Estimating age‐specific cumulative incidence for the 2009 influenza pandemic: a meta‐analysis of <scp>A</scp>(<scp>H</scp>1<scp>N</scp>1)pdm09 serological studies from 19 countries

Kerkhove, Maria D. Van; Hirve, Siddhivinayak; Koukounari, Artemis; Mounts, Anthony W.

doi:10.1111/irv.12074

Cited by 166 publications

(156 citation statements)

References 57 publications

Supporting

Mentioning

143

Contrasting

Unclassified

Order By: Relevance

“…However, the model indicates increasing immunity with age to be another significant factor that is essential in reproducing the observed pattern of attack rates in the different age-groups (figure 4c). This result reaffirms similar conclusions made by previous serological studies [40][41][42] as well as modelling studies of the pandemic in other countries [20,[43][44][45]. Nonetheless, it should be noted that the differences in susceptibility between individuals in the 0-4 age-group and individuals in the 5-19 and 20 -44 age-groups, as estimated by our model, might rsif.royalsocietypublishing.org J. R. Soc.…”

Section: Discussionsupporting

confidence: 92%

Model-based reconstruction of an epidemic using multiple datasets: understanding influenza A/H1N1 pandemic dynamics in Israel

Yaari

Katriel

Stone

et al. 2016

J. R. Soc. Interface.

View full text Add to dashboard Cite

Intensified surveillance during the 2009 A/H1N1 influenza pandemic in Israel resulted in large virological and serological datasets, presenting a unique opportunity for investigating the pandemic dynamics. We employ a conditional likelihood approach for fitting a disease transmission model to virological and serological data, conditional on clinical data. The model is used to reconstruct the temporal pattern of the pandemic in Israel in five age-groups and evaluate the factors that shaped it. We estimate the reproductive number at the beginning of the pandemic to be R ¼ 1.4. We find that the combined effect of varying absolute humidity conditions and school vacations (SVs) is responsible for the infection pattern, characterized by three epidemic waves. Overall attack rate is estimated at 32% (28-35%) with a large variation among the age-groups: the highest attack rates within school children and the lowest within the elderly. This pattern of infection is explained by a combination of the age-group contact structure and increasing immunity with age. We assess that SVs increased the overall attack rates by prolonging the pandemic into the winter. Vaccinating school children would have been the optimal strategy for minimizing infection rates in all age-groups.

show abstract

Section: Discussionsupporting

confidence: 92%

Model-based reconstruction of an epidemic using multiple datasets: understanding influenza A/H1N1 pandemic dynamics in Israel

Yaari

Katriel

Stone

et al. 2016

J. R. Soc. Interface.

View full text Add to dashboard Cite

show abstract

“…2 Global infection rates were estimated at 24%, more than a billion persons, with as many as 200,000 deaths. 3 These data indicate the breadth of the toll that influenza infection takes on humankind.…”

mentioning

confidence: 97%

Epigenetic and Transcriptomic Regulation of Lung Repair during Recovery from Influenza Infection

Pociask

Robinson

Chen

et al. 2017

The American Journal of Pathology

View full text Add to dashboard Cite

Seasonal and pandemic influenza is a cause of morbidity and mortality worldwide. Most people infected with influenza virus display mild-to-moderate disease phenotypes and recover within a few weeks. Influenza is known to cause persistent alveolitis in animal models; however, little is known about the molecular pathways involved in this phenotype. We challenged C57BL/6 mice with influenza A/PR/8/34 and examined lung pathologic processes and inflammation, as well as transcriptomic and epigenetic changes at 21 to 60 days after infection. Influenza induced persistent parenchymal lung inflammation, alveolar epithelial metaplasia, and epithelial endoplasmic reticulum stress that were evident after the clearance of virus and resolution of morbidity. Influenza infection induced robust changes in the lung transcriptome, including a significant impact on inflammatory and extracellular matrix protein expression. Despite the robust changes in lung gene expression, preceding influenza (21 days) did not exacerbate secondary Staphylococcus aureus infection. Finally, we examined the impact of influenza on miRNA expression in the lung and found an increase in miR-155. miR-155 knockout mice recovered from influenza infection faster than controls and had decreased lung inflammation and endoplasmic reticulum stress. These data illuminate the dynamic molecular changes in the lung in the weeks after influenza infection and characterize the repair process, identifying a novel role for miR-155. (Am J Pathol 2017, 187: 851e863; http://dx

show abstract

“…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)(5)(6)(7). During the pandemic in 2009, a disproportionately high number of young adults were hospitalized due to pneumonia and eventually died (6)(7)(8)(9).…”

mentioning

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

View full text Add to dashboard Cite

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 ...

show abstract

Estimating age‐specific cumulative incidence for the 2009 influenza pandemic: a meta‐analysis of A(H1N1)pdm09 serological studies from 19 countries

Cited by 166 publications

References 57 publications

Model-based reconstruction of an epidemic using multiple datasets: understanding influenza A/H1N1 pandemic dynamics in Israel

Model-based reconstruction of an epidemic using multiple datasets: understanding influenza A/H1N1 pandemic dynamics in Israel

Epigenetic and Transcriptomic Regulation of Lung Repair during Recovery from Influenza Infection

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

Contact Info

Product

Resources

About