Inferring influenza global transmission networks without complete phylogenetic information

Aris‐Brosou, Stéphane

doi:10.1111/eva.12138

Cited by 4 publications

(3 citation statements)

References 38 publications

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“…Only H1N1 sequences circulating in humans for the hemagglutinin (HA) and neuraminidase (NA) genes were downloaded. These two genes are also very commonly studied and largely sampled in public databases 22 , 23 . Two types of data sets were constructed: one containing pandemic and non-pandemic sequences circulating in 2009, the pandemic year, and one containing pandemic sequences circulating from August 1 to July 31 of each season in the Northern temperate region between 2009/2010 and 2015/2016 (seven seasons in total).…”

Section: Methodsmentioning

confidence: 99%

Viral outbreaks involve destabilized evolutionary networks: evidence from Ebola, Influenza and Zika

Aris‐Brosou

Ibeh

Noël

2017

Sci Rep

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Recent history has provided us with one pandemic (Influenza A/H1N1) and two severe viral outbreaks (Ebola and Zika). In all three cases, post-hoc analyses have given us deep insights into what triggered these outbreaks, their timing, evolutionary dynamics, and phylogeography, but the genomic characteristics of outbreak viruses are still unclear. To address this outstanding question, we searched for a common denominator between these recent outbreaks, positing that the genome of outbreak viruses is in an unstable evolutionary state, while that of non-outbreak viruses is stabilized by a network of correlated substitutions. Here, we show that during regular epidemics, viral genomes are indeed stabilized by a dense network of weakly correlated sites, and that these networks disappear during pandemics and outbreaks when rates of evolution increase transiently. Post-pandemic, these evolutionary networks are progressively re-established. We finally show that destabilization is not caused by substitutions targeting epitopes, but more likely by changes in the environment sensu lato. Our results prompt for a new interpretation of pandemics as being associated with evolutionary destabilized viruses.

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Section: Methodsmentioning

confidence: 99%

Viral outbreaks involve destabilized evolutionary networks: evidence from Ebola, Influenza and Zika

Aris‐Brosou

Ibeh

Noël

2017

Sci Rep

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“…Molecular epidemiological surveillance can be used to infer the dynamics of disease transmission based on the genetic relatedness of viral sequences derived from the population, as shown for human immunodeficiency virus (HIV) 17 18 19 , influenza virus 20 21 , echovirus 22 and ebola virus 23 , amongst others. Although HMPV is one of the main causative agents of RTIs worldwide, little is known about the temporal dynamics of HMPV transmission in the population.…”

mentioning

confidence: 99%

Genetic diversity, seasonality and transmission network of human metapneumovirus: identification of a unique sub-lineage of the fusion and attachment genes

Chow

Chan

Oong

et al. 2016

Sci Rep

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Human metapneumovirus (HMPV) is an important viral respiratory pathogen worldwide. Current knowledge regarding the genetic diversity, seasonality and transmission dynamics of HMPV among adults and children living in tropical climate remains limited. HMPV prevailed at 2.2% (n = 86/3,935) among individuals presented with acute respiratory tract infections in Kuala Lumpur, Malaysia between 2012 and 2014. Seasonal peaks were observed during the northeast monsoon season (November–April) and correlated with higher relative humidity and number of rainy days (P < 0.05). Phylogenetic analysis of the fusion and attachment genes identified the co-circulation of three known HMPV sub-lineages, A2b and B1 (30.2% each, 26/86) and B2 (20.9%, 18/86), with genotype shift from sub-lineage B1 to A2b observed in 2013. Interestingly, a previously unrecognized sub-lineage of A2 was identified in 18.6% (16/86) of the population. Using a custom script for network construction based on the TN93 pairwise genetic distance, we identified up to nine HMPV transmission clusters circulating as multiple sub-epidemics. Although no apparent major outbreak was observed, the increased frequency of transmission clusters (dyads) during seasonal peaks suggests the potential roles of transmission clusters in driving the spread of HMPV. Our findings provide essential information for therapeutic research, prevention strategies, and disease outbreak monitoring of HMPV.

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“…Nucleotide sequences were retrieved for three viruses: Influenza A, Ebola, and Zika, for select protein-coding genes, chosen because they represent the most sequenced / studied genes for each of these viruses [11, 21, 22, 23]. All sequences were downloaded in May 2016 (Table S1).…”

Section: Methodsmentioning

confidence: 99%

Viral outbreaks involve destabilized evolutionary networks: evidence from Ebola, Influenza and Zika

Aris‐Brosou

Ibeh

Noël

2016

Preprint

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9Recent history has provided us with two severe viral outbreaks (Ebola and Zika) and 10 one pandemic (Influenza A/H1N1). In all three cases, post-hoc analyses have given us 11 deep insights into what triggered these outbreaks, their timing, evolutionary dynamics, 12 and their phylogeography, but the genomic characteristics of outbreak viruses are still 13 unclear. To address this outstanding question, we searched for a common denominator of 14 these recent outbreaks, positing that genomes of outbreak viruses are in an unstable evolu-15 tionary state, while those of non-outbreak viruses are stabilized by a network of correlated 16 substitutions that have been found to be prevalent. Here, we show that during regular 17 epidemics, viral genomes are indeed stabilized by a dense network of weakly correlated 18 sites, and that these networks disappear during pandemics and outbreaks when rates of 19 evolution increase transiently. Post-pandemic, these evolutionary networks are progres-20 sively re-established. We finally show that destabilization is not caused by mutations 21 targeting epitopes, but more likely by changes in the environment sensu lato. Our results 22 prompt for a new interpretation of pandemics as being caused by, from an evolutionary 23 standpoint, destabilized, unhealthy viruses. 24 lution 26 29 situation, where both the virus and the hosts coexist. Such a stable evolutionary strategy 30 can however break down when the virus becomes extremely virulent, which can lead to a 31 severe outbreak or even a pandemic. Recent history is rich in such examples with an Ebola 32 virus outbreak in 2014 [2], a Zika outbreak in 2015 [3], and an Influenza pandemic in 2009 33 [4]. Despite all of these recent examples, in which the phylodymanics of these events were 34 meticulously reconstructed, we still do not know what characterizes the evolutionary 35 dynamics of outbreaks and pandemics. Here we address this outstanding question by 36contrasting the evolutionary dynamics of pandemic and non-pandemic viruses. 37As theory tells us that regular epidemics are the result of a dynamic equilibrium 38[5], we posit that outbreaks are associated with a disequilibrium at the genomic level. 39More specifically, we suggest that outbreaks involve destabilized viral genomes, where 40 evolutionary stability is maintained by compensatory mutations, that can be epistatic or 41 not, but that result in signals of correlated evolution. We predict that such signals are 42 severely weakened during an outbreak. As these signals often lead to complex networks 43 of interactions [6, 7], we test how the structure of these correlation networks is affected 44 during an outbreak. We show that during an outbreak, viral genes are destabilized. 45 Results 46Networks of correlated sites are destabilized during outbreaks. In search for 47 trasted the glycoprotein precursor (GP) sequences of the Ebola virus that circulated 49 4 before, and during 2014/2016 outbreak. For this, we identified the pairs of nucleotides 50 that show evidence for co...

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Inferring influenza global transmission networks without complete phylogenetic information

Cited by 4 publications

References 38 publications

Viral outbreaks involve destabilized evolutionary networks: evidence from Ebola, Influenza and Zika

Viral outbreaks involve destabilized evolutionary networks: evidence from Ebola, Influenza and Zika

Genetic diversity, seasonality and transmission network of human metapneumovirus: identification of a unique sub-lineage of the fusion and attachment genes

Viral outbreaks involve destabilized evolutionary networks: evidence from Ebola, Influenza and Zika

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