Comparison of pandemic (H1N1) 2009 and seasonal influenza viral loads, Singapore.
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ABSTRACT:
SUBMITTER: Lee CK
PROVIDER: S-EPMC3204747 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundPersons with influenza can develop complications that result in hospitalization and death. These are most commonly respiratory related, but cardiovascular or neurologic complications or exacerbations of underlying chronic medical conditions may also occur. Patterns of complications observed during pandemics may differ from typical influenza seasons, and characterizing variations in influenza-related complications can provide a better understanding of the impact of pandemics and guide appropriate clinical management and planning for the future.MethodsUsing a population-based surveillance system, we compared clinical complications using International Classification of Diseases, Ninth Revision (ICD-9) discharge diagnosis codes in adults hospitalized with seasonal influenza (n = 5270) or 2009 pandemic influenza A(H1N1) (H1N1pdm09; n = 4962).ResultsAdults hospitalized with H1N1pdm09 were younger (median age, 47 years) than those with seasonal influenza (median age, 68 years; P < .01), and differed in the frequency of certain underlying medical conditions. Whereas there was similar risk for many influenza-associated complications, after controlling for age and type of underlying medical condition, adults hospitalized with H1N1pdm09 were more likely to have lower respiratory tract complications, shock/sepsis, and organ failure than those with seasonal influenza. They were also more likely to be admitted to the intensive care unit, require mechanical ventilation, or die. Young adults, in particular, had 2-4 times the risk of severe outcomes from H1N1pdm09 than persons of the same ages with seasonal influenza.ConclusionsAlthough H1N1pdm09 was thought of as a relatively mild pandemic, these data highlight the impact of the 2009 pandemic on the risk of severe influenza, especially among younger adults, and the impact this virus may continue to have.
| S-EPMC7314251 | biostudies-literature
Project description:To further understand the molecular pathogenesis of the 2009 pandemic H1N1 influenza virus infection, we profiled cellular miRNAs of lung tissue from BALB/c mice infected with influenza virus BJ501 and a mouse-adapted influenza virus A/Puerto Rico/8/34 (H1N1)(PR8) as a comparison.
2013-04-17 | GSE46087 | GEO
Project description:BACKGROUND:The mortality burden of the 2009 A/H1N1 pandemic remains unclear in many countries due to delays in reporting of death statistics. We estimate the age- and cause-specific excess mortality impact of the pandemic in France, relative to that of other countries and past epidemic and pandemic seasons. METHODS:We applied Serfling and Poisson excess mortality approaches to model weekly age- and cause-specific mortality rates from June 1969 through May 2010 in France. Indicators of influenza activity, time trends, and seasonal terms were included in the models. We also reviewed the literature for country-specific estimates of 2009 pandemic excess mortality rates to characterize geographical differences in the burden of this pandemic. RESULTS:The 2009 A/H1N1 pandemic was associated with 1.0 (95% Confidence Intervals (CI) 0.2-1.9) excess respiratory deaths per 100,000 population in France, compared to rates per 100,000 of 44 (95% CI 43-45) for the A/H3N2 pandemic and 2.9 (95% CI 2.3-3.7) for average inter-pandemic seasons. The 2009 A/H1N1 pandemic had a 10.6-fold higher impact than inter-pandemic seasons in people aged 5-24 years and 3.8-fold lower impact among people over 65 years. CONCLUSIONS:The 2009 pandemic in France had low mortality impact in most age groups, relative to past influenza seasons, except in school-age children and young adults. The historical A/H3N2 pandemic was associated with much larger mortality impact than the 2009 pandemic, across all age groups and outcomes. Our 2009 pandemic excess mortality estimates for France fall within the range of previous estimates for high-income regions. Based on the analysis of several mortality outcomes and comparison with laboratory-confirmed 2009/H1N1 deaths, we conclude that cardio-respiratory and all-cause mortality lack precision to accurately measure the impact of this pandemic in high-income settings and that use of more specific mortality outcomes is important to obtain reliable age-specific estimates.
| S-EPMC3447811 | biostudies-literature
Project description:In contrast to seasonal influenza virus infections, which typically cause significant morbidity and mortality in the elderly, the 2009 H1N1 virus caused severe infection in young adults. This phenomenon was attributed to the presence of cross-protective antibodies acquired by older individuals during previous exposures to H1N1 viruses. However, this hypothesis could not be empirically tested. To address this question, we compared viral replication and the development of the immune response in naïve young adult and aged female rhesus macaques infected with A/California/04/2009 H1N1 (CA04) virus. We show higher viral loads in the bronchoalveolar lavage (BAL) fluid and nasal and ocular swabs in aged animals, suggesting increased viral replication in both the lower and upper respiratory tracts. T cell proliferation was higher in the BAL fluid but delayed and reduced in peripheral blood in aged animals. This delay in proliferation correlated with a reduced frequency of effector CD4 T cells in old animals. Aged animals also mobilized inflammatory cytokines to higher levels in the BAL fluid. Finally, we compared changes in gene expression using microarray analysis of BAL fluid samples. Our analyses revealed that the largest difference in host response between aged and young adult animals was detected at day 4 postinfection, with a significantly higher induction of genes associated with inflammation and the innate immune response in aged animals. Overall, our data suggest that, in the absence of preexisting antibodies, CA04 infection in aged macaques is associated with changes in innate and adaptive immune responses that were shown to correlate with increased disease severity in other respiratory disease models.
| S-EPMC3457171 | biostudies-literature
Project description:BackgroundSeasonal influenza activity varies with geography and time of year.ObjectiveTo describe how pandemic influenza A(H1N1)2009 [A(H1N1)pdm09] activity varied during the 2009-2010 pandemic.MethodsWe analyzed influenza virological data compiled by the World Health Organization from June 2009-August 2010. We calculated weekly proportions of A(H1N1)pdm09-positive specimens out of all A(H1N1)pdm09-positive specimens detected during the study period for each country. We compared parameters of pandemic activity (e.g., peak A[H1N1]pdm09 weekly proportion [peak activity], number of weeks between the 5th and 95th percentiles of A(H1N1)pdm09 cumulative weekly proportion [duration of activity]) between countries in temperate and tropical-subtropical regions. We quantified the proportion of A(H1N1)pdm09 out of all influenza A specimens by country and correlated it with countries' central latitudes.ResultsWe analyzed data from 80 countries (47 temperate, 33 tropical-subtropical). The median proportion of cases identified during the peak week was higher in temperate (0·12) than in tropical-subtropical (0·09) regions (P<0·01). The median duration of activity was longer in tropical-subtropical (27 weeks) than in temperate countries (20 weeks) (P < 0·01). In most temperate countries (98%), peak pandemic activity occurred during the fall-winter period. There was a positive correlation between country central latitude and proportion of A(H1N1)pdm09 out of all influenza A specimens (r: 0·76; P<0·01).ConclusionsThe transmission of A(H1N1)pdm09 exhibited similarities with seasonal influenza transmission in that activity varied between temperate and tropical-subtropical countries and by time of year. Our findings suggest the potential utility of accounting for these factors during future pandemic planning.
| S-EPMC4634296 | biostudies-literature
Project description:BackgroundData about influenza mortality burden in northern China are limited. This study estimated mortality burden in Beijing associated with seasonal influenza from 2007 to 2013 and the 2009 H1N1 pandemic.MethodsWe estimated influenza-associated excess mortality by fitting a negative binomial model using weekly mortality data as the outcome of interest with the percent of influenza-positive samples by type/subtype as predictor variables.ResultsFrom 2007 to 2013, an average of 2375 (CI 1002-8688) deaths was attributed to influenza per season, accounting for 3% of all deaths. Overall, 81% of the deaths attributed to influenza occurred in adults aged ?65 years, and the influenza-associated mortality rate in this age group was higher than the rate among those aged <65 years (113.6 [CI 49.5-397.4] versus 4.4 [CI 1.7-18.6] per 100 000, P < .05). The mortality rate associated with the 2009 H1N1 pandemic in 2009/2010 was comparable to that of seasonal influenza during the seasonal years (19.9 [CI 10.4-33.1] vs 17.2 [CI 7.2-67.5] per 100 000). People aged <65 years represented a greater proportion of all deaths during the influenza A(H1N1)pdm09 pandemic period than during the seasonal epidemics (27.0% vs 17.7%, P < .05).ConclusionsInfluenza is an important contributor to mortality in Beijing, especially among those aged ?65 years. These results support current policies to give priority to older adults for seasonal influenza vaccination and help to define the populations at highest risk for death that could be targeted for pandemic influenza vaccination.
| S-EPMC5818349 | biostudies-literature
Project description:A total of 828 community-dwelling adults were studied during the course of the pandemic (H1N1) 2009 outbreak in Singapore during June-September 2009. Baseline blood samples were obtained before the outbreak, and 2 additional samples were obtained during follow-up. Seroconversion was defined as a >4-fold increase in antibody titers to pandemic (H1N1) 2009, determined by using hemagglutination inhibition. Men were more likely than women to seroconvert (mean adjusted hazards ratio [HR] 2.23, mean 95% confidence interval [CI] 1.26-3.93); Malays were more likely than Chinese to seroconvert (HR 2.67, 95% CI 1.04-6.91). Travel outside Singapore during the study period was associated with seroconversion (HR 1.76, 95% CI 1.11-2.78) as was use of public transport (HR 1.81, 95% CI 1.05-3.09). High baseline antibody titers were associated with reduced seroconversion. This study suggests possible areas for intervention to reduce transmission during future influenza outbreaks.
| S-EPMC3381584 | biostudies-literature
Project description:To further understand the molecular pathogenesis of the 2009 pandemic H1N1 influenza virus infection, we profiled cellular miRNAs of lung tissue from BALB/c mice infected with influenza virus BJ501 and a mouse-adapted influenza virus A/Puerto Rico/8/34 (H1N1)(PR8) as a comparison. Five groups of mice were selected, and three of each group were used to profile the miRNA, two were in case for unqualified RNA extraction. Whole lungs from mice infected by BJ501 or PR8 were harvested on 2,5 days post infection (dpi), and compared with lung samples from 5 uninfected mice.
2013-04-17 | E-GEOD-46087 | biostudies-arrayexpress
Project description:Influenza A(H7N9) viruses isolated from humans show features suggesting partial adaptation to mammals. To provide insights into the pathogenesis of H7N9 virus infection, we compared risk factors, clinical presentation, and progression of patients hospitalized with H7N9, H5N1, and 2009 pandemic H1N1 (pH1N1) virus infections.We compared individual-level data from patients hospitalized with infection by H7N9 (n = 123), H5N1 (n = 119; 43 China, 76 Vietnam), and pH1N1 (n = 3486) viruses. We assessed risk factors for hospitalization after adjustment for age- and sex-specific prevalence of risk factors in the general Chinese population.The median age of patients with H7N9 virus infection was older than other patient groups (63 years; P < .001) and a higher proportion was male (71%; P < .02). After adjustment for age and sex, chronic heart disease was associated with an increased risk of hospitalization with H7N9 (relative risk, 9.68; 95% confidence interval, 5.24-17.9). H7N9 patients had similar patterns of leukopenia, thrombocytopenia, and elevated alanine aminotransferase, creatinine kinase, C-reactive protein, and lactate dehydrogenase to those seen in H5N1 patients, which were all significantly different from pH1N1 patients (P < .005). H7N9 patients had a longer duration of hospitalization than either H5N1 or pH1N1 patients (P < .001), and the median time from onset to death was 18 days for H7N9 (P = .002) vs 11 days for H5N1 and 15 days for pH1N1 (P = .154).The identification of known risk factors for severe seasonal influenza and the more protracted clinical course compared with that of H5N1 suggests that host factors are an important contributor to H7N9 severity.
| S-EPMC3967826 | biostudies-other
Project description:Adamantane and oseltamivir resistance among influenza viruses is a major concern to public health officials. To determine the prevalence of antiviral-resistant influenza viruses in Guangdong, China, 244 seasonal A (H1N1) and 222 pandemic A (H1N1) 2009 viruses were screened for oseltamivir resistance by a fluorescence-based neuraminidase (NA) inhibition assay along with NA gene sequencing. Also, 147 seasonal A (H1N1) viruses were sequenced to detect adamantane resistance markers in M2. Adamantane-resistant seasonal A (H1N1) viruses clustering to clade 2C were dominant in 2008, followed by oseltamivir-resistant seasonal A (H1N1) viruses, clustering to clade 2B during January and May 2009. In June 2009, a lineage of double-resistant seasonal A (H1N1) viruses emerged, until it was replaced by the pandemic A (H1N1) 2009 viruses. The lineage most likely resulted from reassortment under the pressure of the overuse of adamantanes. As all viruses were resistant to at least one of the two types of antiviral agents, the need for close monitoring of the prevalence of antiviral resistance is stressed.
| S-EPMC3147846 | biostudies-literature