A Survey-Based Assessment of United States Clinical Laboratory Response to the 2009 H1N1 Influenza Outbreak

2010 ◽  
Vol 134 (11) ◽  
pp. 1671-1678
Author(s):  
Randall T. Hayden ◽  
Megan T. Wick ◽  
Alicia B. Rodriguez ◽  
Angela M. Caliendo ◽  
Michael J. Mitchell ◽  
...  

Abstract Context.—The recent outbreak of pandemic influenza created enormous economic, logistical, and analytical challenges for clinical laboratories. Laboratory response represented a critical element in the care of affected patients, but little has been published regarding this aspect of the pandemic. Objective.—To assess the overall response of clinical diagnostic laboratories across the United States to the initial phase of the 2009 H1N1 influenza A pandemic. Design.—A 24-question survey was developed and distributed by e-mail to determine current influenza testing practices and how those practices were changed in response to the outbreak of 2009 H1N1 influenza. The survey was distributed to participants in the College of American Pathologists proficiency testing programs related to viral diagnostics. Survey questions focused on laboratory safety, communication of results, testing volume and resources, and whether changes in resource allocation or laboratory practice were anticipated in preparation for the 2009–2010 influenza season. Results.—A total of 24.3% (931) of laboratories responded to the survey. Overall, few laboratories reported changes in methodology in response to the 2009 H1N1 influenza outbreak, although, notably, the number of centers using molecular amplification methods more than doubled, from 41 to 91. Turn-around time for result reporting and safety methods used were largely as expected for individual testing modalities. Shortages in staffing, testing supplies, and personal protective equipment were reported, but most sites were able to maintain operations and did not feel that patient care was negatively affected. Conclusion.—This report provides a comprehensive picture of clinical laboratory responses in the early stages of the 2009 H1N1 influenza pandemic. These data should assist in the continued laboratory management of this outbreak and in planning for future emerging infections.

2009 ◽  
Vol 14 (41) ◽  
Author(s):  
S Towers ◽  
Z Feng

We use data on confirmed cases of pandemic influenza A(H1N1), disseminated by the United States Centers for Disease Control and Prevention(US CDC), to fit the parameters of a seasonally forced Susceptible, Infective, Recovered (SIR) model. We use the resulting model to predict the course of the H1N1 influenza pandemic in autumn 2009, and we assess the efficacy of the planned CDC H1N1 vaccination campaign. The model predicts that there will be a significant wave in autumn, with 63% of the population being infected, and that this wave will peak so early that the planned CDC vaccination campaign will likely not have a large effect on the total number of people ultimately infected by the pandemic H1N1 influenza virus.


2015 ◽  
Vol 105 (1) ◽  
pp. 13-18 ◽  
Author(s):  
Richard N. Danila ◽  
Ellen S. Laine ◽  
Franci Livingston ◽  
Kathryn Como-Sabetti ◽  
Lauren Lamers ◽  
...  

2011 ◽  
Vol 39 (2) ◽  
pp. 229-243 ◽  
Author(s):  
Supriya Kumar ◽  
Sandra Crouse Quinn ◽  
Kevin H. Kim ◽  
Donald Musa ◽  
Karen M. Hilyard ◽  
...  

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Ignacio Mena ◽  
Martha I Nelson ◽  
Francisco Quezada-Monroy ◽  
Jayeeta Dutta ◽  
Refugio Cortes-Fernández ◽  
...  

Asia is considered an important source of influenza A virus (IAV) pandemics, owing to large, diverse viral reservoirs in poultry and swine. However, the zoonotic origins of the 2009 A/H1N1 influenza pandemic virus (pdmH1N1) remain unclear, due to conflicting evidence from swine and humans. There is strong evidence that the first human outbreak of pdmH1N1 occurred in Mexico in early 2009. However, no related swine viruses have been detected in Mexico or any part of the Americas, and to date the most closely related ancestor viruses were identified in Asian swine. Here, we use 58 new whole-genome sequences from IAVs collected in Mexican swine to establish that the swine virus responsible for the 2009 pandemic evolved in central Mexico. This finding highlights how the 2009 pandemic arose from a region not considered a pandemic risk, owing to an expansion of IAV diversity in swine resulting from long-distance live swine trade.


2021 ◽  
Vol 118 (5) ◽  
pp. e2012327118
Author(s):  
Rebecca K. Borchering ◽  
Christian E. Gunning ◽  
Deven V. Gokhale ◽  
K. Bodie Weedop ◽  
Arash Saeidpour ◽  
...  

The 2019/2020 influenza season in the United States began earlier than any season since the 2009 H1N1 pandemic, with an increase in influenza-like illnesses observed as early as August. Also noteworthy was the numerical domination of influenza B cases early in this influenza season, in contrast to their typically later peak in the past. Here, we dissect the 2019/2020 influenza season not only with regard to its unusually early activity, but also with regard to the relative dynamics of type A and type B cases. We propose that the recent expansion of a novel influenza B/Victoria clade may be associated with this shift in the composition and kinetics of the influenza season in the United States. We use epidemiological transmission models to explore whether changes in the effective reproduction number or short-term cross-immunity between these viruses can explain the dynamics of influenza A and B seasonality. We find support for an increase in the effective reproduction number of influenza B, rather than support for cross-type immunity-driven dynamics. Our findings have clear implications for optimal vaccination strategies.


2013 ◽  
Vol 9 (5) ◽  
pp. 20130331 ◽  
Author(s):  
J. Hedge ◽  
S. J. Lycett ◽  
A. Rambaut

Early characterization of the epidemiology and evolution of a pandemic is essential for determining the most appropriate interventions. During the 2009 H1N1 influenza A pandemic, public databases facilitated widespread sharing of genetic sequence data from the outset. We use Bayesian phylogenetics to simulate real-time estimates of the evolutionary rate, date of emergence and intrinsic growth rate ( r 0 ) of the pandemic from whole-genome sequences. We investigate the effects of temporal range of sampling and dataset size on the precision and accuracy of parameter estimation. Parameters can be accurately estimated as early as two months after the first reported case, from 100 genomes and the choice of growth model is important for accurate estimation of r 0 . This demonstrates the utility of simple coalescent models to rapidly inform intervention strategies during a pandemic.


mBio ◽  
2010 ◽  
Vol 1 (1) ◽  
Author(s):  
Brett W. Jagger ◽  
Matthew J. Memoli ◽  
Zong-Mei Sheng ◽  
Li Qi ◽  
Rachel J. Hrabal ◽  
...  

ABSTRACTThe swine-origin H1N1 influenza A virus emerged in early 2009 and caused the first influenza pandemic in 41 years. The virus has spread efficiently to both the Northern and the Southern Hemispheres and has been associated with over 16,000 deaths. Given the virus’s recent zoonotic origin, there is concern that the virus could acquire signature mutations associated with the enhanced pathogenicity of previous pandemic viruses or H5N1 viruses with pandemic potential. We tested the hypothesis that mutations in the polymerase PB2 gene at residues 627 and 701 would enhance virulence but found that influenza viruses containing these mutations in the context of the pandemic virus polymerase complex are attenuated in cell culture and mice.IMPORTANCEInfluenza A virus (IAV) evolution is characterized by host-specific lineages, and IAVs derived in whole or in part from animal reservoirs have caused pandemics in humans. Because IAVs are known to acquire host-adaptive genome mutations, and since the PB2 gene of the 2009 H1N1 virus is of recent avian derivation, there exists concern that the pathogenicity of the 2009 H1N1 influenza A pandemic virus could be potentiated by acquisition of the host-adaptive PB2-E627K or -D701N mutations, which have been shown to enhance the virulence of other influenza viruses. We present data from a mouse model of influenza infection showing that such mutations do not increase the virulence of viruses containing the 2009 H1N1 viral polymerase.


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