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    <title>eLife: latest articles by subject</title>
    <link>https://elifesciences.org</link>
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      <title>Rift Valley fever virus dynamics in a transhumant cattle system in The Gambia</title>
      <link>https://elifesciences.org/articles/107346</link>
      <description>Rift Valley fever (RVF) is a zoonotic disease of global concern, driven by environmental conditions, vector activity, and livestock mobility. Although RVF has been reported in The Gambia, its epidemiology remains poorly understood. This study developed a compartmental model to study RVF dynamics in the cattle population of the country. The model incorporated seasonally dynamic transmission parameters reflecting transhumant movement and ecological differences between two distinct ecoclimatic regions: the Sahelian area and the Gambia river. Parameterised using serological data linked to household survey data, the model predicted endemic RVF virus (RVFV) circulation within The Gambia and captured temporal infection trends that closely match empirical data. Weak decay rates of seropositivity were required to match predicted and observed age-seroprevalence. Results indicated sustained RVFV transmission during the dry season in the Gambia river eco-region, with a high risk of seasonal virus introductions to the Sahelian eco-region at the start of the wet season via the returning transhumant cattle. Our study highlighted the role of livestock mobility in RVFV epidemiology in The Gambia and the need for targeted control strategies that might include, for example, targeted cattle vaccination or application of topical insecticide treatments for transhumant herds.</description>
      <author>jarraessa@yahoo.com (Daniel T Haydon)</author>
      <author>jarraessa@yahoo.com (Divine Ekwem)</author>
      <author>jarraessa@yahoo.com (Essa Jarra)</author>
      <author>jarraessa@yahoo.com (Sarah Cleaveland)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.107346</guid>
      <category>Ecology</category>
      <category>Epidemiology and Global Health</category>
      <pubDate>Fri, 27 Feb 2026 00:00:00 +0000</pubDate>
      <dc:date>2026-02-27T00:00:00Z</dc:date>
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    <item>
      <title>Prediction of SARS-CoV-2 transmission dynamics based on population-level cycle threshold values: An epidemic transmission and machine learning modeling study</title>
      <link>https://elifesciences.org/articles/95666</link>
      <description>Polymerase chain reaction (PCR) cycle threshold (Ct) values can be used to estimate the viral burden of Severe Acute Respiratory Syndrome Coronavirus type 2 (SARS-CoV-2) and predict population-level epidemic trends. We investigated the use of epidemic transmission modeling and machine learning (ML) based on Ct value distribution for SARS-CoV-2 incidence prediction in British Columbia, Canada, during an Omicron subvariant BA.1-predominant period from November 2021 to January 2022. Using real-world data, we developed an epidemic transmission model that was first validated on outbreak data and subsequently fitted to province-level data to predict incidence. Using simulated data, we developed a ML pipeline including five models to predict the reproductive number as a measure of transmission potential based on Ct value distribution and validated it on out-of-sample province-level data. The epidemic transmission model demonstrated accurate prediction with the real incidence falling within the 95% credible interval of the predicted MCMC chains for both the long-term care facility outbreak and province-level data. The ML models demonstrated good performance with a mean squared error (MSE) lower than 0.17 across all models and improved performance with increasing sample size. The variability of the Ct distribution around the mean was the strongest predictor of the reproductive number. These modeling approaches demonstrated utility for incidence and reproductive number prediction and have potential to complement traditional surveillance in real time to guide public health interventions.</description>
      <author>catherine.hogan@bccdc.ca (Aamir Bharmal)</author>
      <author>catherine.hogan@bccdc.ca (Afraz Arif Khan)</author>
      <author>catherine.hogan@bccdc.ca (Agatha N Jassem)</author>
      <author>catherine.hogan@bccdc.ca (Amanda Wilmer)</author>
      <author>catherine.hogan@bccdc.ca (Bonnie Henry)</author>
      <author>catherine.hogan@bccdc.ca (Braeden Klaver)</author>
      <author>catherine.hogan@bccdc.ca (Carmen H Ng)</author>
      <author>catherine.hogan@bccdc.ca (Catherine A Hogan)</author>
      <author>catherine.hogan@bccdc.ca (Chris D Fjell)</author>
      <author>catherine.hogan@bccdc.ca (Hind Sbihi)</author>
      <author>catherine.hogan@bccdc.ca (John Galbraith)</author>
      <author>catherine.hogan@bccdc.ca (Linda MN Hoang)</author>
      <author>catherine.hogan@bccdc.ca (Marc G Romney)</author>
      <author>catherine.hogan@bccdc.ca (Marthe K Charles)</author>
      <author>catherine.hogan@bccdc.ca (Mel Krajden)</author>
      <author>catherine.hogan@bccdc.ca (Michael A Irvine)</author>
      <author>catherine.hogan@bccdc.ca (Miguel Imperial)</author>
      <author>catherine.hogan@bccdc.ca (Naveed Janjua)</author>
      <author>catherine.hogan@bccdc.ca (Susan Roman)</author>
      <author>catherine.hogan@bccdc.ca (Yayuk Joffres)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.95666</guid>
      <category>Epidemiology and Global Health</category>
      <pubDate>Mon, 16 Feb 2026 00:00:00 +0000</pubDate>
      <dc:date>2026-02-16T00:00:00Z</dc:date>
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    <item>
      <title>Heterogeneous associations of polygenic indices of 35 traits with mortality: a register-linked population-based follow-up study</title>
      <link>https://elifesciences.org/articles/107496</link>
      <author>hannu.lahtinen@helsinki.fi (Andrea Ganna)</author>
      <author>hannu.lahtinen@helsinki.fi (Hannu Lahtinen)</author>
      <author>hannu.lahtinen@helsinki.fi (Jaakko Kaprio)</author>
      <author>hannu.lahtinen@helsinki.fi (Kaarina Korhonen)</author>
      <author>hannu.lahtinen@helsinki.fi (Karri Silventoinen)</author>
      <author>hannu.lahtinen@helsinki.fi (Pekka Martikainen)</author>
      <author>hannu.lahtinen@helsinki.fi (Stefano Lombardi)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.107496</guid>
      <category>Epidemiology and Global Health</category>
      <category>Genetics and Genomics</category>
      <pubDate>Wed, 11 Feb 2026 00:00:00 +0000</pubDate>
      <dc:date>2026-02-11T00:00:00Z</dc:date>
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    <item>
      <title>Global risk mapping of highly pathogenic avian influenza H5N1 and H5Nx in the light of epidemic episodes occurring from 2020 onwards</title>
      <link>https://elifesciences.org/articles/104748</link>
      <description>Avian influenza (AI) is a highly contagious viral disease affecting poultry and wild water birds, posing significant global challenges due to its high mortality rates and economic impacts. Highly pathogenic avian influenza (HPAI) outbreaks, particularly those caused by H5N1 and its variants, have surged since 1959. The HPAI H5N1 clade 2.3.4.4b viruses have notably expanded their geographical reach, affecting numerous countries, diverse avian species, and now mammals. Using an ecological niche modelling approach, this study aims to elucidate the environmental factors associated with increased HPAI H5 cases since 2020, investigate potential shifts in ecological niches, and predict new areas suitable for viral circulation. We developed ecological niche models for HPAI cases in wild and domestic birds across two distinct periods: 2015–2020 and 2020–2022. Key environmental predictors include chicken and duck population density, human density, distance to water bodies, and land cover variables. Post-2020, we observe increased relative influence of predictors such as intensive chicken population density and cultivated vegetation. Risk maps reveal notable ecological suitability for HPAI H5 circulation in Europe, Asia, and the Americas, with significant expansions of at-risk areas post-2020. Wild bird H5 occurrences appear primarily correlated with urban areas and open water regions. Our analyses also highlight a potential shift in affected wild bird species diversity, with more avian species, particularly sea birds, impacted post-2020. Overall, these results further contribute to the understanding of HPAI epidemiology and identify regions where surveillance and control measures should be prioritised.</description>
      <author>dupas.mc@gmail.com (Cedric Marsboom)</author>
      <author>dupas.mc@gmail.com (Claire Guinat)</author>
      <author>dupas.mc@gmail.com (Guy Hendrickx)</author>
      <author>dupas.mc@gmail.com (Madhur Dhingra)</author>
      <author>dupas.mc@gmail.com (Maria F Vincenti-Gonzalez)</author>
      <author>dupas.mc@gmail.com (Marie-Cécile Dupas)</author>
      <author>dupas.mc@gmail.com (Marius Gilbert)</author>
      <author>dupas.mc@gmail.com (Simon Dellicour)</author>
      <author>dupas.mc@gmail.com (Timothée Vergne)</author>
      <author>dupas.mc@gmail.com (William Wint)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.104748</guid>
      <category>Epidemiology and Global Health</category>
      <pubDate>Wed, 28 Jan 2026 00:00:00 +0000</pubDate>
      <dc:date>2026-01-28T00:00:00Z</dc:date>
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    </item>
    <item>
      <title>Timely vaccine strain selection and genomic surveillance improve evolutionary forecast accuracy of seasonal influenza A/H3N2</title>
      <link>https://elifesciences.org/articles/104282</link>
      <description>Evolutionary forecasting models inform seasonal influenza vaccine design by predicting which current genetic variants will dominate in the influenza season 12 months later. Forecasting models depend on hemagglutinin sequences from global public health networks to identify current genetic variants (clades) and estimate clade fitnesses. The lag between collection of a clinical sample and public availability of its sequence averages ∼3 months, complicating the 12-month forecasting problem by reducing our understanding of current clade frequencies. Despite continued methodological improvements to forecasting models, these constraints of a 12-month forecast horizon and 3-month submission lags impose an upper bound on any model’s accuracy. The SARS-CoV-2 pandemic revealed that modern vaccine technology reduces forecast horizons to 6 months and expanded sequencing support reduces submission lags to 1 month on average. We quantified the potential effects of these public health policy changes on forecast accuracy for A/H3N2 populations. Reducing forecast horizons to 6 months reduced average absolute forecasting errors to 25% of the 12-month average, while reducing submission lags decreased uncertainty in current clade frequencies by 50%. These results show the potential to improve the accuracy of existing forecasting models through realistic changes to public health policy.</description>
      <author>jhuddles@fredhutch.org (John Huddleston)</author>
      <author>jhuddles@fredhutch.org (Trevor Bedford)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.104282</guid>
      <category>Epidemiology and Global Health</category>
      <category>Microbiology and Infectious Disease</category>
      <pubDate>Thu, 04 Dec 2025 00:00:00 +0000</pubDate>
      <dc:date>2025-12-04T00:00:00Z</dc:date>
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    <item>
      <title>Using step selection functions to analyse human mobility using telemetry data in infectious disease epidemiology: a case study of leptospirosis</title>
      <link>https://elifesciences.org/articles/107153</link>
      <author>p.ruizcuenca@lancaster.ac.uk (Ariane Goncalves da Silva)</author>
      <author>p.ruizcuenca@lancaster.ac.uk (Cleber Cremonese)</author>
      <author>p.ruizcuenca@lancaster.ac.uk (Daiana de Oliveira)</author>
      <author>p.ruizcuenca@lancaster.ac.uk (Diogo C de Carvalho Santiago)</author>
      <author>p.ruizcuenca@lancaster.ac.uk (Emanuele Giorgi)</author>
      <author>p.ruizcuenca@lancaster.ac.uk (Emile V Ribeiro de Souza)</author>
      <author>p.ruizcuenca@lancaster.ac.uk (Fabiana G Palma)</author>
      <author>p.ruizcuenca@lancaster.ac.uk (Fábio N Souza)</author>
      <author>p.ruizcuenca@lancaster.ac.uk (Federico Costa)</author>
      <author>p.ruizcuenca@lancaster.ac.uk (Hussein Khalil)</author>
      <author>p.ruizcuenca@lancaster.ac.uk (Jonathan M Read)</author>
      <author>p.ruizcuenca@lancaster.ac.uk (Juliet O Santana)</author>
      <author>p.ruizcuenca@lancaster.ac.uk (Max T Eyre)</author>
      <author>p.ruizcuenca@lancaster.ac.uk (Pablo Ruiz Cuenca)</author>
      <author>p.ruizcuenca@lancaster.ac.uk (Priscilla Elizabeth Ferreira dos Santos)</author>
      <author>p.ruizcuenca@lancaster.ac.uk (Priscyla dos Santos Ribeiro)</author>
      <author>p.ruizcuenca@lancaster.ac.uk (Roberta Coutinho do Nascimento)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.107153</guid>
      <category>Epidemiology and Global Health</category>
      <pubDate>Mon, 01 Dec 2025 00:00:00 +0000</pubDate>
      <dc:date>2025-12-01T00:00:00Z</dc:date>
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    </item>
    <item>
      <title>Measuring changes in &lt;i&gt;Plasmodium falciparum&lt;/i&gt; census population size in response to sequential malaria control interventions</title>
      <link>https://elifesciences.org/articles/91411</link>
      <description>Here, we introduce a new endpoint ‘census population size’ to evaluate the epidemiology and control of &lt;i&gt;Plasmodium falciparum&lt;/i&gt; infections, where the parasite, rather than the infected human host, is the unit of measurement. To calculate census population size, we rely on a definition of parasite variation known as multiplicity of infection (MOI&lt;i&gt;&lt;sub&gt;var&lt;/sub&gt;&lt;/i&gt;), based on the hyper-diversity of the &lt;i&gt;var&lt;/i&gt; multigene family. We present a Bayesian approach to estimate MOI&lt;i&gt;&lt;sub&gt;var&lt;/sub&gt;&lt;/i&gt; from sequencing and counting the number of unique DBLα tags (or DBLα types) of &lt;i&gt;var&lt;/i&gt; genes, and derive from it census population size by summation of MOI&lt;i&gt;&lt;sub&gt;var&lt;/sub&gt;&lt;/i&gt; in the human population. We track changes in this parasite population size and structure through sequential malaria interventions by indoor residual spraying (IRS) and seasonal malaria chemoprevention (SMC) from 2012 to 2017 in an area of high, seasonal malaria transmission in northern Ghana. Following IRS, which reduced transmission intensity by &amp;gt;90% and decreased parasite prevalence by ~40–50%, significant reductions in &lt;i&gt;var&lt;/i&gt; diversity, MOI&lt;i&gt;&lt;sub&gt;var&lt;/sub&gt;&lt;/i&gt;, and population size were observed in ~2000 humans across all ages. These changes, consistent with the loss of diverse parasite genomes, were short-lived and 32 months after IRS was discontinued and SMC was introduced, &lt;i&gt;var&lt;/i&gt; diversity and population size rebounded in all age groups except for the younger children (1–5 years) targeted by SMC. Despite major perturbations from IRS and SMC interventions, the parasite population remained very large and retained the &lt;i&gt;var&lt;/i&gt; population genetic characteristics of a high-transmission system (high &lt;i&gt;var&lt;/i&gt; diversity; low &lt;i&gt;var&lt;/i&gt; repertoire similarity), demonstrating the resilience of &lt;i&gt;P. falciparum&lt;/i&gt; to short-term interventions in high-burden countries of sub-Saharan Africa.</description>
      <author>karen.day@unimelb.edu.au (Abraham R Oduro)</author>
      <author>karen.day@unimelb.edu.au (Anita Ghansah)</author>
      <author>karen.day@unimelb.edu.au (Dionne C Argyropoulos)</author>
      <author>karen.day@unimelb.edu.au (Gerry Tonkin-Hill)</author>
      <author>karen.day@unimelb.edu.au (Karen P Day)</author>
      <author>karen.day@unimelb.edu.au (Kathryn E Tiedje)</author>
      <author>karen.day@unimelb.edu.au (Kwadwo A Koram)</author>
      <author>karen.day@unimelb.edu.au (Mercedes Pascual)</author>
      <author>karen.day@unimelb.edu.au (Mun Hua Tan)</author>
      <author>karen.day@unimelb.edu.au (Oscar Bangre)</author>
      <author>karen.day@unimelb.edu.au (Qixin He)</author>
      <author>karen.day@unimelb.edu.au (Qi Zhan)</author>
      <author>karen.day@unimelb.edu.au (Samantha Deed)</author>
      <author>karen.day@unimelb.edu.au (Shazia Ruybal-Pésantez)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.91411</guid>
      <category>Epidemiology and Global Health</category>
      <pubDate>Tue, 28 Oct 2025 00:00:00 +0000</pubDate>
      <dc:date>2025-10-28T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>Forecasting the spatial spread of an Ebola epidemic in real time: Comparing predictions of mathematical models and experts</title>
      <link>https://elifesciences.org/articles/98005</link>
      <author>james.munday@swisstph.ch (Alicia Rosello)</author>
      <author>james.munday@swisstph.ch (James D Munday)</author>
      <author>james.munday@swisstph.ch (Sebastian Funk)</author>
      <author>james.munday@swisstph.ch (W John Edmunds)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.98005</guid>
      <category>Epidemiology and Global Health</category>
      <pubDate>Fri, 10 Oct 2025 00:00:00 +0000</pubDate>
      <dc:date>2025-10-10T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>Reassessing the link between adiposity and head and neck cancer: a Mendelian randomization study</title>
      <link>https://elifesciences.org/articles/106075</link>
      <author>dy20206@bristol.ac.uk (Caroline L Relton)</author>
      <author>dy20206@bristol.ac.uk (Elmira Ebrahimi)</author>
      <author>dy20206@bristol.ac.uk (Fernanda Morales Berstein)</author>
      <author>dy20206@bristol.ac.uk (George Davey Smith)</author>
      <author>dy20206@bristol.ac.uk (James D McKay)</author>
      <author>dy20206@bristol.ac.uk (Jasmine Khouja)</author>
      <author>dy20206@bristol.ac.uk (Mark Gormley)</author>
      <author>dy20206@bristol.ac.uk (M Carolina Borges)</author>
      <author>dy20206@bristol.ac.uk (Paul Brennan)</author>
      <author>dy20206@bristol.ac.uk (Rebecca C Richmond)</author>
      <author>dy20206@bristol.ac.uk (Shama Virani)</author>
      <author>dy20206@bristol.ac.uk (Tom Dudding)</author>
      <author>dy20206@bristol.ac.uk (Tom G Richardson)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.106075</guid>
      <category>Epidemiology and Global Health</category>
      <pubDate>Thu, 09 Oct 2025 00:00:00 +0000</pubDate>
      <dc:date>2025-10-09T00:00:00Z</dc:date>
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    </item>
    <item>
      <title>Understanding the global rise of artemisinin resistance: Insights from over 100,000 &lt;i&gt;Plasmodium falciparum&lt;/i&gt; samples</title>
      <link>https://elifesciences.org/articles/105544</link>
      <description>Artemisinin partial resistance (ART-R) in &lt;i&gt;Plasmodium falciparum&lt;/i&gt; is a major challenge to malaria control globally. Over the last two decades, ART-R has spread widely across Southeast Asia, undermining public health strategies and hindering elimination. As of 2024, ART-R has now emerged in East Africa, with the potential to dramatically impact current efforts to control malaria in the region. Mitigating its spread requires detailed genomic surveillance of point mutations in the &lt;i&gt;kelch13&lt;/i&gt; gene, the primary known determinant of artemisinin resistance. Although extensive surveillance data on these markers is available, it is distributed across many literature studies and open databases. In this review, we aggregate spatiotemporal data for 112,933 &lt;i&gt;P. falciparum&lt;/i&gt; samples collected between 1980 and 2023 into a single resource, providing the most comprehensive overview of &lt;i&gt;kelch13&lt;/i&gt; markers to date. We outline the history and current status of these mutations globally, with particular focus on their emergence in Southeast Asia and East/Northeast Africa. Concerningly, we find the recent increases in ART-R in Africa mirror patterns observed in Southeast Asia 10–15 years ago. We examine factors that may influence its spread, including fitness costs, treatment strategies, and local epidemiological dynamics, before discussing potential scenarios for how resistance may spread in Africa in coming years. This review provides a comprehensive account of how the situation of ART-R has unfolded globally so far, highlighting insights for researchers and public health bodies which aim to reduce its negative effects.</description>
      <author>cristina.ariani@gmail.com (Andrew J Balmer)</author>
      <author>cristina.ariani@gmail.com (Chiyun Lee)</author>
      <author>cristina.ariani@gmail.com (Cristina Ariani)</author>
      <author>cristina.ariani@gmail.com (Eyyüb S Ünlü)</author>
      <author>cristina.ariani@gmail.com (Jacob Almagro-Garcia)</author>
      <author>cristina.ariani@gmail.com (Nina FD White)</author>
      <author>cristina.ariani@gmail.com (Richard D Pearson)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.105544</guid>
      <category>Epidemiology and Global Health</category>
      <category>Genetics and Genomics</category>
      <pubDate>Thu, 02 Oct 2025 00:00:00 +0000</pubDate>
      <dc:date>2025-10-02T00:00:00Z</dc:date>
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    </item>
    <item>
      <title>Improving SARS-CoV-2 variants monitoring in the absence of genomic surveillance capabilities: a serological study in Bolivian blood donors in October 2021 and June 2022</title>
      <link>https://elifesciences.org/articles/94475</link>
      <author>lucia-paola.inchauste-jordan@univ-amu.fr (Elif Nurtop)</author>
      <author>lucia-paola.inchauste-jordan@univ-amu.fr (Etzel Arancibia Cardozo)</author>
      <author>lucia-paola.inchauste-jordan@univ-amu.fr (Juan Cansio Garcia Copa)</author>
      <author>lucia-paola.inchauste-jordan@univ-amu.fr (Juan Carlos Pavel Suarez)</author>
      <author>lucia-paola.inchauste-jordan@univ-amu.fr (Katty Mina Villafan)</author>
      <author>lucia-paola.inchauste-jordan@univ-amu.fr (Lissete Bautista Machicado)</author>
      <author>lucia-paola.inchauste-jordan@univ-amu.fr (Lucia Inchauste)</author>
      <author>lucia-paola.inchauste-jordan@univ-amu.fr (Marcelo Ramos Espinoza)</author>
      <author>lucia-paola.inchauste-jordan@univ-amu.fr (Maria Luisa Herrera)</author>
      <author>lucia-paola.inchauste-jordan@univ-amu.fr (Pedro Mamani Mamani)</author>
      <author>lucia-paola.inchauste-jordan@univ-amu.fr (Pierre Gallian)</author>
      <author>lucia-paola.inchauste-jordan@univ-amu.fr (Shirley Lenz Gonzales)</author>
      <author>lucia-paola.inchauste-jordan@univ-amu.fr (Stéphane Priet)</author>
      <author>lucia-paola.inchauste-jordan@univ-amu.fr (Xavier de Lamballerie)</author>
      <author>lucia-paola.inchauste-jordan@univ-amu.fr (Yanine Leigue Roth)</author>
      <author>lucia-paola.inchauste-jordan@univ-amu.fr (Yitzhak Leigue Zabala)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.94475</guid>
      <category>Epidemiology and Global Health</category>
      <category>Microbiology and Infectious Disease</category>
      <pubDate>Fri, 18 Jul 2025 00:00:00 +0000</pubDate>
      <dc:date>2025-07-18T00:00:00Z</dc:date>
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    </item>
    <item>
      <title>A sex-specific Mendelian randomization-phenome-wide association study of body mass index</title>
      <link>https://elifesciences.org/articles/102573</link>
      <author>mary.schooling@sph.cuny.edu (C Mary Schooling)</author>
      <author>mary.schooling@sph.cuny.edu (Io Ieong Chan)</author>
      <author>mary.schooling@sph.cuny.edu (Jack Chun Man Ng)</author>
      <author>mary.schooling@sph.cuny.edu (Zhu Liduzi Jiesisibieke)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.102573</guid>
      <category>Epidemiology and Global Health</category>
      <pubDate>Wed, 11 Jun 2025 00:00:00 +0000</pubDate>
      <dc:date>2025-06-11T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>Assessing healthy vaccinee effect in COVID-19 vaccine effectiveness studies: a national cohort study in Qatar</title>
      <link>https://elifesciences.org/articles/103690</link>
      <author>hsc2001@qatar-med.cornell.edu (Abdullatif Al-Khal)</author>
      <author>hsc2001@qatar-med.cornell.edu (Adeel A Butt)</author>
      <author>hsc2001@qatar-med.cornell.edu (Ali Nizar Latif)</author>
      <author>hsc2001@qatar-med.cornell.edu (Andrew Jeremijenko)</author>
      <author>hsc2001@qatar-med.cornell.edu (Anvar Hassan Kaleeckal)</author>
      <author>hsc2001@qatar-med.cornell.edu (Asmaa A Al Thani)</author>
      <author>hsc2001@qatar-med.cornell.edu (Einas Al-Kuwari)</author>
      <author>hsc2001@qatar-med.cornell.edu (Gheyath K Nasrallah)</author>
      <author>hsc2001@qatar-med.cornell.edu (Hadi M Yassine)</author>
      <author>hsc2001@qatar-med.cornell.edu (Hamad Eid Al-Romaihi)</author>
      <author>hsc2001@qatar-med.cornell.edu (Hanan F Abdul-Rahim)</author>
      <author>hsc2001@qatar-med.cornell.edu (Hiam Chemaitelly)</author>
      <author>hsc2001@qatar-med.cornell.edu (Houssein H Ayoub)</author>
      <author>hsc2001@qatar-med.cornell.edu (Laith J Abu-Raddad)</author>
      <author>hsc2001@qatar-med.cornell.edu (Mohamed Ghaith Al-Kuwari)</author>
      <author>hsc2001@qatar-med.cornell.edu (Mohamed H Al-Thani)</author>
      <author>hsc2001@qatar-med.cornell.edu (Mohammad R Hasan)</author>
      <author>hsc2001@qatar-med.cornell.edu (Patrick Tang)</author>
      <author>hsc2001@qatar-med.cornell.edu (Peter Coyle)</author>
      <author>hsc2001@qatar-med.cornell.edu (Riyazuddin Mohammad Shaik)</author>
      <author>hsc2001@qatar-med.cornell.edu (Roberto Bertollini)</author>
      <author>hsc2001@qatar-med.cornell.edu (Zaina Al-Kanaani)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.103690</guid>
      <category>Epidemiology and Global Health</category>
      <pubDate>Mon, 09 Jun 2025 00:00:00 +0000</pubDate>
      <dc:date>2025-06-09T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>Menopausal hormone therapy and the female brain: Leveraging neuroimaging and prescription registry data from the UK Biobank cohort</title>
      <link>https://elifesciences.org/articles/99538</link>
      <author>claudia.barth@medisin.uio.no (Ann-Marie G de Lange)</author>
      <author>claudia.barth@medisin.uio.no (Bonnie H Lee)</author>
      <author>claudia.barth@medisin.uio.no (Claudia Barth)</author>
      <author>claudia.barth@medisin.uio.no (Emily G Jacobs)</author>
      <author>claudia.barth@medisin.uio.no (Lars T Westlye)</author>
      <author>claudia.barth@medisin.uio.no (Liisa AM Galea)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.99538</guid>
      <category>Epidemiology and Global Health</category>
      <category>Neuroscience</category>
      <pubDate>Thu, 29 May 2025 00:00:00 +0000</pubDate>
      <dc:date>2025-05-29T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>Lifestyles and their relative contribution to biological aging across multiple-organ systems: Change analysis from the China Multi-Ethnic Cohort study</title>
      <link>https://elifesciences.org/articles/99924</link>
      <author>yinjianzhong2005@sina.com (Dan Tang)</author>
      <author>yinjianzhong2005@sina.com (Jianzhong Yin)</author>
      <author>yinjianzhong2005@sina.com (Ning Zhang)</author>
      <author>yinjianzhong2005@sina.com (Wen Qian)</author>
      <author>yinjianzhong2005@sina.com (Xianbin Ding)</author>
      <author>yinjianzhong2005@sina.com (Xing Zhao)</author>
      <author>yinjianzhong2005@sina.com (Xiong Xiao)</author>
      <author>yinjianzhong2005@sina.com (Yangji Baima)</author>
      <author>yinjianzhong2005@sina.com (Yifan Hu)</author>
      <author>yinjianzhong2005@sina.com (Yi Xiang)</author>
      <author>yinjianzhong2005@sina.com (Yuan Zhang)</author>
      <author>yinjianzhong2005@sina.com (Ziyun Wang)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.99924</guid>
      <category>Epidemiology and Global Health</category>
      <pubDate>Fri, 07 Mar 2025 00:00:00 +0000</pubDate>
      <dc:date>2025-03-07T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>Protection afforded by post-infection SARS-CoV-2 vaccine doses: A cohort study in Shanghai</title>
      <link>https://elifesciences.org/articles/94990</link>
      <author>yyao@fudan.edu.cn (Bo Zheng)</author>
      <author>yyao@fudan.edu.cn (Bronner P Gonçalves)</author>
      <author>yyao@fudan.edu.cn (Caoyi Xue)</author>
      <author>yyao@fudan.edu.cn (Jie Tian)</author>
      <author>yyao@fudan.edu.cn (Pengfei Deng)</author>
      <author>yyao@fudan.edu.cn (Weibing Wang)</author>
      <author>yyao@fudan.edu.cn (Xueyao Liang)</author>
      <author>yyao@fudan.edu.cn (Ye Yao)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.94990</guid>
      <category>Epidemiology and Global Health</category>
      <category>Microbiology and Infectious Disease</category>
      <pubDate>Mon, 17 Feb 2025 00:00:00 +0000</pubDate>
      <dc:date>2025-02-17T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>Persistent cross-species transmission systems dominate Shiga toxin-producing &lt;i&gt;Escherichia coli&lt;/i&gt; O157:H7 epidemiology in a high incidence region: A genomic epidemiology study</title>
      <link>https://elifesciences.org/articles/97643</link>
      <description>Several areas of the world suffer a notably high incidence of Shiga toxin-producing &lt;i&gt;Escherichia coli&lt;/i&gt;. To assess the impact of persistent cross-species transmission systems on the epidemiology of &lt;i&gt;E. coli&lt;/i&gt; O157:H7 in Alberta, Canada, we sequenced and assembled &lt;i&gt;E. coli&lt;/i&gt; O157:H7 isolates originating from collocated cattle and human populations, 2007–2015. We constructed a timed phylogeny using BEAST2 using a structured coalescent model. We then extended the tree with human isolates through 2019 to assess the long-term disease impact of locally persistent lineages. During 2007–2015, we estimated that 88.5% of human lineages arose from cattle lineages. We identified 11 persistent lineages local to Alberta, which were associated with 38.0% (95% CI 29.3%, 47.3%) of human isolates. During the later period, six locally persistent lineages continued to be associated with human illness, including 74.7% (95% CI 68.3%, 80.3%) of reported cases in 2018 and 2019. Our study identified multiple locally evolving lineages transmitted between cattle and humans persistently associated with &lt;i&gt;E. coli&lt;/i&gt; O157:H7 illnesses for up to 13 y. Locally persistent lineages may be a principal cause of the high incidence of &lt;i&gt;E. coli&lt;/i&gt; O157:H7 in locations such as Alberta and provide opportunities for focused control efforts.</description>
      <author>gtarr@umn.edu (Chad R Laing)</author>
      <author>gtarr@umn.edu (Emmanuel W Bumunang)</author>
      <author>gtarr@umn.edu (Gillian AM Tarr)</author>
      <author>gtarr@umn.edu (Kim Stanford)</author>
      <author>gtarr@umn.edu (Linda Chui)</author>
      <author>gtarr@umn.edu (Rahat Zaheer)</author>
      <author>gtarr@umn.edu (Stephen B Freedman)</author>
      <author>gtarr@umn.edu (Tim A McAllister)</author>
      <author>gtarr@umn.edu (Vincent Li)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.97643</guid>
      <category>Epidemiology and Global Health</category>
      <category>Microbiology and Infectious Disease</category>
      <pubDate>Wed, 29 Jan 2025 00:00:00 +0000</pubDate>
      <dc:date>2025-01-29T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>Leveraging mobility data to analyze persistent SARS-CoV-2 mutations and inform targeted genomic surveillance</title>
      <link>https://elifesciences.org/articles/94045</link>
      <description>Given the rapid cross-country spread of SARS-CoV-2 and the resulting difficulty in tracking lineage spread, we investigated the potential of combining mobile service data and fine-granular metadata (such as postal codes and genomic data) to advance integrated genomic surveillance of the pandemic in the federal state of Thuringia, Germany. We sequenced over 6500 SARS-CoV-2 Alpha genomes (B.1.1.7) across 7 months within Thuringia while collecting patients’ isolation dates and postal codes. Our dataset is complemented by over 66,000 publicly available German Alpha genomes and mobile service data for Thuringia. We identified the existence and spread of nine persistent mutation variants within the Alpha lineage, seven of which formed separate phylogenetic clusters with different spreading patterns in Thuringia. The remaining two are subclusters. Mobile service data can indicate these clusters’ spread and highlight a potential sampling bias, especially of low-prevalence variants. Thereby, mobile service data can be used either retrospectively to assess surveillance coverage and efficiency from already collected data or to actively guide part of a surveillance sampling process to districts where these variants are expected to emerge. The latter concept was successfully implemented as a proof-of-concept for a mobility-guided sampling strategy in response to the surveillance of Omicron sublineage BQ.1.1. The combination of mobile service data and SARS-CoV-2 surveillance by genome sequencing is a valuable tool for more targeted and responsive surveillance.</description>
      <author>riccardo.spott@gmail.com (Aurelia Kimmig)</author>
      <author>riccardo.spott@gmail.com (Carolin Fleischmann-Struzek)</author>
      <author>riccardo.spott@gmail.com (Christian Brandt)</author>
      <author>riccardo.spott@gmail.com (Christiane Hadlich)</author>
      <author>riccardo.spott@gmail.com (Denise Kühnert)</author>
      <author>riccardo.spott@gmail.com (Mara Lohde)</author>
      <author>riccardo.spott@gmail.com (Martin Hölzer)</author>
      <author>riccardo.spott@gmail.com (Mateusz Jundzill)</author>
      <author>riccardo.spott@gmail.com (Mathias W Pletz)</author>
      <author>riccardo.spott@gmail.com (Matthias Hauert)</author>
      <author>riccardo.spott@gmail.com (Mike Marquet)</author>
      <author>riccardo.spott@gmail.com (Petra Dickmann)</author>
      <author>riccardo.spott@gmail.com (Riccardo Spott)</author>
      <author>riccardo.spott@gmail.com (Ruben Schüchner)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.94045</guid>
      <category>Epidemiology and Global Health</category>
      <pubDate>Wed, 15 Jan 2025 00:00:00 +0000</pubDate>
      <dc:date>2025-01-15T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>Serum metabolome indicators of early childhood development in the Brazilian National Survey on Child Nutrition (ENANI-2019)</title>
      <link>https://elifesciences.org/articles/97982</link>
      <author>gilberto.kac@gmail.com (Dayana R Farias)</author>
      <author>gilberto.kac@gmail.com (Elisa MA Lacerda)</author>
      <author>gilberto.kac@gmail.com (Felipe M Delpino)</author>
      <author>gilberto.kac@gmail.com (Gilberto Kac)</author>
      <author>gilberto.kac@gmail.com (Inês RR de Castro)</author>
      <author>gilberto.kac@gmail.com (Marina Padilha)</author>
      <author>gilberto.kac@gmail.com (Meera Shanmuganathan)</author>
      <author>gilberto.kac@gmail.com (Nathalia C Freitas-Costa)</author>
      <author>gilberto.kac@gmail.com (Paula Normando)</author>
      <author>gilberto.kac@gmail.com (Philip Britz-Mckibbin)</author>
      <author>gilberto.kac@gmail.com (Raquel M Schincaglia)</author>
      <author>gilberto.kac@gmail.com (Samary SR Freire)</author>
      <author>gilberto.kac@gmail.com (Victor Nahuel Keller)</author>
      <author>gilberto.kac@gmail.com (Zachary Kroezen)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.97982</guid>
      <category>Epidemiology and Global Health</category>
      <pubDate>Wed, 15 Jan 2025 00:00:00 +0000</pubDate>
      <dc:date>2025-01-15T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>Livestock abortion surveillance in Tanzania reveals disease priorities and importance of timely collection of vaginal swab samples for attribution</title>
      <link>https://elifesciences.org/articles/95296</link>
      <description>Lack of data on the aetiology of livestock diseases constrains effective interventions to improve livelihoods, food security and public health. Livestock abortion is an important disease syndrome affecting productivity and public health. Several pathogens are associated with livestock abortions but across Africa surveillance data rarely include information from abortions, little is known about aetiology and impacts, and data are not available to inform interventions. This paper describes outcomes from a surveillance platform established in Tanzania spanning pastoral, agropastoral and smallholder systems to investigate causes and impacts of livestock abortion. Abortion events were reported by farmers to livestock field officers (LFO) and on to investigation teams. Events were included if the research team or LFO could attend within 72 hr. If so, samples and questionnaire data were collected to investigate (a) determinants of attribution; (b) patterns of events, including species and breed, previous abortion history, and seasonality; (c) determinants of reporting, investigation and attribution; (d) cases involving zoonotic pathogens. Between 2017–2019, 215 events in cattle (n=71), sheep (n=44), and goats (n=100) were investigated. Attribution, achieved for 19.5% of cases, was significantly affected by delays in obtaining samples. Histopathology proved less useful than PCR due to rapid deterioration of samples. Vaginal swabs provided practical and sensitive material for pathogen detection. Livestock abortion surveillance, even at a small scale, can generate valuable information on causes of disease outbreaks, reproductive losses and can identify pathogens not easily captured through other forms of livestock disease surveillance. This study demonstrated the feasibility of establishing a surveillance system, achieved through engagement of community-based field officers, establishment of practical sample collection and application of molecular diagnostic platforms.</description>
      <author>felix.lankester@wsu.edu (Blandina T Mmbaga)</author>
      <author>felix.lankester@wsu.edu (Elisabeth A Innes)</author>
      <author>felix.lankester@wsu.edu (Emanuel Swai)</author>
      <author>felix.lankester@wsu.edu (Felix Lankester)</author>
      <author>felix.lankester@wsu.edu (Frank Katzer)</author>
      <author>felix.lankester@wsu.edu (Jo E Halliday)</author>
      <author>felix.lankester@wsu.edu (John R Claxton)</author>
      <author>felix.lankester@wsu.edu (Joram J Buza)</author>
      <author>felix.lankester@wsu.edu (Kate M Thomas)</author>
      <author>felix.lankester@wsu.edu (Kathryn J Allan)</author>
      <author>felix.lankester@wsu.edu (Nick Wheelhouse)</author>
      <author>felix.lankester@wsu.edu (Obed M Nyasebwa)</author>
      <author>felix.lankester@wsu.edu (Sarah Cleaveland)</author>
      <author>felix.lankester@wsu.edu (Tito J Kibona)</author>
      <author>felix.lankester@wsu.edu (William de Glanville)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.95296</guid>
      <category>Epidemiology and Global Health</category>
      <category>Microbiology and Infectious Disease</category>
      <pubDate>Mon, 16 Dec 2024 00:00:00 +0000</pubDate>
      <dc:date>2024-12-16T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>Systematic evaluation of multifactorial causal associations for Alzheimer’s disease and an interactive platform MRAD developed based on Mendelian randomization analysis</title>
      <link>https://elifesciences.org/articles/96224</link>
      <description>Alzheimer’s disease (AD) is a complex degenerative disease of the central nervous system, and elucidating its pathogenesis remains challenging. In this study, we used the inverse-variance weighted (IVW) model as the major analysis method to perform hypothesis-free Mendelian randomization (MR) analysis on the data from MRC IEU OpenGWAS (18,097 exposure traits and 16 AD outcome traits), and conducted sensitivity analysis with six models, to assess the robustness of the IVW results, to identify various classes of risk or protective factors for AD, early-onset AD, and late-onset AD. We generated 400,274 data entries in total, among which the major analysis method of the IVW model consists of 73,129 records with 4840 exposure traits, which fall into 10 categories: Disease, Medical laboratory science, Imaging, Anthropometric, Treatment, Molecular trait, Gut microbiota, Past history, Family history, and Lifestyle trait. More importantly, a freely accessed online platform called MRAD (&lt;a href="https://gwasmrad.com/mrad/"&gt;https://gwasmrad.com/mrad/&lt;/a&gt;) has been developed using the Shiny package with MR analysis results. Additionally, novel potential AD therapeutic targets (CD33, TBCA, VPS29, GNAI3, PSME1) are identified, among which CD33 was positively associated with the main outcome traits of AD, as well as with both EOAD and LOAD. TBCA and VPS29 were negatively associated with the main outcome traits of AD, as well as with both EOAD and LOAD. GNAI3 and PSME1 were negatively associated with the main outcome traits of AD, as well as with LOAD, but had no significant causal association with EOAD. The findings of our research advance our understanding of the etiology of AD.</description>
      <author>chenl@jlu.edu.cn (Hui Li)</author>
      <author>chenl@jlu.edu.cn (Li Chen)</author>
      <author>chenl@jlu.edu.cn (Meishuang Zhang)</author>
      <author>chenl@jlu.edu.cn (Ming Zhang)</author>
      <author>chenl@jlu.edu.cn (Tianyu Zhao)</author>
      <author>chenl@jlu.edu.cn (Yang Xu)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.96224</guid>
      <category>Epidemiology and Global Health</category>
      <category>Genetics and Genomics</category>
      <pubDate>Fri, 11 Oct 2024 00:00:00 +0000</pubDate>
      <dc:date>2024-10-11T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>Noncaloric monosaccharides induce excessive sprouting angiogenesis in zebrafish via foxo1a-marcksl1a signal</title>
      <link>https://elifesciences.org/articles/95427</link>
      <description>Artificially sweetened beverages containing noncaloric monosaccharides were suggested as healthier alternatives to sugar-sweetened beverages. Nevertheless, the potential detrimental effects of these noncaloric monosaccharides on blood vessel function remain inadequately understood. We have established a zebrafish model that exhibits significant excessive angiogenesis induced by high glucose, resembling the hyperangiogenic characteristics observed in proliferative diabetic retinopathy (PDR). Utilizing this model, we observed that glucose and noncaloric monosaccharides could induce excessive formation of blood vessels, especially intersegmental vessels (ISVs). The excessively branched vessels were observed to be formed by ectopic activation of quiescent endothelial cells (ECs) into tip cells. Single-cell transcriptomic sequencing analysis of the ECs in the embryos exposed to high glucose revealed an augmented ratio of capillary ECs, proliferating ECs, and a series of upregulated proangiogenic genes. Further analysis and experiments validated that reduced &lt;i&gt;foxo1a&lt;/i&gt; mediated the excessive angiogenesis induced by monosaccharides via upregulating the expression of &lt;i&gt;marcksl1a&lt;/i&gt;. This study has provided new evidence showing the negative effects of noncaloric monosaccharides on the vascular system and the underlying mechanisms.</description>
      <author>liuxia_fd@ntu.edu.cn (Bowen Li)</author>
      <author>liuxia_fd@ntu.edu.cn (Dong Liu)</author>
      <author>liuxia_fd@ntu.edu.cn (Gangcai Xie)</author>
      <author>liuxia_fd@ntu.edu.cn (Jiehuan Xu)</author>
      <author>liuxia_fd@ntu.edu.cn (Jinxiang Zhao)</author>
      <author>liuxia_fd@ntu.edu.cn (Xia Liu)</author>
      <author>liuxia_fd@ntu.edu.cn (Xiaoning Wang)</author>
      <author>liuxia_fd@ntu.edu.cn (Xuchu Duan)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.95427</guid>
      <category>Epidemiology and Global Health</category>
      <pubDate>Fri, 04 Oct 2024 00:00:00 +0000</pubDate>
      <dc:date>2024-10-04T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>Antigenic drift and subtype interference shape A(H3N2) epidemic dynamics in the United States</title>
      <link>https://elifesciences.org/articles/91849</link>
      <description>Influenza viruses continually evolve new antigenic variants, through mutations in epitopes of their major surface proteins, hemagglutinin (HA) and neuraminidase (NA). Antigenic drift potentiates the reinfection of previously infected individuals, but the contribution of this process to variability in annual epidemics is not well understood. Here, we link influenza A(H3N2) virus evolution to regional epidemic dynamics in the United States during 1997—2019. We integrate phenotypic measures of HA antigenic drift and sequence-based measures of HA and NA fitness to infer antigenic and genetic distances between viruses circulating in successive seasons. We estimate the magnitude, severity, timing, transmission rate, age-specific patterns, and subtype dominance of each regional outbreak and find that genetic distance based on broad sets of epitope sites is the strongest evolutionary predictor of A(H3N2) virus epidemiology. Increased HA and NA epitope distance between seasons correlates with larger, more intense epidemics, higher transmission, greater A(H3N2) subtype dominance, and a greater proportion of cases in adults relative to children, consistent with increased population susceptibility. Based on random forest models, A(H1N1) incidence impacts A(H3N2) epidemics to a greater extent than viral evolution, suggesting that subtype interference is a major driver of influenza A virus infection ynamics, presumably via heterosubtypic cross-immunity.</description>
      <author>amanda.perofsky@nih.gov (Amanda C Perofsky)</author>
      <author>amanda.perofsky@nih.gov (Burcu Ermetal)</author>
      <author>amanda.perofsky@nih.gov (Cécile Viboud)</author>
      <author>amanda.perofsky@nih.gov (Chelsea L Hansen)</author>
      <author>amanda.perofsky@nih.gov (David E Wentworth)</author>
      <author>amanda.perofsky@nih.gov (Florian Krammer)</author>
      <author>amanda.perofsky@nih.gov (Hideki Hasegawa)</author>
      <author>amanda.perofsky@nih.gov (Ian G Barr)</author>
      <author>amanda.perofsky@nih.gov (John Huddleston)</author>
      <author>amanda.perofsky@nih.gov (John R Barnes)</author>
      <author>amanda.perofsky@nih.gov (John W McCauley)</author>
      <author>amanda.perofsky@nih.gov (Kanta Subbarao)</author>
      <author>amanda.perofsky@nih.gov (Kazuya Nakamura)</author>
      <author>amanda.perofsky@nih.gov (Lynne Whittaker)</author>
      <author>amanda.perofsky@nih.gov (Monica Galiano)</author>
      <author>amanda.perofsky@nih.gov (Nicola Lewis)</author>
      <author>amanda.perofsky@nih.gov (Noriko Kishida)</author>
      <author>amanda.perofsky@nih.gov (Rebecca Kondor)</author>
      <author>amanda.perofsky@nih.gov (Rodney Stuart Daniels)</author>
      <author>amanda.perofsky@nih.gov (Ruth Harvey)</author>
      <author>amanda.perofsky@nih.gov (Seiichiro Fujisaki)</author>
      <author>amanda.perofsky@nih.gov (Sheena G Sullivan)</author>
      <author>amanda.perofsky@nih.gov (Shinji Watanabe)</author>
      <author>amanda.perofsky@nih.gov (Thomas Rowe)</author>
      <author>amanda.perofsky@nih.gov (Trevor Bedford)</author>
      <author>amanda.perofsky@nih.gov (Xiyan Xu)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.91849</guid>
      <category>Epidemiology and Global Health</category>
      <category>Microbiology and Infectious Disease</category>
      <pubDate>Wed, 25 Sep 2024 00:00:00 +0000</pubDate>
      <dc:date>2024-09-25T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>Ethnic and region-specific genetic risk variants of stroke and its comorbid conditions can define the variations in the burden of stroke and its phenotypic traits</title>
      <link>https://elifesciences.org/articles/94088</link>
      <description>Burden of stroke differs by region, which could be attributed to differences in comorbid conditions and ethnicity. Genomewide variation acts as a proxy marker for ethnicity, and comorbid conditions. We present an integrated approach to understand this variation by considering prevalence and mortality rates of stroke and its comorbid risk for 204 countries from 2009 to 2019, and Genome-wide association studies (GWAS) risk variant for all these conditions. Global and regional trend analysis of rates using linear regression, correlation, and proportion analysis, signifies ethnogeographic differences. Interestingly, the comorbid conditions that act as risk drivers for stroke differed by regions, with more of metabolic risk in America and Europe, in contrast to high systolic blood pressure in Asian and African regions. GWAS risk loci of stroke and its comorbid conditions indicate distinct population stratification for each of these conditions, signifying for population-specific risk. Unique and shared genetic risk variants for stroke, and its comorbid and followed up with ethnic-specific variation can help in determining regional risk drivers for stroke. Unique ethnic-specific risk variants and their distinct patterns of linkage disequilibrium further uncover the drivers for phenotypic variation. Therefore, identifying population- and comorbidity-specific risk variants might help in defining the threshold for risk, and aid in developing population-specific prevention strategies for stroke.</description>
      <author>mbanerjee@rgcb.res.in (Achuthsankar S Nair)</author>
      <author>mbanerjee@rgcb.res.in (Moinak Banerjee)</author>
      <author>mbanerjee@rgcb.res.in (Rashmi Sukumaran)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.94088</guid>
      <category>Epidemiology and Global Health</category>
      <category>Genetics and Genomics</category>
      <pubDate>Fri, 13 Sep 2024 00:00:00 +0000</pubDate>
      <dc:date>2024-09-13T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>Recent evolutionary origin and localized diversity hotspots of mammalian coronaviruses</title>
      <link>https://elifesciences.org/articles/91745</link>
      <description>Several coronaviruses infect humans, with three, including the SARS-CoV2, causing diseases. While coronaviruses are especially prone to induce pandemics, we know little about their evolutionary history, host-to-host transmissions, and biogeography. One of the difficulties lies in dating the origination of the family, a particularly challenging task for RNA viruses in general. Previous cophylogenetic tests of virus-host associations, including in the Coronaviridae family, have suggested a virus-host codiversification history stretching many millions of years. Here, we establish a framework for robustly testing scenarios of ancient origination and codiversification &lt;i&gt;versus&lt;/i&gt; recent origination and diversification by host switches. Applied to coronaviruses and their mammalian hosts, our results support a scenario of recent origination of coronaviruses in bats and diversification by host switches, with preferential host switches within mammalian orders. Hotspots of coronavirus diversity, concentrated in East Asia and Europe, are consistent with this scenario of relatively recent origination and localized host switches. Spillovers from bats to other species are rare, but have the highest probability to be towards humans than to any other mammal species, implicating humans as the evolutionary intermediate host. The high host-switching rates within orders, as well as between humans, domesticated mammals, and non-flying wild mammals, indicates the potential for rapid additional spreading of coronaviruses across the world. Our results suggest that the evolutionary history of extant mammalian coronaviruses is recent, and that cases of long-term virus–host codiversification have been largely over-estimated.</description>
      <author>renanmaestri@gmail.com (Anna Zhukova)</author>
      <author>renanmaestri@gmail.com (Benoît Perez-Lamarque)</author>
      <author>renanmaestri@gmail.com (Hélène Morlon)</author>
      <author>renanmaestri@gmail.com (Renan Maestri)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.91745</guid>
      <category>Epidemiology and Global Health</category>
      <category>Evolutionary Biology</category>
      <pubDate>Wed, 28 Aug 2024 00:00:00 +0000</pubDate>
      <dc:date>2024-08-28T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>Disentangling the relationship between cancer mortality and COVID-19 in the US</title>
      <link>https://elifesciences.org/articles/93758</link>
      <description>Cancer is considered a risk factor for COVID-19 mortality, yet several countries have reported that deaths with a primary code of cancer remained within historic levels during the COVID-19 pandemic. Here, we further elucidate the relationship between cancer mortality and COVID-19 on a population level in the US. We compared pandemic-related mortality patterns from underlying and multiple cause (MC) death data for six types of cancer, diabetes, and Alzheimer’s. Any pandemic-related changes in coding practices should be eliminated by study of MC data. Nationally in 2020, MC cancer mortality rose by only 3% over a pre-pandemic baseline, corresponding to ~13,600 excess deaths. Mortality elevation was measurably higher for less deadly cancers (breast, colorectal, and hematological, 2–7%) than cancers with a poor survival rate (lung and pancreatic, 0–1%). In comparison, there was substantial elevation in MC deaths from diabetes (37%) and Alzheimer’s (19%). To understand these differences, we simulated the expected excess mortality for each condition using COVID-19 attack rates, life expectancy, population size, and mean age of individuals living with each condition. We find that the observed mortality differences are primarily explained by differences in life expectancy, with the risk of death from deadly cancers outcompeting the risk of death from COVID-19.</description>
      <author>chelsea.hansen@nih.gov (Cécile Viboud)</author>
      <author>chelsea.hansen@nih.gov (Chelsea L Hansen)</author>
      <author>chelsea.hansen@nih.gov (Lone Simonsen)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.93758</guid>
      <category>Cancer Biology</category>
      <category>Epidemiology and Global Health</category>
      <pubDate>Tue, 27 Aug 2024 00:00:00 +0000</pubDate>
      <dc:date>2024-08-27T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>Associations of age at diagnosis of breast cancer with incident myocardial infarction and heart failure: A prospective cohort study</title>
      <link>https://elifesciences.org/articles/95901</link>
      <author>xiewuxiang@hsc.pku.edu.cn (Darui Gao)</author>
      <author>xiewuxiang@hsc.pku.edu.cn (Fanfan Zheng)</author>
      <author>xiewuxiang@hsc.pku.edu.cn (Jie Liang)</author>
      <author>xiewuxiang@hsc.pku.edu.cn (Wenya Zhang)</author>
      <author>xiewuxiang@hsc.pku.edu.cn (Wuxiang Xie)</author>
      <author>xiewuxiang@hsc.pku.edu.cn (Yang Pan)</author>
      <author>xiewuxiang@hsc.pku.edu.cn (Yongqian Wang)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.95901</guid>
      <category>Epidemiology and Global Health</category>
      <pubDate>Thu, 22 Aug 2024 00:00:00 +0000</pubDate>
      <dc:date>2024-08-22T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>Maternal smoking DNA methylation risk score associated with health outcomes in offspring of European and South Asian ancestry</title>
      <link>https://elifesciences.org/articles/93260</link>
      <author>dengwq@mcmaster.ca (Amel Lamri)</author>
      <author>dengwq@mcmaster.ca (Elinor Simons)</author>
      <author>dengwq@mcmaster.ca (Guillaume Paré)</author>
      <author>dengwq@mcmaster.ca (Katherine M Morrison)</author>
      <author>dengwq@mcmaster.ca (Koon K Teo)</author>
      <author>dengwq@mcmaster.ca (Meghan B Azad)</author>
      <author>dengwq@mcmaster.ca (Natalie Campbell)</author>
      <author>dengwq@mcmaster.ca (Nathan Cawte)</author>
      <author>dengwq@mcmaster.ca (Padmaja Subbarao)</author>
      <author>dengwq@mcmaster.ca (Piush J Mandhane)</author>
      <author>dengwq@mcmaster.ca (Russell J de Souza)</author>
      <author>dengwq@mcmaster.ca (Sandi M Azab)</author>
      <author>dengwq@mcmaster.ca (Sonia S Anand)</author>
      <author>dengwq@mcmaster.ca (Stephanie A Atkinson)</author>
      <author>dengwq@mcmaster.ca (Stuart E Turvey)</author>
      <author>dengwq@mcmaster.ca (Theo J Moraes)</author>
      <author>dengwq@mcmaster.ca (Wei Q Deng)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.93260</guid>
      <category>Epidemiology and Global Health</category>
      <category>Genetics and Genomics</category>
      <pubDate>Wed, 14 Aug 2024 00:00:00 +0000</pubDate>
      <dc:date>2024-08-14T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
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