metricas
covid
Buscar en
Enfermedades Infecciosas y Microbiología Clínica
Toda la web
Inicio Enfermedades Infecciosas y Microbiología Clínica Influenza A(H1N1)pdm09 virus: viral characteristics and genetic evolution
Información de la revista
Vol. 30. Núm. S4.
The first influenza pandemic of the 21st century. The REIPI/SEIMC experience
Páginas 10-17 (octubre 2012)
Compartir
Compartir
Descargar PDF
Más opciones de artículo
Vol. 30. Núm. S4.
The first influenza pandemic of the 21st century. The REIPI/SEIMC experience
Páginas 10-17 (octubre 2012)
Acceso a texto completo
Influenza A(H1N1)pdm09 virus: viral characteristics and genetic evolution
Virus de la gripe A(H1N1)pdm09: características virales y evolución genética
Visitas
5652
Andrés Antóna,b,
Autor para correspondencia
ananton@clinic.ub.es

Corresponding author.
, Francisco Pozoc, Jordi Niubód, Inmaculada Casasc, Tomás Pumarolaa,b
a Virology Section, Department of Microbiology, Barcelona Centre for International Health Research (CRESIB, Hospital Clínic-Universitat de Barcelona), Barcelona, Spain
b National Influenza Centre-Barcelona, Universitat de Barcelona, Barcelona, Spain
c National Influenza Centre-Madrid, Majadahonda, Madrid, Spain
d Virology Section, Microbiology Service, IDIBELL, Hospital Universitari de Bellvitge, L’Hospitalet de Llobregat, Barcelona, Spain
Este artículo ha recibido
Información del artículo
Abstract

From April 2009 to the present, the influenza A(H1N1)pdm09 virus has been evolving continuously, acquiring new amino acid changes that may alter its antigenic characteristics, virulence, and its antiviral drug susceptibility. Phylogenetic analysis of the hemagglutinin (HA) gene of A(H1N1)pdm09 viruses showed that it clustered into 8 genetic groups relative to A/California/7/2009, in addition to others reported by regional influenza surveillance networks. However, none were considered antigenically distinct from the vaccine virus A/California/7/2009, which was recommended for use during the 2012–2013 influenza season in the Northern Hemisphere. Amino acid substitution D222G in the HA1 subunit of HA was the first potential virulence marker of the influenza A(H1N1)pdm09 virus that was associated with severe clinical outcomes. The vast majority of influenza A(H1N1)pdm2009 viruses tested by the WHO-GISRS (World Health Organization-Global Influenza Surveillance and Response System) laboratories were sensitive to neuraminidase inhibitor (NAI) drugs, and during the 2011–2012 influenza season the resistance prevalence was low (1%) or undetectable in the United States and Europe. Resistance to NAIs was detected predominantly in patients with severe conditions, most of whom were immunosuppressed. The resistance was usually associated with the H275Y mutation in the NA protein sequence, although other amino acid substitutions were also reported to confer resistance or decreased susceptibility to 1 or more NAIs. Global virological surveillance should be strengthened for new influenza variants carrying new mutations or reassorted segments that may affect viral features such as virulence, transmission, or antiviral susceptibility.

Keywords:
Surveillance
Resistance
Vaccine
Oseltamivir
H275Y
Resumen

El virus de la gripe A(H1N1)pdm09 ha estado evolucionando continuamente desde abril de 2009 hasta la actualidad. Los cambios experimentados en los aminoácidos del virus pueden alterar sus características antigénicas, su virulencia y su sensibilidad a los fármacos antivirales. Mediante el análisis filogenético del gen hemaglutinina (HA) del virus A(H1N1)pdm09 se han observado 8 grupos genéticos relacionados con el A/California/7/2009, además de otros informados por las redes regionales de vigilancia de la gripe, si bien ninguno de estos grupos genéticos ha sido considerado antigénicamente distinto del virus de la vacuna A/California/7/2009, cuyo uso se recomendó durante la estación de gripe 2012–2013 en el hemisferio norte. El primer marcador de virulencia potencial del virus de la gripe A(H1N1)pdm09 que fue asociado con una mayor severidad clínica de la enfermedad fue la sustitución del aminoácido D222G en la subunidad HA1 del HA. La inmensa mayoría de los virus de la gripe A(H1N1)pdm2009 estudiados por los laboratorios del WHO-GISRS (World Health Organization-Global Influenza Surveillance and Response System) eran sensibles a los fármacos inhibidores de la neuraminidasa (INA). Tanto en Estados Unidos como en Europa, el predominio de resistencia fue bajo (1%) o indetectable durante la temporada de gripe 2011–2012. Los pacientes con enfermedad grave, la mayoría de los cuales eran inmunodeprimidos, fueron principalmente los que presentaron resistencia a los INA. Habitualmente, la resistencia estaba asociada a la mutación de H275Y en la secuencia de la proteína NA, aunque también se apreciaron otras sustituciones de aminoácido que conferían resistencia o disminución de la sensibilidad a uno o más INA. Los autores recomiendan extremar la vigilancia virológica global para detectar nuevas variantes de la gripe debidas a nuevas mutaciones o reordenamientos genómicos que pueden afectar características virales como la virulencia, la transmisión o la sensibilidad a los antivirales.

Palabras clave:
Vigilancia
Resistencia
Vacuna
Oseltamivir
H275Y
El Texto completo está disponible en PDF
References
[1.]
D.M. Knipe, P.M. Howley.
Fields Virology.
5th Ed, Lippincott Williams & Wilkins, (2006),
[2.]
R.A. Lamb, P.W. Choppin.
The gene structure and replication of influenza virus.
Annu Rev Biochem, 52 (1983), pp. 467-506
[3.]
P. Suárez, J. Valcarcel, J. Ortín.
Heterogeneity of the mutation rates of influenza A viruses: isolation of mutator mutants.
J Virol, 66 (1992), pp. 2491-2494
[4.]
J.D. Mathews, J.M. Chesson, J.M. McCaw, J. McVernon.
Understanding influenza transmission, immunity and pandemic threats.
Influenza Other Respi Viruses, 3 (2009), pp. 143-149
[5.]
Centers for Disease Control, Prevention (CDC).
Swine influenza A (H1N1) infection in two children—Southern California, March–April 2009.
MMWR Morb Mortal Wkly Rep, 58 (2009), pp. 400-402
[6.]
Y. Itoh, K. Shinya, M. Kiso, T. Watanabe, Y. Sakoda, M. Hatta, et al.
In vitro and in vivo characterization of new swine-origin H1N1 influenza viruses.
Nature, 460 (2009), pp. 1021-1025
[7.]
G.J. Smith, D. Vijaykrishna, J. Bahl, S.J. Lycett, M. Worobey, O.G. Pybus, et al.
Origins and evolutionary genomics of the 2009 swine-origin H1N1 influenza A epidemic.
Nature, 459 (2009), pp. 1122-1125
[8.]
R.J. Garten, C.T. Davis, C.A. Russell, B. Shu, S. Lindstrom, A. Balish, et al.
Antigenic and genetic characteristics of swine-origin 2009 A(H1N1) influenza viruses circulating in humans.
Science, 325 (2009), pp. 197-201
[9.]
Centers for Disease Control and Prevention (CDC).
Update: drug susceptibility of swine-origin influenza A (H1N1) viruses, April 2009.
MMWR Morb Mortal Wkly Rep, 58 (2009), pp. 433-435
[10.]
O. Hungnes.
The role of genetic analysis in influenza virus surveillance and strain characterisation.
Vaccine, 20 (2002), pp. B45-B49
[11.]
M. Nelson, D. Spiro, D. Wentworth, E. Beck, J. Fan, E. Ghedin, et al.
The early diversification of influenza A/H1N1pdm.
PLoS Curr, 1 (2009), pp. RRN1126
[12.]
M.I. Nelson, Y. Tan, E. Ghedin, D.E. Wentworth, K. St George, L. Edelman, et al.
Phylogeography of the spring and fall waves of the H1N1/09 pandemic influenza virus in the United States.
J Virol, 85 (2011), pp. 828-834
[13.]
M.C. Christman, A. Kedwaii, J. Xu, R.O. Donis, G. Lu.
Pandemic (H1N1) 2009 virus revisited: an evolutionary retrospective.
Infect Genet Evol, 11 (2011), pp. 803-811
[14.]
M.B. Valli, S. Meschi, M. Selleri, P. Zaccaro, G. Ippolito, M.R. Capobianchi, et al.
Evolutionary pattern of pandemic influenza (H1N1) 2009 virus in the late phases of the 2009 pandemic.
PLoS Curr, 2 (2010),
[15.]
E.E. Espínola.
Genome Stability of Pandemic Influenza A (H1N1) 2009 Based on Analysis of Hemagglutinin and Neuraminidase Genes.
Open Virol J, 6 (2012), pp. 59-63
[16.]
W. Li, W. Shi, H. Qiao, S.Y. Ho, A. Luo, Y. Zhang, et al.
Positive selection on hemagglutinin and neuraminidase genes of H1N1 influenza viruses.
[17.]
J. Mullick, S.S. Cherian, V.A. Potdar, M.S. Chadha, A.C. Mishra.
Evolutionary dynamics of the influenza A pandemic (H1N1) 2009 virus with emphasis on Indian isolates:evidence for adaptive evolution in the HA gene.
Infect Genet Evol, 11 (2011), pp. 997-1005
[18.]
X. Ding, L. Jiang, C. Ke, Z. Yang, C. Lei, K. Cao, et al.
Amino acid sequence analysis and identification of mutations under positive selection in hemagglutinin of 2009 influenza A (H1N1) isolates.
Virus Genes, 41 (2010), pp. 329-340
[19.]
W.M. Fitch, J.M. Leiter, X.Q. Li, P. Palese.
Positive Darwinian evolution in human influenza A viruses.
Proc Natl Acad Sci U S A, 88 (1991), pp. 4270-4274
[20.]
European Centre For Disease Prevention and Control (ECDC). Influenza virus characterization. Summary Europe, February 2012. Available at: http://ecdc.europa.eu/en/publications/Publications/1203_TED_CNRL_report_Feb2011.pdf.
[21.]
J. Ledesma, F. Pozo, G. Reina, M. Blasco, G. Rodríguez, M. Montes, et al.
Spanish Influenza Surveillance System (SISS). Genetic diversity of influenza A(H1N1)2009 virus circulating during the season 2010–2011 in Spain.
J Clin Virol, 53 (2012), pp. 16-21
[22.]
J.J. Skehel, D.C. Wiley.
Receptor binding and membrane fusion in virus entry: the influenza hemagglutinin.
Annu Rev Biochem, 69 (2000), pp. 531-569
[23.]
A.J. Caton, G.G. Brownlee, J.W. Yewdell, W. Gerhard.
The antigenic structure of the influenza virus A/PR/8/34 hemagglutinin (H1 subtype).
Cell, 31 (1982), pp. 417-427
[24.]
G. Winter, S. Fields, G.G. Brownlee.
Nucleotide sequence of the haemagglutinin gene of a human influenza virus H1 subtype.
Nature, 292 (1981), pp. 72-75
[25.]
R. Xu, D.C. Ekiert, J.C. Krause, R. Hai, J.E. Crowe Jr., I.A. Wilson.
Structural basis of preexisting immunity to the 2009 H1N1 pandemic influenza virus.
Science, 328 (2010), pp. 357-360
[26.]
W. Gerhard, J. Yewdell, M.E. Frankel, R. Webster.
Antigenic structure of influenza virus haemagglutinin defined by hybridoma antibodies.
Nature, 290 (1981), pp. 713-717
[27.]
T. Han, W.A. Marasco.
Structural basis of influenza virus neutralization.
Ann N Y Acad Sci, 1217 (2011), pp. 178-190
[28.]
R. Xu, R. McBride, C.M. Nycholat, J.C. Paulson, I.A. Wilson.
Structural characterization of the hemagglutinin receptor specificity from the 2009 H1N1 influenza pandemic.
J Virol, 86 (2012), pp. 982-990
[29.]
G. Neumann, Y. Kawaoka.
The first influenza pandemic of the new millennium.
Influenza Other Respi Viruses, 5 (2011), pp. 157-166
[30.]
M. Igarashi, K. Ito, R. Yoshida, D. Tomabechi, H. Kida, A. Takada.
Predicting the antigenic structure of the pandemic (H1N1) 2009 influenza virus hemagglutinin.
[31.]
B. Manicassamy, R.A. Medina, R. Hai, T. Tsibane, S. Stertz, E. Nistal-Villan, et al.
Protection of mice against lethal challenge with 2009 H1N1 influenza A virus by 1918-like and classical swine H1N1 based vaccines.
PLoS Pathog, 6 (2010), pp. e1000745
[32.]
N. Ikonen, M. Strengell, L. Kinnunen, P. Osterlund, J. Pirhonen, M. Broman, et al.
High frequency of cross-reacting antibodies against 2009 pandemic influenza A(H1N1) virus among the elderly in Finland.
Euro Surveill, 15 (2010), pp. 19478
[33.]
E. Miller, K. Hoschler, P. Hardelid, E. Stanford, N. Andrews, M. Zambon.
Incidence of 2009 pandemic influenza A H1N1 infection in England: a cross-sectional serological study.
Lancet, 375 (2010), pp. 1100-1108
[34.]
K. Hancock, V. Veguilla, X. Lu, W. Zhong, E.N. Butler, H. Sun, et al.
Cross-reactive antibody responses to the 2009 pandemic H1N1 influenza virus.
N Engl J Med, 361 (2009), pp. 1945-1952
[35.]
P. Hardelid, N.J. Andrews, K. Hoschler, E. Stanford, M. Baguelin, P.A. Waight, et al.
Assessment of baseline age-specific antibody prevalence and incidence of infection to novel influenza A/H1N1 2009.
Health Technol Assess, 14 (2010), pp. 115-192
[36.]
Recommended composition of influenza virus vaccines for use in the 2012–2013 northern hemisphere influenza season. Wkly Epidemiol Rec. 2012;87:83–95.
[37.]
WHO Collaborating Centre for Reference and Research on Influenza. Report prepared for the WHO annual consultation on the composition of influenza vaccine for the Northern Hemisphere. 2012 20th February 2012. Available at: http://www.nimr.mrc.ac.uk/documents/about/interim-report-feb-2012.pdf.
[38.]
M. Graham, B. Liang, G. Van Domselaar, N. Bastien, C. Beaudoin, S. Tyler, et al.
Nationwide molecular surveillance of pandemic H1N1 influenza A virus genomes: Canada, 2009.
[39.]
M. Galiano, P.M. Agapow, C. Thompson, S. Platt, A. Underwood, J. Ellis, et al.
Evolutionary pathways of the pandemic influenza A (H1N1) 2009 in the UK.
[40.]
I.G. Barr, L. Cui, N. Komadina, R.T. Lee, R.T. Lin, Y. Deng, et al.
A new pandemic influenza A(H1N1) genetic variant predominated in the winter 2010 influenza season in Australia, New Zealand and Singapore.
Euro Surveill, 15 (2010), pp. 19692
[41.]
S. Maurer-Stroh, R.T. Lee, F. Eisenhaber, L. Cui, S.P. Phuah, R.T. Lin.
A new common mutation in the hemagglutinin of the 2009 (H1N1) influenza A virus.
PLoS Curr, 2 (2010),
[42.]
D.C. Ekiert, G. Bhabha, M.A. Elsliger, R.H. Friesen, M. Jongeneelen, M. Throsby, et al.
Antibody recognition of a highly conserved influenza virus epitope.
Science, 324 (2009), pp. 246-251
[43.]
R.J. Russell, P.S. Kerry, D.J. Stevens, D.A. Steinhauer, S.R. Martin, S.J. Gamblin, et al.
Structure of influenza hemagglutinin in complex with an inhibitor of membrane fusion.
Proc Natl Acad Sci U S A, 105 (2008), pp. 17736-17741
[44.]
H. Yang, P. Carney, J. Stevens.
Structure and receptor binding properties of a pandemic H1N1 virus hemagglutinin.
PLoS Curr, 2 (2010),
[45.]
P. Suphaphiphat, M. Franti, A. Hekele, A. Lilja, T. Spencer, E. Settembre, et al.
Mutations at positions 186 and 194 in the HA gene of the 2009 H1N1 pandemic influenza virus improve replication in cell culture and eggs.
[46.]
M.P. Girard, J.S. Tam, O.M. Assossou, M.P. Kieny.
The 2009 A (H1N1) influenza virus pandemic: a review.
Vaccine, 28 (2010), pp. 4895-4902
[47.]
A.R. Everitt, S. Clare, T. Pertel, S.P. John, R.S. Wash, S.E. Smith, et al.
IFITM3 restricts the morbidity and mortality associated with influenza.
Nature, 484 (2012), pp. 519-523
[48.]
Y. Kawaoka, R.G. Webster.
Sequence requirements for cleavage activation of influenza virus hemagglutinin expressed in mammalian cells.
Proc Natl Acad Sci U S A, 85 (1988), pp. 324-328
[49.]
M. Hatta, P. Gao, P. Halfmann, Y. Kawaoka.
Molecular basis for high virulence of Hong Kong H5N1 influenza A viruses.
Science, 293 (2001), pp. 1840-1842
[50.]
J. Steel, A.C. Lowen, S. Mubareka, P. Palese.
Transmission of influenza virus in a mammalian host is increased by PB2 amino acids 627K or 627E/701N.
PLoS Pathog, 5 (2009), pp. e1000252
[51.]
E.K. Subbarao, W. London, B.R. Murphy.
A single amino acid in the PB2 gene of influenza A virus is a determinant of host range.
J Virol, 67 (1993), pp. 1761-1764
[52.]
D. Jackson, M.J. Hossain, D. Hickman, D.R. Perez, R.A. Lamb.
A new influenza virus virulence determinant: the NS1 protein four C-terminal residues modulate pathogenicity.
Proc Natl Acad Sci U S A, 105 (2008), pp. 4381-4386
[53.]
D. Zamarin, M.B. Ortigoza, P. Palese.
Influenza A virus PB1-F2 protein contributes to viral pathogenesis in mice.
J Virol, 80 (2006), pp. 7976-7983
[54.]
G. Neumann, T. Noda, Y. Kawaoka.
Emergence and pandemic potential of swine-origin H1N1 influenza virus.
Nature, 459 (2009), pp. 931-939
[55.]
D.M. Tscherne, A. Garcia-Sastre.
Virulence determinants of pandemic influenza viruses.
J Clin Invest, 121 (2011), pp. 6-13
[56.]
K. Shinya, M. Ebina, S. Yamada, M. Ono, N. Kasai, Y. Kawaoka.
Avian flu: influenza virus receptors in the human airway.
Nature, 440 (2006), pp. 435-436
[57.]
D. Van Riel, V.J. Munster, E. De Wit, G.F. Rimmelzwaan, R.A. Fouchier, A.D. Osterhaus, et al.
H5N1 Virus Attachment to Lower Respiratory Tract.
Science, 312 (2006), pp. 399
[58.]
G.N. Rogers, J.C. Paulson.
Receptor determinants of human and animal influenza virus isolates: differences in receptor specificity of the H3 hemagglutinin based on species of origin.
Virology, 127 (1983), pp. 361-373
[59.]
R.J. Connor, Y. Kawaoka, R.G. Webster, J.C. Paulson.
Receptor specificity in human, avian, and equine H2 and H3 influenza virus isolates.
Virology, 205 (1994), pp. 17-23
[60.]
J. Stevens, O. Blixt, L. Glaser, J.K. Taubenberger, P. Palese, J.C. Paulson, et al.
Glycan microarray analysis of the hemagglutinins from modern and pandemic influenza viruses reveals different receptor specificities.
J Mol Biol, 355 (2006), pp. 1143-1155
[61.]
T.R. Maines, A. Jayaraman, J.A. Belser, D.A. Wadford, C. Pappas, H. Zeng, et al.
Transmission and pathogenesis of swine-origin 2009 A(H1N1) influenza viruses in ferrets and mice.
Science, 325 (2009), pp. 484-487
[62.]
V. Soundararajan, K. Tharakaraman, R. Raman, S. Raguram, Z. Shriver, V. Sasisekharan, et al.
Extrapolating from sequence—the 2009 H1N1 ‘swine’ influenza virus.
Nat Biotechnol, 27 (2009), pp. 510-513
[63.]
R.A. Childs, A.S. Palma, S. Wharton, T. Matrosovich, Y. Liu, W. Chai, et al.
Receptorbinding specificity of pandemic influenza A (H1N1) 2009 virus determined by carbohydrate microarray.
Nat Biotechnol, 27 (2009), pp. 797-799
[64.]
A. Antón, M.A. Marcos, M.J. Martínez, S. Ramón, A. Martínez, N. Cardeñosa, et al.
D225G mutation in the hemagglutinin protein found in 3 severe cases of 2009 pandemic influenza A (H1N1) in Spain.
Diagn Microbiol Infect Dis, 67 (2010), pp. 207-208
[65.]
J. Ellis, M. Galiano, R. Pebody, A. Lackenby, C. Thompson, A. Bermingham, et al.
Virological analysis of fatal influenza cases in the United Kingdom during the early wave of influenza in winter 2010/11.
Euro Surveill, 16 (2011), pp. 19760
[66.]
A. Kilander, R. Rykkvin, S.G. Dudman, O. Hungnes.
Observed association between the HA1 mutation D222G in the 2009 pandemic influenza A(H1N1) virus and severe clinical outcome, Norway 2009–2010.
Euro Surveill, 15 (2010), pp. 19498
[67.]
J. Ledesma, F. Pozo, M.P. Ruiz, J.M. Navarro, L. Piñeiro, M. Montes, et al.
Spanish Influenza Surveillance System (SISS). Substitutions in position 222 of haemagglutinin of pandemic influenza A (H1N1) 2009 viruses in Spain.
J Clin Virol, 51 (2011), pp. 75-78
[68.]
S. Puzelli, M. Facchini, D. Spagnolo, M.A. De Marco, L. Calzoletti, A. Zanetti, et al.
Transmission of hemagglutinin D222G mutant strain of pandemic (H1N1) 2009 virus.
Emerg Infect Dis, 16 (2010), pp. 863-865
[69.]
J.R. Yang, Y.P. Huang, F.Y. Chang, L.C. Hsu, Y.C. Lin, C.H. Su, et al.
New variants and age shift to high fatality groups contribute to severe successive waves in the 2009 influenza pandemic in Taiwan.
[70.]
G.C. Mak, K.W. Au, L.S. Tai, K.C. Chuang, K.C. Cheng, T.C. Shiu, et al.
Association of D222G substitution in haemagglutinin of 2009 pandemic influenza A (H1N1) with severe disease.
Euro Surveill, 15 (2010), pp. 19534
[71.]
R.R. Miller, A.R. MacLean, R.N. Gunson, W.F. Carman.
Occurrence of haemagglutinin mutation D222G in pandemic influenza A(H1N1) infected patients in the West of Scotland, United Kingdom. 2009–10.
Euro Surveill, 15 (2010), pp. 19546
[72.]
F. Baldanti, G. Campanini, A. Piralla, F. Rovida, A. Braschi, F. Mojoli, et al.
Severe outcome of influenza A/H1N1/09v infection associated with 222G/N polymorphisms in the haemagglutinin: a multicentre study.
Clin Microbiol Infect, 17 (2011), pp. 1166-1169
[73.]
I.A. Wilson, J.J. Skehel, D.C. Wiley.
Structure of the haemagglutinin membrane glycoprotein of influenza virus at 3 A resolution.
Nature, 289 (1981), pp. 366-373
[74.]
J.A. Belser, A. Jayaraman, R. Raman, C. Pappas, H. Zeng, N.J. Cox, et al.
Effect of D222G mutation in the hemagglutinin protein on receptor binding, pathogenesis and transmissibility of the 2009 pandemic H1N1 influenza virus.
[75.]
S. Chutinimitkul, S. Herfst, J. Steel, A.C. Lowen, J. Ye, D. Van Riel, et al.
Virulence-associated substitution D222G in the hemagglutinin of 2009 pandemic influenza A(H1N1) virus affects receptor binding.
J Virol, 84 (2010), pp. 11802-11813
[76.]
Y. Liu, R.A. Childs, T. Matrosovich, S. Wharton, A.S. Palma, W. Chai, et al.
Altered receptor specificity and cell tropism of D222G hemagglutinin mutants isolated from fatal cases of pandemic A(H1N1) 2009 influenza virus.
J Virol, 84 (2010), pp. 12069-12074
[77.]
S.M. Brookes, A. Núñez, B. Choudhury, M. Matrosovich, S.C. Essen, D. Clifford, et al.
Replication, pathogenesis and transmission of pandemic (H1N1) 2009 virus in non-immune pigs.
[78.]
R. Almansa, A. Anton, P. Ramirez, I. Martin-Loeches, D. Banner, T. Pumarola, et al.
Direct association between pharyngeal viral secretion and host cytokine response in severe pandemic influenza.
BMC Infect Dis, 11 (2011), pp. 232
[79.]
H.S. Houng, J. Garner, Y. Zhou, A. Lyons, R. Kuschner, G. Deye, et al.
Emergent 2009 influenza A(H1N1) viruses containing HA D222N mutation associated with severe clinical outcomes in the Americas.
J Clin Virol, 53 (2012), pp. 12-15
[80.]
S. Kumar, K.J. Henrickson.
Update on influenza diagnostics: lessons from the novel H1N1 influenza A pandemic.
Clin Microbiol Rev, 25 (2012), pp. 344-361
[81.]
WHO Global Influenza Surveillance and Response System (GISRS). Summary of influenza antiviral susceptibility surveillance findings, September 2010 - March 2011. 2011. Available at: http://www.who.int/influenza/gisrs_laboratory/updates/antiviral_susceptibility/en/index.html.
[82.]
A.C. Hurt, T. Chotpitayasunondh, N.J. Cox, R. Daniels, A.M. Fry, L.V. Gubareva, et al.
Antiviral resistance during the 2009 influenza A H1N1 pandemic: public health, laboratory, and clinical perspectives.
Lancet Infect Dis, 12 (2012), pp. 240-248
[83.]
Y.S. Babu, P. Chand, S. Bantia, P. Kotian, A. Dehghani, Y. El-Kattan, et al.
BCX-1812 (RWJ-270201): discovery of a novel, highly potent, orally active, and selective influenza neuraminidase inhibitor through structure-based drug design.
J Med Chem, 43 (2000), pp. 3482-3486
[84.]
H.T. Nguyen, A.M. Fry, L.V. Gubareva.
Neuraminidase inhibitor resistance in influenza viruses and laboratory testing methods.
Antivir Ther, 17 (2012), pp. 159-173
[85.]
World Health Organization. Influenza Update N° 160. 2012. Available at: http://www.who.int/influenza/surveillance_monitoring/updates/2012_05_25_surveilance_update_160.pdf.
[86.]
V. Lopez Chavarrias, E. Broberg, A. Nicoll.
Preliminary implications for Europe of the 2011 influenza season in five temperate southern hemisphere countries.
Euro Surveill, 16 (2011), pp. 20044
[87.]
A.C. Hurt, K. Hardie, N.J. Wilson, Y.M. Deng, M. Osbourn, N. Gehrig, et al.
Community transmission of oseltamivir-resistant A(H1N1)pdm09 influenza.
N Engl J Med, 365 (2011), pp. 2541-2542
[88.]
M.J. Memoli, A.S. Davis, K. Proudfoot, D.S. Chertow, R.J. Hrabal, T. Bristol, et al.
Multidrug-resistant 2009 pandemic influenza A(H1N1) viruses maintain fitness and transmissibility in ferrets.
J Infect Dis, 203 (2011), pp. 348-357
[89.]
C.W. Seibert, M. Kaminski, J. Philipp, D. Rubbenstroth, R.A. Albrecht, F. Schwalm, et al.
Oseltamivir-resistant variants of the 2009 pandemic H1N1 influenza A virus are not attenuated in the guinea pig and ferret transmission models.
J Virol, 84 (2010), pp. 11219-11226
[90.]
M.E. Hamelin, M. Baz, Y. Abed, C. Couture, P. Joubert, E. Beaulieu, et al.
Oseltamivir-resistant pandemic A/H1N1 virus is as virulent as its wild-type counterpart in mice and ferrets.
PLoS Pathog, 6 (2010), pp. e1001015
[91.]
S. Duan, D.A. Boltz, P. Seiler, J. Li, K. Bragstad, L.P. Nielsen, et al.
Oseltamivir-resistant pandemic H1N1/2009 influenza virus possesses lower transmissibility and fitness in ferrets.
PLoS Pathog, 6 (2010), pp. e1001022
[92.]
D.W. Brookes, S. Miah, A. Lackenby, L. Hartgroves, W.S. Barclay.
Pandemic H1N1 2009 influenza virus with the H275Y oseltamivir resistance neuraminidase mutation shows a small compromise in enzyme activity and viral fitness.
J Antimicrob Chemother, 66 (2011), pp. 466-470
[93.]
J.D. Bloom, L.I. Gong, D. Baltimore.
Permissive secondary mutations enable the evolution of influenza oseltamivir resistance.
Science, 328 (2010), pp. 1272-1275
[94.]
S.E. Hensley, S.R. Das, J.S. Gibbs, A.L. Bailey, L.M. Schmidt, J.R. Bennink, et al.
Influenza A virus hemagglutinin antibody escape promotes neuraminidase antigenic variation and drug resistance.
[95.]
A. Lackenby, J. Moran Gilad, R. Pebody, S. Miah, L. Calatayud, S. Bolotin, et al.
Continued emergence and changing epidemiology of oseltamivir-resistant influenza A(H1N1)2009 virus, United Kingdom, winter 2010/11.
Euro Surveill, 16 (2011), pp. 19784
[96.]
P.J. Collins, L.F. Haire, Y.P. Lin, J. Liu, R.J. Russell, P.A. Walker, et al.
Structural basis for oseltamivir resistance of influenza viruses.
Vaccine, 27 (2009), pp. 6317-6323
[97.]
A.C. Hurt, K. Hardie, N.J. Wilson, Y.M. Deng, M. Osbourn, S.K. Leang, et al.
Characteristics of a widespread community cluster of H275Y oseltamivir-resistant A(H1N1)pdm09 influenza in Australia.
J Infect Dis, 206 (2012), pp. 148-157
[98.]
A. Pizzorno, X. Bouhy, Y. Abed, G. Boivin.
Generation and characterization of recombinant pandemic influenza A(H1N1) viruses resistant to neuraminidase inhibitors.
J Infect Dis, 203 (2011), pp. 25-31
[99.]
A.C. Hurt, S.K. Leang, D.J. Speers, I.G. Barr, S. Maurer-Stroh.
Mutations I117V and I117M and oseltamivir sensitivity of pandemic (H1N1) 2009 viruses.
Emerg Infect Dis, 18 (2012), pp. 109-112
[100.]
H.T. Nguyen, A.M. Fry, P.A. Loveless, A.I. Klimov, L.V. Gubareva.
Recovery of a multidrug-resistant strain of pandemic influenza A 2009 (H1N1) virus carrying a dual H275Y/I223R mutation from a child after prolonged treatment with oseltamivir.
Clin Infect Dis, 51 (2010), pp. 983-984
[101.]
E. Van der Vries, F.F. Stelma, C.A. Boucher.
Emergence of a multidrug-resistant pandemic influenza A (H1N1) virus.
N Engl J Med, 363 (2010), pp. 1381-1382
[102.]
A. Eshaghi, S.N. Patel, A. Sarabia, R.R. Higgins, A. Savchenko, P.J. Stojios, et al.
Multidrug-resistant pandemic (H1N1) 2009 infection in immunocompetent child.
Emerg Infect Dis, 17 (2011), pp. 1472-1474
[103.]
A. Pizzorno, Y. Abed, X. Bouhy, E. Beaulieu, C. Mallett, R. Russell, et al.
Impact of mutations at residue I223 of the neuraminidase protein on the resistance profile, replication level, and virulence of the 2009 pandemic influenza virus.
Antimicrob Agents Chemother, 56 (2012), pp. 1208-1214
[104.]
A.C. Hurt, R.T. Lee, S.K. Leang, L. Cui, Y.M. Deng, S.P. Phuah, et al.
Increased detection in Australia and Singapore of a novel influenza A(H1N1)2009 variant with reduced oseltamivir and zanamivir sensitivity due to a S247N neuraminidase mutation.
Euro Surveill, 16 (2011), pp. 19884
[105.]
E. Ghedin, J. Laplante, J. DePasse, D.E. Wentworth, R.P. Santos, M.L. Lepow, et al.
Deep sequencing reveals mixed infection with 2009 pandemic influenza A (H1N1) virus strains and the emergence of oseltamivir resistance.
J Infect Dis, 203 (2011), pp. 168-174
[106.]
A. Anton, T. Pumarola.
Influenza in immunocompromised patients: considerations for therapy.
Future Virology, 6 (2011), pp. 855-868
[107.]
B.D. Greenbaum, O.T. Li, L.L. Poon, A.J. Levine, R. Rabadan.
Viral reassortment as an information exchange between viral segments.
Proc Natl Acad Sci U S A, 109 (2012), pp. 3341-3346
[108.]
K. Nagarajan, G. Saikumar, R.S. Arya, A. Gupta, R. Somvanshi, B. Pattnaik.
Influenza A H1N1 virus in Indian pigs & its genetic relatedness with pandemic human influenza A 2009 H1N1.
Indian J Med Res, 132 (2010), pp. 160-167
[109.]
S. Rith, P. Netrabukkana, S. Sorn, E. Mumford, C. Mey, D. Holl, et al.
Serologic evidence of human influenza virus infections in swine populations, Cambodia.
Influenza Other Respi Viruses, (2012),
[110.]
W. Ma, R.E. Kahn, J.A. Richt.
The pig as a mixing vessel for influenza viruses: Human and veterinary implications.
J Mol Genet Med, 3 (2008), pp. 158-166
[111.]
Q. Liu, J. Ma, H. Liu, W. Qi, J. Anderson, S.C. Henry, et al.
Emergence of novel reassortant H3N2 swine influenza viruses with the 2009 pandemic H1N1 genes in the United States.
Arch Virol, 157 (2012), pp. 555-562
[112.]
D. Vijaykrishna, L.L. Poon, H.C. Zhu, S.K. Ma, O.T. Li, C.L. Cheung, et al.
Reassortment of pandemic H1N1/2009 influenza A virus in swine.
Science, 328 (2010), pp. 1529
[113.]
E. Starick, E. Lange, C. Grund, E. Grosse Beilage, S. Dohring, A. Maas, et al.
Reassortants of pandemic influenza A virus H1N1/2009 and endemic porcine HxN2 viruses emerge in swine populations in Germany.
J Gen Virol, (2012),
[114.]
X. Fan, H. Zhu, B. Zhou, D.K. Smith, X. Chen, T.T. Lam, et al.
Emergence and dissemination of a swine H3N2 reassortant influenza virus with 2009 pandemic H1N1 genes in pigs in China.
J Virol, 86 (2012), pp. 2375-2378
[115.]
J.Y. Han, S.J. Park, H.K. Kim, S. Rho, G.V. Nguyen, D. Song, et al.
Identification of reassortant pandemic H1N1 influenza virus in Korean pigs.
J Microbiol Biotechnol, 22 (2012), pp. 699-707
[116.]
M.F. Ducatez, B. Hause, E. Stigger-Rosser, D. Darnell, C. Corzo, K. Juleen, et al.
Multiple reassortment between pandemic (H1N1) 2009 and endemic influenza viruses in pigs, United States.
Emerg Infect Dis, 17 (2011), pp. 1624-1629
[117.]
B. Shu, R. Garten, S. Emery, A. Balish, L. Cooper, W. Sessions, et al.
Genetic analysis and antigenic characterization of swine origin influenza viruses isolated from humans in the United States. 1990–2010.
Virology, 422 (2012), pp. 151-160
[118.]
Centers for Disease Control and Prevention (CDC).
Limited human-to-human transmission of novel influenza A (H3N2) virus—Iowa, November 2011.
MMWR Morb Mortal Wkly Rep, 60 (2011), pp. 1615-1617
[119.]
S. Lindstrom, R. Garten, A. Balish, B. Shu, S. Emery, L. Berman, et al.
Human infections with novel reassortant influenza A(H3N2)v viruses, United States. 2011.
Emerg Infect Dis, 18 (2012), pp. 834-837
[120.]
Centers for Disease Control, Prevention (CDC).
Update: Influenza A (H3N2)v transmission and guidelines - five states. 2011.
MMWR Morb Mortal Wkly Rep, 60 (2012), pp. 1741-1744
Copyright © 2012. Elsevier España, S.L.. All rights reserved
Descargar PDF
Opciones de artículo
es en pt

¿Es usted profesional sanitario apto para prescribir o dispensar medicamentos?

Are you a health professional able to prescribe or dispense drugs?

Você é um profissional de saúde habilitado a prescrever ou dispensar medicamentos