Last data update: May 20, 2024. (Total: 46824 publications since 2009)
Records 1-7 (of 7 Records) |
Query Trace: Lemey P[original query] |
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Virus genomes reveal factors that spread and sustained the Ebola epidemic.
Dudas G , Carvalho LM , Bedford T , Tatem AJ , Baele G , Faria NR , Park DJ , Ladner JT , Arias A , Asogun D , Bielejec F , Caddy SL , Cotten M , D'Ambrozio J , Dellicour S , Caro AD , Diclaro JW , Duraffour S , Elmore MJ , Fakoli LS , Faye O , Gilbert ML , Gevao SM , Gire S , Gladden-Young A , Gnirke A , Goba A , Grant DS , Haagmans BL , Hiscox JA , Jah U , Kugelman JR , Liu D , Lu J , Malboeuf CM , Mate S , Matthews DA , Matranga CB , Meredith LW , Qu J , Quick J , Pas SD , Phan MV , Pollakis G , Reusken CB , Sanchez-Lockhart M , Schaffner SF , Schieffelin JS , Sealfon RS , Simon-Loriere E , Smits SL , Stoecker K , Thorne L , Tobin EA , Vandi MA , Watson SJ , West K , Whitmer S , Wiley MR , Winnicki SM , Wohl S , Wolfel R , Yozwiak NL , Andersen KG , Blyden SO , Bolay F , Carroll MW , Dahn B , Diallo B , Formenty P , Fraser C , Gao GF , Garry RF , Goodfellow I , Gunther S , Happi CT , Holmes EC , Kargbo B , Keita S , Kellam P , Koopmans MP , Kuhn JH , Loman NJ , Magassouba N , Naidoo D , Nichol ST , Nyenswah T , Palacios G , Pybus OG , Sabeti PC , Sall A , Stroher U , Wurie I , Suchard MA , Lemey P , Rambaut A . Nature 2017 544 (7650) 309-315 The 2013-2016 West African epidemic caused by the Ebola virus was of unprecedented magnitude, duration and impact. Here we reconstruct the dispersal, proliferation and decline of Ebola virus throughout the region by analysing 1,610 Ebola virus genomes, which represent over 5% of the known cases. We test the association of geography, climate and demography with viral movement among administrative regions, inferring a classic 'gravity' model, with intense dispersal between larger and closer populations. Despite attenuation of international dispersal after border closures, cross-border transmission had already sown the seeds for an international epidemic, rendering these measures ineffective at curbing the epidemic. We address why the epidemic did not spread into neighbouring countries, showing that these countries were susceptible to substantial outbreaks but at lower risk of introductions. Finally, we reveal that this large epidemic was a heterogeneous and spatially dissociated collection of transmission clusters of varying size, duration and connectivity. These insights will help to inform interventions in future epidemics. |
1970s and 'Patient 0' HIV-1 genomes illuminate early HIV/AIDS history in North America.
Worobey M , Watts TD , McKay RA , Suchard MA , Granade T , Teuwen DE , Koblin BA , Heneine W , Lemey P , Jaffe HW . Nature 2016 539 (7627) 98-101 The emergence of HIV-1 group M subtype B in North American men who have sex with men was a key turning point in the HIV/AIDS pandemic. Phylogenetic studies have suggested cryptic subtype B circulation in the United States (US) throughout the 1970s and an even older presence in the Caribbean. However, these temporal and geographical inferences, based upon partial HIV-1 genomes that postdate the recognition of AIDS in 1981, remain contentious and the earliest movements of the virus within the US are unknown. We serologically screened >2,000 1970s serum samples and developed a highly sensitive approach for recovering viral RNA from degraded archival samples. Here, we report eight coding-complete genomes from US serum samples from 1978-1979-eight of the nine oldest HIV-1 group M genomes to date. This early, full-genome 'snapshot' reveals that the US HIV-1 epidemic exhibited extensive genetic diversity in the 1970s but also provides strong evidence for its emergence from a pre-existing Caribbean epidemic. Bayesian phylogenetic analyses estimate the jump to the US at around 1970 and place the ancestral US virus in New York City with 0.99 posterior probability support, strongly suggesting this was the crucial hub of early US HIV/AIDS diversification. Logistic growth coalescent models reveal epidemic doubling times of 0.86 and 1.12 years for the US and Caribbean, respectively, suggesting rapid early expansion in each location. Comparisons with more recent data reveal many of these insights to be unattainable without archival, full-genome sequences. We also recovered the HIV-1 genome from the individual known as 'Patient 0' (ref. 5) and found neither biological nor historical evidence that he was the primary case in the US or for subtype B as a whole. We discuss the genesis and persistence of this belief in the light of these evolutionary insights. |
Global circulation patterns of seasonal influenza viruses vary with antigenic drift.
Bedford T , Riley S , Barr IG , Broor S , Chadha M , Cox NJ , Daniels RS , Gunasekaran CP , Hurt AC , Kelso A , Klimov A , Lewis NS , Li X , McCauley JW , Odagiri T , Potdar V , Rambaut A , Shu Y , Skepner E , Smith DJ , Suchard MA , Tashiro M , Wang D , Xu X , Lemey P , Russell CA . Nature 2015 523 (7559) 217-20 Understanding the spatiotemporal patterns of emergence and circulation of new human seasonal influenza virus variants is a key scientific and public health challenge. The global circulation patterns of influenza A/H3N2 viruses are well characterized, but the patterns of A/H1N1 and B viruses have remained largely unexplored. Here we show that the global circulation patterns of A/H1N1 (up to 2009), B/Victoria, and B/Yamagata viruses differ substantially from those of A/H3N2 viruses, on the basis of analyses of 9,604 haemagglutinin sequences of human seasonal influenza viruses from 2000 to 2012. Whereas genetic variants of A/H3N2 viruses did not persist locally between epidemics and were reseeded from East and Southeast Asia, genetic variants of A/H1N1 and B viruses persisted across several seasons and exhibited complex global dynamics with East and Southeast Asia playing a limited role in disseminating new variants. The less frequent global movement of influenza A/H1N1 and B viruses coincided with slower rates of antigenic evolution, lower ages of infection, and smaller, less frequent epidemics compared to A/H3N2 viruses. Detailed epidemic models support differences in age of infection, combined with the less frequent travel of children, as probable drivers of the differences in the patterns of global circulation, suggesting a complex interaction between virus evolution, epidemiology, and human behaviour. |
Geographic and temporal trends in the molecular epidemiology and genetic mechanisms of transmitted HIV-1 drug resistance: an individual-patient- and sequence-level meta-analysis.
Rhee SY , Blanco JL , Jordan MR , Taylor J , Lemey P , Varghese V , Hamers RL , Bertagnolio S , de Wit TF , Aghokeng AF , Albert J , Avi R , Avila-Rios S , Bessong PO , Brooks JI , Boucher CA , Brumme ZL , Busch MP , Bussmann H , Chaix ML , Chin BS , D'Aquin TT , De Gascun CF , Derache A , Descamps D , Deshpande AK , Djoko CF , Eshleman SH , Fleury H , Frange P , Fujisaki S , Harrigan PR , Hattori J , Holguin A , Hunt GM , Ichimura H , Kaleebu P , Katzenstein D , Kiertiburanakul S , Kim JH , Kim SS , Li Y , Lutsar I , Morris L , Ndembi N , Ng KP , Paranjape RS , Peeters M , Poljak M , Price MA , Ragonnet-Cronin ML , Reyes-Teran G , Rolland M , Sirivichayakul S , Smith DM , Soares MA , Soriano VV , Ssemwanga D , Stanojevic M , Stefani MA , Sugiura W , Sungkanuparph S , Tanuri A , Tee KK , Truong HH , van de Vijver DA , Vidal N , Yang C , Yang R , Yebra G , Ioannidis JP , Vandamme AM , Shafer RW . PLoS Med 2015 12 (4) e1001810 BACKGROUND: Regional and subtype-specific mutational patterns of HIV-1 transmitted drug resistance (TDR) are essential for informing first-line antiretroviral (ARV) therapy guidelines and designing diagnostic assays for use in regions where standard genotypic resistance testing is not affordable. We sought to understand the molecular epidemiology of TDR and to identify the HIV-1 drug-resistance mutations responsible for TDR in different regions and virus subtypes. METHODS AND FINDINGS: We reviewed all GenBank submissions of HIV-1 reverse transcriptase sequences with or without protease and identified 287 studies published between March 1, 2000, and December 31, 2013, with more than 25 recently or chronically infected ARV-naive individuals. These studies comprised 50,870 individuals from 111 countries. Each set of study sequences was analyzed for phylogenetic clustering and the presence of 93 surveillance drug-resistance mutations (SDRMs). The median overall TDR prevalence in sub-Saharan Africa (SSA), south/southeast Asia (SSEA), upper-income Asian countries, Latin America/Caribbean, Europe, and North America was 2.8%, 2.9%, 5.6%, 7.6%, 9.4%, and 11.5%, respectively. In SSA, there was a yearly 1.09-fold (95% CI: 1.05-1.14) increase in odds of TDR since national ARV scale-up attributable to an increase in non-nucleoside reverse transcriptase inhibitor (NNRTI) resistance. The odds of NNRTI-associated TDR also increased in Latin America/Caribbean (odds ratio [OR] = 1.16; 95% CI: 1.06-1.25), North America (OR = 1.19; 95% CI: 1.12-1.26), Europe (OR = 1.07; 95% CI: 1.01-1.13), and upper-income Asian countries (OR = 1.33; 95% CI: 1.12-1.55). In SSEA, there was no significant change in the odds of TDR since national ARV scale-up (OR = 0.97; 95% CI: 0.92-1.02). An analysis limited to sequences with mixtures at less than 0.5% of their nucleotide positions-a proxy for recent infection-yielded trends comparable to those obtained using the complete dataset. Four NNRTI SDRMs-K101E, K103N, Y181C, and G190A-accounted for >80% of NNRTI-associated TDR in all regions and subtypes. Sixteen nucleoside reverse transcriptase inhibitor (NRTI) SDRMs accounted for >69% of NRTI-associated TDR in all regions and subtypes. In SSA and SSEA, 89% of NNRTI SDRMs were associated with high-level resistance to nevirapine or efavirenz, whereas only 27% of NRTI SDRMs were associated with high-level resistance to zidovudine, lamivudine, tenofovir, or abacavir. Of 763 viruses with TDR in SSA and SSEA, 725 (95%) were genetically dissimilar; 38 (5%) formed 19 sequence pairs. Inherent limitations of this study are that some cohorts may not represent the broader regional population and that studies were heterogeneous with respect to duration of infection prior to sampling. CONCLUSIONS: Most TDR strains in SSA and SSEA arose independently, suggesting that ARV regimens with a high genetic barrier to resistance combined with improved patient adherence may mitigate TDR increases by reducing the generation of new ARV-resistant strains. A small number of NNRTI-resistance mutations were responsible for most cases of high-level resistance, suggesting that inexpensive point-mutation assays to detect these mutations may be useful for pre-therapy screening in regions with high levels of TDR. In the context of a public health approach to ARV therapy, a reliable point-of-care genotypic resistance test could identify which patients should receive standard first-line therapy and which should receive a protease-inhibitor-containing regimen. |
Global migration of influenza A viruses in swine.
Nelson Martha I, Viboud Cécile, Vincent Amy L, Culhane Marie R, Detmer Susan E, Wentworth David E, Rambaut Andrew, Suchard Marc A, Holmes Edward C, Lemey Philippe. Nature communications 2015 Mar 66696 . Nature communications 2015 Mar 66696 Nelson Martha I, Viboud Cécile, Vincent Amy L, Culhane Marie R, Detmer Susan E, Wentworth David E, Rambaut Andrew, Suchard Marc A, Holmes Edward C, Lemey Philippe. Nature communications 2015 Mar 66696 |
The phylogeography and spatiotemporal spread of south-central skunk rabies virus
Kuzmina NA , Lemey P , Kuzmin IV , Mayes BC , Ellison JA , Orciari LA , Hightower D , Taylor ST , Rupprecht CE . PLoS One 2013 8 (12) e82348 The south-central skunk rabies virus (SCSK) is the most broadly distributed terrestrial viral lineage in North America. Skunk rabies has not been efficiently targeted by oral vaccination campaigns and represents a natural system of pathogen invasion, yielding insights to rabies emergence. In the present study we reconstructed spatiotemporal spread of SCSK in the whole territory of its circulation using a combination of Bayesian methods. The analysis based on 241 glycoprotein gene sequences demonstrated that SCSK is much more divergent phylogenetically than was appreciated previously. According to our analyses the SCSK originated in the territory of Texas ~170 years ago, and spread geographically during the following decades. The wavefront velocity in the northward direction was significantly greater than in the eastward and westward directions. Rivers (except the Mississippi River and Rio Grande River) did not constitute significant barriers for epizootic spread, in contrast to deserts and mountains. The mean dispersal rate of skunk rabies was lower than that of the raccoon and fox rabies. Viral lineages circulate in their areas with limited evidence of geographic spread during decades. However, spatiotemporal reconstruction shows that after a long period of stability the dispersal rate and wavefront velocity of SCSK are increasing. Our results indicate that there is a need to develop control measures for SCSK, and suggest how such measure can be implemented most efficiently. Our approach can be extrapolated to other rabies reservoirs and used as a tool for investigation of epizootic patterns and planning interventions towards disease elimination. |
Phylogeographical footprint of colonial history in the global dispersal of human immunodeficiency virus type 2 group A
Faria NR , Hodges-Mameletzis I , Silva JC , Rodes B , Erasmus S , Paolucci S , Ruelle J , Pieniazek D , Taveira N , Trevino A , Goncalves MF , Jallow S , Xu L , Camacho RJ , Soriano V , Goubau P , de Sousa JD , Vandamme AM , Suchard MA , Lemey P . J Gen Virol 2012 93 889-99 Human immunodeficiency virus type 2 (HIV-2) emerged in West Africa and has spread further to countries that share socio-historical ties with this region. However, viral origins and dispersal patterns at a global scale remain poorly understood. Here, we adopt a Bayesian phylogeographic approach to investigate the spatial dynamics of HIV-2 group A (HIV-2A) using a collection of 320 partial pol and 248 partial env sequences sampled throughout 19 countries worldwide. We extend phylogenetic diffusion models that simultaneously draw information from multiple loci to estimate location states throughout distinct phylogenies and explicitly attempt to incorporate human migratory fluxes. Our study highlights that Guinea-Bissau, together with Cote d'Ivoire and Senegal, have acted as the main viral sources in the early stages of the epidemic. We show that convenience sampling can obfuscate the estimation of the spatial root of HIV-2A. We explicitly attempt to circumvent this by incorporating rate priors that reflect the ratio of human flow from and to West Africa. We recover four main routes of HIV-2A dispersal that are laid out along colonial ties: Guinea-Bissau and Cape Verde to Portugal, Cote d'Ivoire and Senegal to France. Within Europe, we find strong support for epidemiological linkage from Portugal to Luxembourg and to the UK. We demonstrate that probabilistic models can uncover global patterns of HIV-2A dispersal providing sampling bias is taken into account and we provide a scenario for the international spread of this virus. |
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