Fitness of Pandemic H1N1 and Seasonal influenza A viruses during Co-infectionEvidence of competitive advantage of pandemic H1N1 influenza versus seasonal influenza

Pérez, Daniel R.; Sorrell, Erin M.; Angel, Matthew; Ye, Jianqiang; Hickman, Danielle; Pena, Lindomar; Ramírez-Nieto, Gloria; Kimble, Brian; Araya, Yonas

doi:10.1371/currents.rrn1011

Cited by 31 publications

(27 citation statements)

References 10 publications

(17 reference statements)

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“…Induction of proinflammatory cytokines was also markedly increased in the lungs of mice and macaques following 2009 S-OIV infection compared with seasonal H1N1 virus infection (54). Aerosol transmission between ferrets was comparable to (50,54,55), or slightly less efficient than (49), seasonal H1N1 viruses. Miniature pigs displayed few disease symptoms after infection with 2009 S-OIV, despite high levels of viral replication in the lungs (54).…”

Section: S-oiv (H1n1) During March and April Of 2009mentioning

confidence: 91%

“…In mice, ferrets, and nonhuman primates, 2009 S-OIV replicated efficiently in the upper and lower respiratory tracts and induced more pronounced lung pathology than seasonal H1N1 viruses (49,50,54,55). Induction of proinflammatory cytokines was also markedly increased in the lungs of mice and macaques following 2009 S-OIV infection compared with seasonal H1N1 virus infection (54).…”

Section: S-oiv (H1n1) During March and April Of 2009mentioning

confidence: 95%

“…The 2009 S-OIV virus contains none of the hallmarks of highly pathogenic influenza viruses (see below), although results from infection of animal models suggest that this virus produces a more severe disease than seasonal H1N1 viruses (49,50,54,55). In mice, ferrets, and nonhuman primates, 2009 S-OIV replicated efficiently in the upper and lower respiratory tracts and induced more pronounced lung pathology than seasonal H1N1 viruses (49,50,54,55).…”

Section: S-oiv (H1n1) During March and April Of 2009mentioning

confidence: 99%

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Virulence determinants of pandemic influenza viruses

2011

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Influenza A viruses cause recurrent, seasonal epidemics and occasional global pandemics with devastating levels of morbidity and mortality. The ability of influenza A viruses to adapt to various hosts and undergo reassortment events ensures constant generation of new strains with unpredictable degrees of pathogenicity, transmissibility, and pandemic potential. Currently, the combination of factors that drives the emergence of pandemic influenza is unclear, making it impossible to foresee the details of a future outbreak. Identification and characterization of influenza A virus virulence determinants may provide insight into genotypic signatures of pathogenicity as well as a more thorough understanding of the factors that give rise to pandemics.

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Section: S-oiv (H1n1) During March and April Of 2009mentioning

confidence: 91%

Section: S-oiv (H1n1) During March and April Of 2009mentioning

confidence: 95%

Section: S-oiv (H1n1) During March and April Of 2009mentioning

confidence: 99%

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Virulence determinants of pandemic influenza viruses

2011

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“…Several studies have tried to evaluate the likelihood of such reassortant events to occur, as well as the pathogenicity and/or transmissibility of progeny viruses in animal models. [31][32][33][34] Perez et al coinfected ferrets with an A(H1N1)pdm09 virus and A(H1N1) or A(H3N2) seasonal human viruses. The results of this study showed that there was no selective advantage for novel reassortants to be generated in this model system and in fact the A(H1N1) pdm09 virus dominated over both seasonal counterparts.…”

Section: Reassortment In Experimental Modelsmentioning

confidence: 99%

“…The results of this study showed that there was no selective advantage for novel reassortants to be generated in this model system and in fact the A(H1N1) pdm09 virus dominated over both seasonal counterparts. 32 Two additional teams demonstrated the possibility of reassortment between A(H1N1)pdm09 and human seasonal viruses in vitro. In both studies, and in contrast with the earlier work, reassortant progeny viruses were generated, and these turned out to be more virulent than their parental strains in the ferret model.…”

Section: Reassortment In Experimental Modelsmentioning

confidence: 99%

Evolution and adaptation of the pandemic A/H1N1 2009 influenza virus

Ducatez¹,

Fabrizio²,

Webby³

2011

VAAT

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Abstract:The emergence of the 2009 H1N1 pandemic influenza virus [A(H1N1)pdm09] has provided the public health community with many challenges, but also the scientific community with an opportunity to monitor closely its evolution through the processes of drift and shift. To date, and despite having circulated in humans for nearly two years, little antigenic variation has been observed in the A(H1N1)pdm09 viruses. However, as the A(H1N1)pdm09 virus continues to circulate and the immunologic pressure within the human population increases, future antigenic change is almost a certainty. Several coinfections of A(H1N1)pdm09 and seasonal A(H1N1) or A(H3N2) viruses have been observed, but no reassortant viruses have been described in humans, suggesting a lack of fitness of reassortant viruses or a lack of opportunities for interaction of different viral lineages. In contrast, multiple reassortment events have been detected in swine populations between A(H1N1) pdm09 and other endemic swine viruses. Somewhat surprisingly, many of the well characterized influenza virus virulence markers appear to have limited impact on the phenotype of the A(H1N1)pdm09 viruses when they have been introduced into mutant viruses in laboratory settings. As such, it is unclear what the evolutionary path of the pandemic virus will be, but the monitoring of any changes in the circulating viruses will remain a global public and animal health priority.

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The 2009 Pandemic Influenza Virus: Where Did It Come from, Where Is It Now, and Where Is It Going?

York

Donis

2012

Swine Influenza

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Around 2008 or 2009, an influenza A virus that had been circulating undetected in swine entered human population. Unlike most swine influenza infections of humans, this virus established sustained human-to-human transmission, leading to a global pandemic. The virus responsible, 2009 pandemic H1N1 (H1N1pdm), is the result of multiple reassortment events that brought together genomic segments from classical H1N1 swine influenza virus, human seasonal H3N2 influenza virus, North American avian influenza virus, and Eurasian avian-origin swine influenza viruses. Genetically, H1N1pdm possesses a number of unusual features, although the genomic characteristics that permitted sustained human-to-human transmission are yet unclear. Human infection with H1N1pdm has generally resulted in low mortality, although certain subgroups (including pregnant women, people with some chronic medical conditions, morbidly obese individuals, and immunosuppressed people) have significantly higher risk of severe disease. As H1N1pdm has spread throughout the human population it continued to evolve. It has also reentered the swine population as a circulating pathogen, and has been transiently identified in other species such as turkeys, cats, and domestic ferrets. Most genetic changes in H1N1pdm to date have not been clearly linked to changes in antigenicity, disease severity, antiviral drug resistance, or transmission efficiency. However, the rapid evolution rate characteristic of influenza viruses suggests that changes in antigenicity are inevitable in future years. Experience with this first pandemic of twenty-first century reemphasizes the importance of influenza surveillance in animals as well as humans, and offers lessons to develop and enhance our ability to identify potentially pandemic influenza viruses in the future.

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Fitness of Pandemic H1N1 and Seasonal influenza A viruses during Co-infectionEvidence of competitive advantage of pandemic H1N1 influenza versus seasonal influenza

Cited by 31 publications

References 10 publications

Virulence determinants of pandemic influenza viruses

Virulence determinants of pandemic influenza viruses

Evolution and adaptation of the pandemic A/H1N1 2009 influenza virus

The 2009 Pandemic Influenza Virus: Where Did It Come from, Where Is It Now, and Where Is It Going?

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