cohorts ,Birth cohorts ,Estado de Saúde e Doença ,resultado del tratamiento ,Vaccination ,Age Factors ,Imprinting ,adulto ,Middle Aged ,multicentre study ,Europe ,Treatment Outcome ,Influenza A virus ,Época 2018-2019 ,Influenza Vaccines ,Population Surveillance ,Female ,Seasons ,imprinting ,influenza ,Birth cohort ,A(H3N2) ,Adult ,Adolescent ,Primary care ,Multicentre study ,vacunación ,03 medical and health sciences ,vigilancia de la población ,Virology ,Influenza, Human ,Humans ,ddc:610 ,Vacina Antigripal ,EuroEVA ,Vaccine Potency ,Aged ,vaccine effectiveness ,business.industry ,Influenza A Virus, H3N2 Subtype ,Research ,Efetividade ,Public Health, Environmental and Occupational Health ,Influenza a ,Influenza ,estaciones (meteorología) ,030104 developmental biology ,influenza vaccination, test negative case control, vaccine effectiveness ,610 Medizin und Gesundheit ,business ,Immunologic Memory ,Sentinel Surveillance ,Demography - Abstract
Introduction Influenza A(H3N2) clades 3C.2a and 3C.3a co-circulated in Europe in 2018/19. Immunological imprinting by first childhood influenza infection may induce future birth cohort differences in vaccine effectiveness (VE). Aim The I-MOVE multicentre primary care test-negative study assessed 2018/19 influenza A(H3N2) VE by age and genetic subgroups to explore VE by birth cohort. Methods We measured VE against influenza A(H3N2) and (sub)clades. We stratified VE by usual age groups (0–14, 15–64, ≥ 65-years). To assess the imprint-regulated effect of vaccine (I-REV) hypothesis, we further stratified the middle-aged group, notably including 32–54-year-olds (1964–86) sharing potential childhood imprinting to serine at haemagglutinin position 159. Results Influenza A(H3N2) VE among all ages was −1% (95% confidence interval (CI): −24 to 18) and 46% (95% CI: 8–68), −26% (95% CI: −66 to 4) and 20% (95% CI: −20 to 46) among 0–14, 15–64 and ≥ 65-year-olds, respectively. Among 15–64-year-olds, VE against clades 3C.2a1b and 3C.3a was 15% (95% CI: −34 to 50) and −74% (95% CI: −259 to 16), respectively. VE was −18% (95% CI: −140 to 41), −53% (95% CI: −131 to −2) and −12% (95% CI: −74 to 28) among 15–31-year-olds (1987–2003), 32–54-year-olds (1964–86) and 55–64-year-olds (1954–63), respectively. Discussion The lowest 2018/19 influenza A(H3N2) VE was against clade 3C.3a and among those born 1964–86, corresponding to the I-REV hypothesis. The low influenza A(H3N2) VE in 15–64-year-olds and the public health impact of the I-REV hypothesis warrant further study.
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- 2019
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3. Start of the 2014/15 influenza season in Europe: drifted influenza A(H3N2) viruses circulate as dominant subtype
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Broberg, E., Snacken, R., Adlhoch, C., Beaute, J., Galinska, M., Pereyaslov, D., Brown, C., Penttinen, P., Who, European Region And The European Influenza Surveillance Network, Kota, Majlinda, Simaku, Artan, Sarkisian, Shushan, Torosyan, Liana, Popow-Kraupp, Therese, Rendi-Wagner, Pamela, Schmid, Daniela, Abdullayeva, Nazakat, Salimov, Oleg, Gribkova, Natalia, Shimanovich, Veronika, Thomas, Isabelle, Hombrouck, Anneleen, Bossuyt, Nathalie, Moreels, Sarah, Casteren, Viviane, Ljubovic, Amela Dedejic, Rodic, Nina Vukmir, Korsun, Neli, Kojouharova, Mira, Georgieva, Teodora, Drazenovic, Vladimir, Bagatzouni, Despo, Koliou, Maria, Havlickova, Martina, Jirincova, Helena, Kyncl, Jan, Knudsen, Lisbet Krause, Mazick, Anne, Trebbien, Ramona, Fischer, Thea Kolsen, Lilje, Liisa, Pokras, Lesja, Kuznetsova, Natalja, Sadikova, Olga, Ikonen, Niina, Lyytikainen, Outi, Murtopuro, Satu, Enouf, Vincent, Lina, Bruno, Valette, Martine, Werf, Sylvie, Bonmarin, Isabelle, Sylvie, Behillil, Thierry, Blanchon, Turbelin, Clement, Belchior, Emmanuel, Machablishvili, Ann, Zakhashvili, Khatuna, Buda, Silke, Schweiger, Brunhilde, Kossivakis, Athanassios, Georgia, Spala, Mentis, Andreas, Malisiovas, Nikolaos, Csohan, Agnes, Rozsa, Monika, Jankovics, Istvan, Molnar, Zsuzsanna, Love, Arthur, Sigmundsdottir, Gudrun, Gudnason, Thorolfur, Domegan, Lisa, O Flanagan, Darina, Igoe, Derval, Waters, Allison, Duffy, Margaret, Coughlan, Suzie, O Donnell, Joan, Kaufman, Zalman, Mandelboim, Michal, Donatelli, Isabella, Bella, Antonino, Rizzo, Caterina, Pompa, Maria Grazia, Puzelli, Simona, Castrucci, Maria Rita, Katrenova, Aigul, Nusupbaeva, Gaukhar, Kasymbekova, Kalia, Otorbaeva, Dinagul, Nikiforova, Raina, Zamjatina, Natalija, Erne, Sabine, Griskevicius, Algirdas, Lipnickiene, Vilnele, Mossong, Joel, Opp, Matthias, Barbara, Christopher, Melillo, Tanya, Melillo, Jackie Maistre, Zahra, Graziella, Rakocevic, Bozidarka, Vratnica, Zoran, Meijer, Adam, Teirlinck, Anne, Dijkstra, Frederika, Donker, Ge, Rimmelzwaan, Guus, Lange, Marit, Hungnes, Olav, Bragstad, Karoline, Hauge, Siri Helene, Tonnessen, Ragnhild, Dudman, Susanne Gjeruldsen, Bednarska, Karolina, Brydak, Lidia B., Zielinski, Andrzej, Guiomar, Raquel, Pechirra, Pedro, Cristovao, Paula, Costa, Ines, Nunes, Baltazar, Rodrigues, Ana, Veronica Eder, Spinu, Constantin, Alexandrescu, Viorel, Lupulescu, Emilia, Popovici, Florin, Burtseva, Elena, Sominina, Anna, Dimitrijevic, Dragana, Adrovic, Slavica Rakic, Staronova, Edita, Mikas, Jan, Prosenc, Katarina, Berginc, Natasa, Socan, Maja, Casas, Inmaculada, Larrauri, Amparo, Pozo, Francisco, Ortiz Lejarazu, Raul, Pumarola, Tomas, Brytting, Mia, Englund, Helene, Wiman, Asa, Mahmud, Nasser Nuru, Born, Rita, Cordey, Samuel, Tishkova, Farida, Kamolov, Mirali, Bosevska, Golubinka, Kuzmanovska, Gordana, Topal, Selmur, Korukluoglu, Gulay, Ashirova, Amansoltan, Ovliyakulova, Gurbangul, Demchyshyna, Iryna, Dykhanovska, Tatiana, Mironenko, Alla, Coyle, Peter, Maclean, Alasdair, Gunson, Rory, Green, Helen, Kearns, Cathriona, Zambon, Maria, Nugent, Christopher, Moore, Catherine, Phin, Nick, Pebody, Richard, Cottrell, Simon, Mcmenamin, Jim, Jessop, Lucy, Dzemileva, Sultana, Rakhimov, Ravshan, Mccauley, John, and Daniels, Rod
4. Novel mutations and phenotypic effect of the splice site modulator IVS3-48C in nine Swedish families with erythropoietic protoporphyria.
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Wiman A, Floderus Y, and Harper P
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- Female, Haplotypes, Humans, Male, Pedigree, Phenotype, Prevalence, RNA, Messenger genetics, RNA, Messenger metabolism, Sweden, Mutation, Porphyria, Hepatoerythropoietic genetics, RNA Splice Sites genetics
- Abstract
Erythropoietic protoporphyria (EPP) is an inherited disorder, caused by a partial deficiency of ferrochelatase (FECH), the last enzyme of the heme biosynthetic pathway. The deficiency results in accumulation of protoporphyrin, primarily in erythroid cells, and the major clinical feature is cutaneous photosensitivity. In addition, some patients may develop liver complications. Several EPP-coupled mutations have been identified in the FECH gene, and the less than 50% of FECH activity seen in patients with overt EPP was recently shown to be due to the in trans inheritance of one deleterious mutation and a IVS3-48T>C transition in intron 3 of the FECH gene. This IVS3-48T>C transition modulates the use of a constitutive aberrant splice site, which results in a decreased FECH mRNA level in the carrier. In the present study, the inheritance of four novel (364C>T, 393delC, 532G>A, and 1088-89insGG) and two previously reported (343C>T and 1001C>T) FECH mutations, and the splice site modulator IVS3-48C was investigated in nine Swedish families with EPP. The methods used for the FECH gene analysis included denaturating gradient gel electrophoresis, sequencing analysis, and restriction enzyme cleavage. Haplotype analysis, based on the polymorphic loci 287(G/A), IVS3-48(T/C), and 921(G/A), revealed that all individuals carrying a mutated allele and IVS3-48C in trans to each other were affected by overt EPP. Mild clinical and biochemical EPP signs may, however, be present in individuals carrying a T at position IVS3-48 in trans to a mutated allele, because this was the case in one of the individuals investigated in the present study.
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- 2003
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5. Two novel mutations and coexistence of the 991C>T and the 1339C>T mutation on a single allele in the coproporphyrinogen oxidase gene in Swedish patients with hereditary coproporphyria.
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Wiman A, Floderus Y, and Harper P
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- Adult, Female, Humans, Male, Middle Aged, Pedigree, Polymorphism, Genetic, Porphyrias, Hepatic enzymology, Coproporphyrinogen Oxidase genetics, Mutation, Missense, Porphyrias, Hepatic genetics
- Abstract
Hereditary coproporphyria (HCP) is an autosomal dominant disorder, resulting from a partial deficiency of the enzyme coproporphyrinogen oxidase (CPO). This enzyme catalyzes the sixth step of the heme biosynthetic pathway, and mutations in the CPO gene have been coupled to HCP. The present study was undertaken to identify disease-producing mutations in the CPOgene in nine Swedish families with HCP. Exon 1 of the CPO gene of the nine probands was analyzed directly by sequencing, and exons 2-7 were screened by denaturating gradient gel electrophoresis, followed by sequencing of exons showing abnormal band pattern. Mutations were detected in five of the nine families. In two of these families, the novel mutations 623C>T (S208F, exon 2) and 982C>T (R328C, exon 5) were identified, respectively. In the affected members of the other three families, the previously reported mutations 991C>T (R331W, exon 5) and 1339C>T (R447C, exon 7) were shown to coexist on one allele. The present study contributes 2 novel mutations to the 34 that have been previously reported to cause HCP. In addition, this is the first report on patients carrying two HCP-coupled mutations on one allele.
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- 2002
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