@inproceedings{conf/eusai/BlacheCDEFPV03, added-at = {2011-07-06T00:00:00.000+0200}, author = {Blache, Fabrice and Chraiet, Naoufel and Daroux, Olivier and Evennou, Frédéric and Flury, Thibaud and Privat, Gilles and Viboud, Jean-Paul}, biburl = {http://www.bibsonomy.org/bibtex/2be19ee3232775fd3b32fc55c59dc83a2/dblp}, booktitle = {EUSAI}, crossref = {conf/eusai/2003}, editor = {Aarts, Emile H. L. and Collier, René and van Loenen, Evert and de Ruyter, Boris E. R.}, ee = {http://dx.doi.org/10.1007/978-3-540-39863-9_15}, interhash = {0a962366901086bb2b4d1ad23a91b2c9}, intrahash = {be19ee3232775fd3b32fc55c59dc83a2}, isbn = {3-540-20418-0}, keywords = {dblp}, pages = {192-207}, publisher = {Springer}, series = {Lecture Notes in Computer Science}, title = {Position-Based Interaction for Indoor Ambient Intelligence Environments.}, url = {http://dblp.uni-trier.de/db/conf/eusai/eusai2003.html#BlacheCDEFPV03}, volume = 2875, year = 2003 } @article{Viboud:2006:Science:16574822, abstract = {Quantifying long-range dissemination of infectious diseases is a key issue in their dynamics and control. Here, we use influenza-related mortality data to analyze the between-state progression of interpandemic influenza in the United States over the past 30 years. Outbreaks show hierarchical spatial spread evidenced by higher pairwise synchrony between more populous states. Seasons with higher influenza mortality are associated with higher disease transmission and more rapid spread than are mild ones. The regional spread of infection correlates more closely with rates of movement of people to and from their workplaces (workflows) than with geographical distance. Workflows are described in turn by a gravity model, with a rapid decay of commuting up to around 100 km and a long tail of rare longer range flow. A simple epidemiological model, based on the gravity formulation, captures the observed increase of influenza spatial synchrony with transmissibility; high transmission allows influenza to spread rapidly beyond local spatial constraints.}, added-at = {2009-12-07T18:24:53.000+0100}, author = {Viboud and Bj\ornstad, O N and Smith, D L and Simonsen, L and Miller, M A and Grenfell, B T}, biburl = {http://www.bibsonomy.org/bibtex/2bbd7923d4b3ac39714327c4baac12f9d/ebo}, description = {Synchrony, waves, and spatial hierarchies in the s... [Science. 2006] - PubMed result}, doi = {10.1126/science.1125237}, interhash = {43995eb243959258b51c873cc5a97b6a}, intrahash = {bbd7923d4b3ac39714327c4baac12f9d}, journal = {Science}, keywords = {epi imported influenza spatial synchrony}, month = Apr, number = 5772, pages = {447-451}, pmid = {16574822}, title = {Synchrony, waves, and spatial hierarchies in the spread of influenza}, url = {http://www.ncbi.nlm.nih.gov/pubmed/16574822?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1}, volume = 312, year = 2006 } @article{LoneSimonsen08012007, abstract = {A dramatic rise in the frequency of resistance to adamantane drugs by influenza A (H3N2) viruses has occurred in recent years--from [~]2% to [~]90% in multiple countries worldwide--and associated with a single S31N amino acid replacement in the viral matrix M2 protein. To explore the emergence and spread of these adamantane resistant viruses we performed a phylogenetic analysis of recently sampled complete A/H3N2 genome sequences. Strikingly, all adamantane resistant viruses belonged to a single lineage (the "N-lineage") characterized by 17 amino acid replacements across the viral genome. Further, our analysis revealed that the genesis of the N-lineage was due to a 4+4 segment reassortment event involving 2 distinct lineages of influenza A/H3N2 virus. A subsequent study of hemagglutinin HA1 sequences suggested that the N-lineage was circulating widely in Asia during 2005, and then dominated the Northern hemisphere 2005-2006 season in Japan and the USA. Given the infrequent use of adamantane drugs in many countries, as well as the decades of use in the US associated with little drug resistance, we propose that the globally increasing frequency of adamantane resistance is more likely attributable to its interaction with fitness-enhancing mutations at other genomic sites rather than to direct drug selection pressure. This implies that adamantanes may not be useful for treatment and prophylaxis against influenza viruses in the long term. More generally, these findings illustrate that drug selection pressure is not the sole factor determining the evolution and maintenance of drug resistance in human pathogens. }, added-at = {2009-10-23T04:28:31.000+0200}, author = {Simonsen, Lone and Viboud, Cecile and Grenfell, Bryan T. and Dushoff, Jonathan and Jennings, Lance and Smit, Marita and Macken, Catherine and Hata, Mami and Gog, Julia and Miller, Mark A. and Holmes, Edward C.}, biburl = {http://www.bibsonomy.org/bibtex/267d2a7b9c80980ef87596e6572d89be3/ebo}, description = {The Genesis and Spread of Reassortment Human Influenza A/H3N2 Viruses Conferring Adamantane Resistance -- Simonsen et al. 24 (8): 1811 -- Molecular Biology and Evolution}, doi = {10.1093/molbev/msm103}, eprint = {http://mbe.oxfordjournals.org/cgi/reprint/24/8/1811.pdf}, interhash = {8c5efa735b7f1973556011f2b727fbfa}, intrahash = {67d2a7b9c80980ef87596e6572d89be3}, journal = {Mol Biol Evol}, keywords = {epi imported influenza popgen}, number = 8, pages = {1811-1820}, title = {{The Genesis and Spread of Reassortment Human Influenza A/H3N2 Viruses Conferring Adamantane Resistance}}, url = {http://mbe.oxfordjournals.org/cgi/content/abstract/24/8/1811}, volume = 24, year = 2007 } @article{Wolf:2006:Biol-Direct:17067369, abstract = {BACKGROUND: The interpandemic evolution of the influenza A virus hemagglutinin (HA) protein is commonly considered a paragon of rapid evolutionary change under positive selection in which amino acid replacements are fixed by virtue of their effect on antigenicity, enabling the virus to evade immune surveillance. RESULTS: We performed phylogenetic analyses of the recently obtained large and relatively unbiased samples of the HA sequences from 1995-2005 isolates of the H3N2 and H1N1 subtypes of influenza A virus. Unexpectedly, it was found that the evolution of H3N2 HA includes long intervals of generally neutral sequence evolution without apparent substantial antigenic change ("stasis" periods) that are characterized by an excess of synonymous over nonsynonymous substitutions per site, lack of association of amino acid replacements with epitope regions, and slow extinction of coexisting virus lineages. These long periods of stasis are punctuated by shorter intervals of rapid evolution under positive selection during which new dominant lineages quickly displace previously coexisting ones. The preponderance of positive selection during intervals of rapid evolution is supported by the dramatic excess of amino acid replacements in the epitope regions of HA compared to replacements in the rest of the HA molecule. In contrast, the stasis intervals showed a much more uniform distribution of replacements over the HA molecule, with a statistically significant difference in the rate of synonymous over nonsynonymous substitution in the epitope regions between the two modes of evolution. A number of parallel amino acid replacements - the same amino acid substitution occurring independently in different lineages - were also detected in H3N2 HA. These parallel mutations were, largely, associated with periods of rapid fitness change, indicating that there are major limitations on evolutionary pathways during antigenic change. The finding that stasis is the prevailing modality of H3N2 evolution suggests that antigenic changes that lead to an increase in fitness typically result from epistatic interactions between several amino acid substitutions in the HA and, perhaps, other viral proteins. The strains that become dominant due to increased fitness emerge from low frequency strains thanks to the last amino acid replacement that completes the set of replacements required to produce a significant antigenic change; no subset of substitutions results in a biologically significant antigenic change and corresponding fitness increase. In contrast to H3N2, no clear intervals of evolution under positive selection were detected for the H1N1 HA during the same time span. Thus, the ascendancy of H1N1 in some seasons is, most likely, caused by the drop in the relative fitness of the previously prevailing H3N2 lineages as the fraction of susceptible hosts decreases during the stasis intervals. CONCLUSION: We show that the common view of the evolution of influenza virus as a rapid, positive selection-driven process is, at best, incomplete. Rather, the interpandemic evolution of influenza appears to consist of extended intervals of stasis, which are characterized by neutral sequence evolution, punctuated by shorter intervals of rapid fitness increase when evolutionary change is driven by positive selection. These observations have implications for influenza surveillance and vaccine formulation; in particular, the possibility exists that parallel amino acid replacements could serve as a predictor of new dominant strains. REVIEWERS: Ron Fouchier (nominated by Andrey Rzhetsky), David Krakauer, Christopher Lee.}, added-at = {2009-07-09T19:38:32.000+0200}, author = {Wolf, Y I and Viboud, C and Holmes, E C and Koonin, E V and Lipman, D J}, biburl = {http://www.bibsonomy.org/bibtex/2b2b43d34748ecaee90474798f7046458/ebo}, description = {Long intervals of stasis punctuated by bursts of p...[Biol Direct. 2006] - PubMed Result}, doi = {10.1186/1745-6150-1-34}, interhash = {4a933a9594971a8ee3d83c35126e9953}, intrahash = {b2b43d34748ecaee90474798f7046458}, journal = {Biol Direct}, keywords = {evolution immunity imported influenza}, pages = {34-34}, pmid = {17067369}, title = {Long intervals of stasis punctuated by bursts of positive selection in the seasonal evolution of influenza A virus}, url = {http://www.ncbi.nlm.nih.gov/pubmed/17067369}, volume = 1, year = 2006 } @article{Nelson:2008:PLoS-Pathog:18725925, abstract = {To determine the spatial and temporal dynamics of influenza A virus during a single epidemic, we examined whole-genome sequences of 284 A/H1N1 and 69 A/H3N2 viruses collected across the continental United States during the 2006-2007 influenza season, representing the largest study of its kind undertaken to date. A phylogenetic analysis revealed that multiple clades of both A/H1N1 and A/H3N2 entered and co-circulated in the United States during this season, even in localities that are distant from major metropolitan areas, and with no clear pattern of spatial spread. In addition, co-circulating clades of the same subtype exchanged genome segments through reassortment, producing both a minor clade of A/H3N2 viruses that appears to have re-acquired sensitivity to the adamantane class of antiviral drugs, as well as a likely antigenically distinct A/H1N1 clade that became globally dominant following this season. Overall, the co-circulation of multiple viral clades during the 2006-2007 epidemic season revealed patterns of spatial spread that are far more complex than observed previously, and suggests a major role for both migration and reassortment in shaping the epidemiological dynamics of human influenza A virus.}, added-at = {2009-07-04T22:24:36.000+0200}, author = {Nelson, M I and Edelman, L and Spiro, D J and Boyne, A R and Bera, J and Halpin, R and Sengamalay, N and Ghedin, E and Miller, M A and Simonsen, L and Viboud, C and Holmes, E C}, biburl = {http://www.bibsonomy.org/bibtex/209e54fc5affafbf32f43266395db93f0/ebo}, description = {Molecular Epidemiology of A/H3N2 and A/H1N1 Influenza Virus during a Single Epidemic Season in the United States}, doi = {10.1371/journal.ppat.1000133}, interhash = {ba566825ac05991e36726c556eb5382f}, intrahash = {09e54fc5affafbf32f43266395db93f0}, journal = {PLoS Pathog}, keywords = {evolution imported influenza phylogenetics}, number = 8, pmid = {18725925}, title = {Molecular epidemiology of A/H3N2 and A/H1N1 influenza virus during a single epidemic season in the United States}, url = {http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2495036&rendertype=abstract}, volume = 4, year = 2008 } @article{andrew2008genomic, added-at = {2009-07-04T22:20:21.000+0200}, author = {Rambaut, Andrew and Pybus, Oliver G. and Nelson, Martha I. and Viboud, Cecile and Taubenberger, Jeffery K. and Holmes, Edward C.}, biburl = {http://www.bibsonomy.org/bibtex/25b5c4d8c51efcdd13b92d1a8d81a2212/ebo}, description = {Access : The genomic and epidemiological dynamics of human influenza A virus : Nature}, interhash = {8397cb3a6f68590ff1bb4a198c493fd9}, intrahash = {5b5c4d8c51efcdd13b92d1a8d81a2212}, issn = {0028-0836}, journal = {Nature}, keywords = {epi evolution imported influenza phylogenetics}, month = {#may#}, number = 7195, pages = {615--619}, publisher = {Nature Publishing Group}, title = {The genomic and epidemiological dynamics of human influenza A virus}, url = {http://dx.doi.org/10.1038/nature06945}, volume = 453, year = 2008 } @article{Nelson:2006:PLoS-Pathog:17140286, abstract = {Understanding the evolutionary dynamics of influenza A virus is central to its surveillance and control. While immune-driven antigenic drift is a key determinant of viral evolution across epidemic seasons, the evolutionary processes shaping influenza virus diversity within seasons are less clear. Here we show with a phylogenetic analysis of 413 complete genomes of human H3N2 influenza A viruses collected between 1997 and 2005 from New York State, United States, that genetic diversity is both abundant and largely generated through the seasonal importation of multiple divergent clades of the same subtype. These clades cocirculated within New York State, allowing frequent reassortment and generating genome-wide diversity. However, relatively low levels of positive selection and genetic diversity were observed at amino acid sites considered important in antigenic drift. These results indicate that adaptive evolution occurs only sporadically in influenza A virus; rather, the stochastic processes of viral migration and clade reassortment play a vital role in shaping short-term evolutionary dynamics. Thus, predicting future patterns of influenza virus evolution for vaccine strain selection is inherently complex and requires intensive surveillance, whole-genome sequencing, and phenotypic analysis.}, added-at = {2009-07-04T22:11:07.000+0200}, author = {Nelson, M I and Simonsen, L and Viboud, C and Miller, M A and Taylor, J and George, K S and Griesemer, S B and Ghedin, E and Ghedi, E and Sengamalay, N A and Spiro, D J and Volkov, I and Grenfell, B T and Lipman, D J and Taubenberger, J K and Holmes, E C}, biburl = {http://www.bibsonomy.org/bibtex/26e4d6248889d275bcfcfb1678069695e/ebo}, description = {Stochastic processes are key determinants of short...[PLoS Pathog. 2006] - PubMed Result}, doi = {10.1371/journal.ppat.0020125}, interhash = {8913d3c1f789b652c42c15045c13058a}, intrahash = {6e4d6248889d275bcfcfb1678069695e}, journal = {PLoS Pathog}, keywords = {epi evolution imported influenza phylogenetics}, month = Dec, number = 12, pmid = {17140286}, title = {Stochastic processes are key determinants of short-term evolution in influenza a virus}, url = {http://www.ncbi.nlm.nih.gov/pubmed/17140286}, volume = 2, year = 2006 } @article{citeulike:4545214, abstract = {10.1056/NEJMp0903906}, added-at = {2009-05-19T18:00:18.000+0200}, author = {Miller, Mark A. and Viboud, Cecile and Balinska, Marta and Simonsen, Lone}, biburl = {http://www.bibsonomy.org/bibtex/23accf660f2173d1f9fe963e864282230/earthfare}, citeulike-article-id = {4545214}, description = {CiteULike: Everyone's library}, doi = {10.1056/NEJMp0903906}, interhash = {8fc6eaa9ea115d2949da05701e1f9989}, intrahash = {3accf660f2173d1f9fe963e864282230}, journal = {N Engl J Med}, keywords = {dynamics, influenza}, month = May, pages = {NEJMp0903906+}, posted-at = {2009-05-19 15:54:20}, priority = {2}, title = {The Signature Features of Influenza Pandemics -- Implications for Policy}, url = {http://dx.doi.org/10.1056/NEJMp0903906}, year = 2009 } @article{lipsitch2009isl, added-at = {2009-05-15T07:48:20.000+0200}, author = {Lipsitch, Marc and Viboud, Cécile}, biburl = {http://www.bibsonomy.org/bibtex/271019bc934df0393ba338ca3934e53d8/ebo}, doi = {10.1073/pnas.0900933106}, institution = {Department of Epidemiology, Harvard School of Public Health, Boston, MA 02130, USA. mlipsitc@hsph.harvard.edu}, interhash = {b48a8c3e10d0d33fc9c5941857ca2999}, intrahash = {71019bc934df0393ba338ca3934e53d8}, journal = {Proceedings of the National Academy of Sciences (USA)}, journalkeywords = {Humans; Influenza, Human, transmission; Seasons; Vapor Pressure}, keywords = {corepape}, month = Mar, number = 10, pages = {3645--3646}, pii = {106/10/3645}, pmid = {19276125}, title = {Influenza seasonality: lifting the fog.}, url = {http://dx.doi.org/10.1073/pnas.0900933106}, volume = 106, year = 2009 } @article{chowell2008t11, abstract = {Spatial variations in disease patterns of the 1918?1919 influenza pandemic remain poorly studied. We explored the association between influenza death rates, transmissibility and several geographical and demographic indicators for the autumn and winter waves of the 1918?1919 pandemic in cities, towns and rural areas of England and Wales. Average measures of transmissibility, estimated by the reproduction number, ranged between 1.3 and 1.9, depending on model assumptions and pandemic wave and showed little spatial variation. Death rates varied markedly with urbanization, with 30?40\% higher rates in cities and towns compared with rural areas. In addition, death rates varied with population size across rural settings, where low population areas fared worse. By contrast, we found no association between transmissibility, death rates and indicators of population density and residential crowding. Further studies of the geographical mortality patterns associated with the 1918?1919 influenza pandemic may be useful for pandemic planning.}, added-at = {2009-05-15T07:47:50.000+0200}, author = {Chowell, Gerardo and Bettencourt, Lu{\'i}s M.A. and Johnson, Niall and Alonso, Wladimir J. and Viboud, C{\'e}cile}, biburl = {http://www.bibsonomy.org/bibtex/222a99ac3fb5ba17c2ff2a4c68b753634/ebo}, doi = {10.1098/rspb.2007.1477}, interhash = {492c1bbd7849ba6d746a56f742aa1381}, intrahash = {22a99ac3fb5ba17c2ff2a4c68b753634}, journal = {Proceedings of the Royal Society of London Series B---Biological Sciences}, journalkeywords = {UBM\_report}, keywords = {corepape}, month = {#mar#}, pages = {501-509}, title = {The 1918-1919 influenza pandemic in England and Wales: spatial patterns in transmissibility and mortality impact}, url = {http://dx.doi.org/10.1098/rspb.2007.1477}, volume = 275, year = 2008 }