Document Type


Peer Reviewed


Publication Date


Journal/Book/Conference Title

PLoS Computational Biology

DOI of Published Version

10.1371/journal. pcbi.1004337

Start Page


Total Pages



While a relationship between environmental forcing and influenza transmission has been established in inter-pandemic seasons, the drivers of pandemic influenza remain debated. In particular, school effects may predominate in pandemic seasons marked by an atypical concentration of cases among children. For the 2009 A/H1N1 pandemic, Mexico is a particularly interesting case study due to its broad geographic extent encompassing temperate and tropical regions, well-documented regional variation in the occurrence of pandemic outbreaks, and coincidence of several school breaks during the pandemic period. Here we fit a series of transmission models to daily laboratory-confirmed influenza data in 32 Mexican states using MCMC approaches, considering a meta-population framework or the absence of spatial coupling between states. We use these models to explore the effect of environmental, school–related and travel factors on the generation of spatially-heterogeneous pandemic waves. We find that the spatial structure of the pandemic is best understood by the interplay between regional differences in specific humidity (explaining the occurrence of pandemic activity towards the end of the school term in late May-June 2009 in more humid southeastern states), school vacations (preventing influenza transmission during July-August in all states), and regional differences in residual susceptibility (resulting in large outbreaks in early fall 2009 in central and northern Mexico that had yet to experience fully-developed outbreaks). Our results are in line with the concept that very high levels of specific humidity, as present during summer in southeastern Mexico, favor influenza transmission, and that school cycles are a strong determinant of pandemic wave timing.



Granting or Sponsoring Agency


Grant Number

1U54GM088558 and ES009089


Funding was provided by the NIH Models of Infectious Disease Agent Study program through cooperative agreement 1U54GM088558 (JT, JS), as well as NIEHS Center grant ES009089 (JS), the RAPIDD program of the Science and Technology Directorate, US Department of Homeland Security (JS), and the in-house influenza research program of the Fogarty International Center, NIH, funded by the Office of Global Affairs’ International Influenza Unit, Office of the Secretary, US Department of Health and Human Services.

Journal Article Version

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Published Article/Book Citation

PLoS Comput Biol 11(8): e1004337. doi: 10.1371/journal.pcbi.1004337


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