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Dive into the research topics where Bahman Davoudi is active.

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Featured researches published by Bahman Davoudi.


Influenza and Other Respiratory Viruses | 2009

Initial human transmission dynamics of the pandemic (H1N1) 2009 virus in North America.

Babak Pourbohloul; Armando Ahued; Bahman Davoudi; Rafael Meza; Lauren Ancel Meyers; Danuta M. Skowronski; Ignacio Villaseñor; Fernando Galván; Patricia Cravioto; David J. D. Earn; Jonathan Dushoff; David N. Fisman; W. John Edmunds; Nathaniel Hupert; Samuel V. Scarpino; Jesús Trujillo; Miguel Lutzow; Jorge Morales; Ada Contreras; Carolina Chávez; David M. Patrick; Robert C. Brunham

Background  Between 5 and 25 April 2009, pandemic (H1N1) 2009 caused a substantial, severe outbreak in Mexico, and subsequently developed into the first global pandemic in 41 years. We determined the reproduction number of pandemic (H1N1) 2009 by analyzing the dynamics of the complete case series in Mexico City during this early period.


BMC Public Health | 2011

Vaccination against 2009 pandemic H1N1 in a population dynamical model of Vancouver, Canada: timing is everything

Jessica M. Conway; Ashleigh R. Tuite; David N. Fisman; Nathaniel Hupert; Rafael Meza; Bahman Davoudi; Krista M. English; P. van den Driessche; Fred Brauer; Junling Ma; Lauren Ancel Meyers; Marek Smieja; Amy L. Greer; Danuta M. Skowronski; David L. Buckeridge; Jeffrey C. Kwong; Jianhong Wu; Seyed M. Moghadas; Daniel Coombs; Robert C. Brunham; Babak Pourbohloul

BackgroundMuch remains unknown about the effect of timing and prioritization of vaccination against pandemic (pH1N1) 2009 virus on health outcomes. We adapted a city-level contact network model to study different campaigns on influenza morbidity and mortality.MethodsWe modeled different distribution strategies initiated between July and November 2009 using a compartmental epidemic model that includes age structure and transmission network dynamics. The model represents the Greater Vancouver Regional District, a major North American city and surrounding suburbs with a population of 2 million, and is parameterized using data from the British Columbia Ministry of Health, published studies, and expert opinion. Outcomes are expressed as the number of infections and deaths averted due to vaccination.ResultsThe model output was consistent with provincial surveillance data. Assuming a basic reproduction number = 1.4, an 8-week vaccination campaign initiated 2 weeks before the epidemic onset reduced morbidity and mortality by 79-91% and 80-87%, respectively, compared to no vaccination. Prioritizing children and parents for vaccination may have reduced transmission compared to actual practice, but the mortality benefit of this strategy appears highly sensitive to campaign timing. Modeling the actual late October start date resulted in modest reductions in morbidity and mortality (13-25% and 16-20%, respectively) with little variation by prioritization scheme.ConclusionDelays in vaccine production due to technological or logistical barriers may reduce potential benefits of vaccination for pandemic influenza, and these temporal effects can outweigh any additional theoretical benefits from population targeting. Careful modeling may provide decision makers with estimates of these effects before the epidemic peak to guide production goals and inform policy. Integration of real-time surveillance data with mathematical models holds the promise of enabling public health planners to optimize the community benefits from proposed interventions before the pandemic peak.


PLOS ONE | 2013

H3N2v and Other Influenza Epidemic Risk Based on Age-Specific Estimates of Sero-Protection and Contact Network Interactions

Danuta M. Skowronski; Flavia Moser; Naveed Z. Janjua; Bahman Davoudi; Krista M. English; Dale Purych; Martin Petric; Babak Pourbohloul

Cases of a novel swine-origin influenza A(H3N2) variant (H3N2v) have recently been identified in the US, primarily among children. We estimated potential epidemic attack rates (ARs) based on age-specific estimates of sero-susceptibility and social interactions. A contact network model previously established for the Greater Vancouver Area (GVA), Canada was used to estimate average epidemic (infection) ARs for the emerging H3N2v and comparator viruses (H1N1pdm09 and an extinguished H3N2 seasonal strain) based on typical influenza characteristics, basic reproduction number (R0), and effective contacts taking into account age-specific sero-protection rates (SPRs). SPRs were assessed in sera collected from the GVA in 2009 or earlier (pre-H1N1pdm09) and fall 2010 (post-H1N1pdm09, seasonal A/Brisbane/10/2007(H3N2), and H3N2v) by hemagglutination inhibition (HI) assay. SPR was assigned per convention based on proportion with HI antibody titre ≥40 (SPR40). Recognizing that the HI titre ≥40 was established as the 50%sero-protective threshold we also explored for ½SPR40, SPR80 and a blended gradient defined as: ¼SPR20, ½SPR40, ¾SPR80, SPR160. Base case analysis assumed R0 = 1.40, but we also explored R0 as high as 1.80. With R0 = 1.40 and SPR40, simulated ARs were well aligned with field observations for H1N1pdm09 incidence (AR: 32%), sporadic detections without a third epidemic wave post-H1N1pdm09 (negligible AR<0.1%) as well as A/Brisbane/10/2007(H3N2) seasonal strain extinction and antigenic drift replacement (negligible AR<0.1%). Simulated AR for the novel swine-origin H3N2v was 6%, highest in children 6–11years (16%). However, with modification to SPR thresholds per above, H3N2v AR ≥20% became possible. At SPR40, H3N2v AR ≥10%, ≥15% or ≥30%, occur if R0≥1.48, ≥1.56 or ≥1.86, respectively. Based on conventional assumptions, the novel swine-origin H3N2v does not currently pose a substantial pandemic threat. If H3N2v epidemics do occur, overall community ARs are unlikely to exceed typical seasonal influenza experience. However risk assessment may change with time and depends crucially upon the validation of epidemiological features of influenza, notably the serologic correlate of protection and R0.


Physical Review X | 2012

Early real-time estimation of the basic reproduction number of emerging infectious diseases

Bahman Davoudi; Joel C. Miller; Rafael Meza; Lauren Ancel Meyers; David J. D. Earn; Babak Pourbohloul

When an infectious disease strikes a population, the number of newly reported cases is often the only available information that one can obtain during early stages of the outbreak. An important goal of early outbreak analysis is to obtain a reliable estimate for the basic reproduction number, R0, from the limited information available. We present a novel method that enables us to make a reliable real-time estimate of the reproduction number at a much earlier stage compared to other available methods. Our method takes into account the possibility that a disease has a wide distribution of infectious period and that the degree distribution of the contact network is heterogeneous. We validate our analytical framework with numerical simulations. 1 Division of Mathematical Modeling, British Columbia Centre for Disease Control, Vancouver, British Columbia, Canada 2 School of Population & Public Health, University of British Columbia, Vancouver, British Columbia, Canada 3 Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, U.S.A. 4 Section of Integrative Biology, Institute for Cellular and Molecular Biology, University of Texas at Austin, Austin, Texas, U.S.A. 5 Department of Mathematics & Statistics, McMaster University, Hamilton, Ontario, Canada Corresponding Author 1


PLOS ONE | 2015

Early real-time estimation of the basic reproduction number of emerging or reemerging infectious diseases in a community with heterogeneous contact pattern: Using data from Hong Kong 2009 H1N1 Pandemic Influenza as an illustrative example.

Kin On Kwok; Bahman Davoudi; Steven Riley; Babak Pourbohloul

Emerging and re-emerging infections such as SARS (2003) and pandemic H1N1 (2009) have caused concern for public health researchers and policy makers due to the increased burden of these diseases on health care systems. This concern has prompted the use of mathematical models to evaluate strategies to control disease spread, making these models invaluable tools to identify optimal intervention strategies. A particularly important quantity in infectious disease epidemiology is the basic reproduction number, R0. Estimation of this quantity is crucial for effective control responses in the early phase of an epidemic. In our previous study, an approach for estimating the basic reproduction number in real time was developed. This approach uses case notification data and the structure of potential transmission contacts to accurately estimate R0 from the limited amount of information available at the early stage of an outbreak. Based on this approach, we extend the existing methodology; the most recent method features intra- and inter-age groups contact heterogeneity. Given the number of newly reported cases at the early stage of the outbreak, with parsimony assumptions on removal distribution and infectivity profile of the diseases, experiments to estimate real time R0 under different levels of intra- and inter-group contact heterogeneity using two age groups are presented. We show that the new method converges more quickly to the actual value of R0 than the previous one, in particular when there is high-level intra-group and inter-group contact heterogeneity. With the age specific contact patterns, number of newly reported cases, removal distribution, and information about the natural history of the 2009 pandemic influenza in Hong Kong, we also use the extended model to estimate R0 and age-specific R0.


Journal of Biological Dynamics | 2013

Epidemic progression on networks based on disease generation time

Bahman Davoudi; Flavia Moser; Fred Brauer; Babak Pourbohloul

We investigate the time evolution of disease spread on a network and present an analytical framework using the concept of disease generation time. Assuming a susceptible–infected–recovered epidemic process, this network-based framework enables us to calculate in detail the number of links (edges) within the network that are capable of producing new infectious nodes (individuals), the number of links that are not transmitting the infection further (non-transmitting links), as well as the number of contacts that individuals have with their neighbours (also known as degree distribution) within each epidemiological class, for each generation period. Using several examples, we demonstrate very good agreement between our analytical calculations and the results of computer simulations.


Physical Review E | 2009

Time evolution of epidemic disease on finite and infinite networks

Pierre-André Noël; Bahman Davoudi; Robert C. Brunham; Louis J. Dubé; Babak Pourbohloul


Journal of Theoretical Biology | 2010

Epidemics with general generation interval distributions

Joel C. Miller; Bahman Davoudi; Rafael Meza; Anja Slim; Babak Pourbohloul


Sexually Transmitted Infections | 2013

O17.4 Evaluating the Cost Effectiveness of Targeted Vaccination Strategies to Reduce Incidence of HPV-Related Cancer and Other Clinical Outcomes in Men Who Have Sex with Men (MSM) in British Columbia, Canada

Krista M. English; Fawziah Marra; Bahman Davoudi; Mark Gilbert; Babak Pourbohloul


arXiv: Statistical Mechanics | 2010

Time Evolution of the Spread of Diseases with a General Infectivity Profile on a Complex Dynamic Network

Bahman Davoudi; Babak Pourbohloul

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Babak Pourbohloul

University of British Columbia

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Danuta M. Skowronski

BC Centre for Disease Control

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Fred Brauer

University of British Columbia

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Krista M. English

University of British Columbia

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Robert C. Brunham

University of British Columbia

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Lauren Ancel Meyers

University of Texas at Austin

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Rafael Meza

BC Centre for Disease Control

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Flavia Moser

Simon Fraser University

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