A global initiative on sharing avian flu data

Bogner, Péter; Capua, Ilaria; Lipman, David J.; Cox, Nancy J.

doi:10.1038/442981a

Cited by 132 publications

(134 citation statements)

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“…Determination of polymorphism frequencies was based on amino acid sequences for the proteins PB2, PA, NP, hemagglutinin (HA), NA, and NS1. Amino acid sequences for 2009 pH1N1 isolates from 2009 to 2014 with respective sampling times (year/month) were downloaded from the GISAID (20) database (see Table S1 in the supplemental material). The numbers of isolates for each segment were as follows: PB2, 3,356; PA, 3,202; NP, 3,319; HA, 9,728; NA, 11,017; and NS1, 3,408.…”

Section: Methodsmentioning

confidence: 99%

Adaptive Mutations That Occurred during Circulation in Humans of H1N1 Influenza Virus in the 2009 Pandemic Enhance Virulence in Mice

Otte

Sauter

Daxer

et al. 2015

J Virol

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During the 2009 H1N1 influenza pandemic, infection attack rates were particularly high among young individuals who suffered from pneumonia with occasional death. Moreover, previously reported determinants of mammalian adaptation and pathogenicity were not present in 2009 pandemic H1N1 influenza A viruses. Thus, it was proposed that unknown viral factors might have contributed to disease severity in humans. In this study, we performed a comparative analysis of two clinical 2009 pandemic H1N1 strains that belong to the very early and later phases of the pandemic. We identified mutations in the viral hemagglutinin (HA) and the nucleoprotein (NP) that occurred during pandemic progression and mediate increased virulence in mice. Lethal disease outcome correlated with elevated viral replication in the alveolar epithelium, increased proinflammatory cytokine and chemokine responses, pneumonia, and lymphopenia in mice. These findings show that viral mutations that have occurred during pandemic circulation among humans are associated with severe disease in mice. IMPORTANCEIn this study, novel determinants of 2009 pandemic H1N1 influenza pathogenicity were identified in the viral hemagglutinin (HA) and the nucleoprotein (NP) genes. In contrast to highly pathogenic avian influenza viruses, increased virulence in mice did not correlate with enhanced polymerase activity but with reduced activity. Lethal 2009 pandemic H1N1 infection in mice correlated with lymphopenia and severe pneumonia. These studies suggest that molecular mechanisms that mediate 2009 pandemic H1N1 influenza pathogenicity are distinct from those that mediate avian influenza virus pathogenicity in mice.T he first pandemic of the 21st century was caused by a novel influenza A virus strain of the H1N1 subtype that contained gene segments from both North American and Eurasian swine lineages (1-3). In the beginning, the 2009 H1N1 influenza pandemic was considered to be relatively mild as the majority of cases underwent an uncomplicated or even an asymptomatic infection course. However, this was partially revoked since infection attack rates were highest among the younger age groups, in contrast to seasonal influenza, where mostly the elderly are affected (4-7). During the pandemic in 2009, a disproportionately high number of young adults were hospitalized due to pneumonia and eventually died (6-9). Retrospective modeling estimates that during the first 12 months of the pandemic, approximately 80% of the overall 201,200 respiratory and additional 83,300 cardiovascular deaths occurred in people younger than 65 years (10). This age-specific mortality pattern among younger individuals has been captured by the "years-of-life-lost" metric (11) as a more accurate parameter to measure pandemic burden. In the United States, the number of years of life lost within the first months of the pandemic was estimated to range between the impact of the more virulent H3N2 influenza epidemics and that of the 1968 Hong Kong pandemic (12).Subsequently, it was postulated that ...

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Section: Methodsmentioning

confidence: 99%

Adaptive Mutations That Occurred during Circulation in Humans of H1N1 Influenza Virus in the 2009 Pandemic Enhance Virulence in Mice

Otte

Sauter

Daxer

et al. 2015

J Virol

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“…In the case of influenza, an international consortium of researchers called GISAID established a framework for good practice in 2006. Largely thanks to this, during the 2009 H1N1 influenza outbreak, the US National Center for Biotechnology Information created a public repository that became a go-to place for the community to deposit and locate H1N1 sequence information 4 . By contrast, the publishing of sequence information in the early stages of the 2012 Middle East respiratory syndrome (MERS) outbreak in Saudi Arabia highlighted uncertainties about intellectualproperty rights, and the resulting disputes hampered subsequent access to samples.…”

Section: Speed Is Everythingmentioning

confidence: 99%

Data sharing: Make outbreak research open access

Yozwiak

Schaffner

Sabeti

2015

Nature

130

116

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“…In recent years we witnessed massive data collection from surveillance platforms, 35,36 sophisticated data analysis and experimental work that is shedding light on the interplay between disease evolution and host immunity, [37][38][39][40] and elaborate theoretical studies already mentioned in the introduction. The latter produced several competing models each of which is, when suitably parametrized, capable of generating realistic phylodynamics patterns.…”

Section: Discussionmentioning

confidence: 99%

Host immunity and pathogen diversity: A computational study

Aquino

Nunes

2016

Virulence

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The distinctive features of human influenza A phylogeny have inspired many mathematical and computational studies of viral infections spreading in a host population, but our understanding of the mechanisms that shape the coupled evolution of host immunity, disease incidence and viral antigenic properties is far from complete. In this paper we explore the epidemiology and the phylogeny of a rapidly mutating pathogen in a host population with a weak immune response, that allows re-infection by the same strain and provides little cross-immunity. We find that mutation generates explosive diversity and that, as diversity grows, the system is driven to a very high prevalence level. This is in stark contrast with the behavior of similar models where mutation gives rise to a large epidemic followed by disease extinction, under the assumption that infection with a strain provides lifelong immunity. For low mutation rates, the behavior of the system shows the main qualitative features of influenza evolution. Our results highlight the importance of heterogeneity in the human immune response for understanding influenza A phenomenology. They are meant as a first step toward computationally affordable, individual based models including more complex host-pathogen interactions.

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A global initiative on sharing avian flu data

Cited by 132 publications

References 1 publication

Adaptive Mutations That Occurred during Circulation in Humans of H1N1 Influenza Virus in the 2009 Pandemic Enhance Virulence in Mice

Adaptive Mutations That Occurred during Circulation in Humans of H1N1 Influenza Virus in the 2009 Pandemic Enhance Virulence in Mice

Data sharing: Make outbreak research open access

Host immunity and pathogen diversity: A computational study

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