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Here, we establish an\n              <jats:italic>in vitro<\/jats:italic>\n              whole-blood model using hirudin, an anticoagulant that preserves complement activity and cellular interactions, to study DENV infection. Our model reveals the susceptibility of all major leukocyte populations to DENV infection, with monocytes and granulocytes demonstrating high permissiveness and production of infectious virus progeny. Notably, granulocytes emerge as previously unrecognized targets of DENV infection, highlighting the importance of studying viral tropism within a physiologically relevant context. We also observed efficient DENV binding to B cells, but limited production of infectious virus, suggesting a potential role in viral sequestration or immune dysregulation. Interestingly, both NK and T cells, while less permissive, were also found to be susceptible to DENV infection. Our\n              <jats:italic>ex vivo<\/jats:italic>\n              analysis of whole blood from DENV-infected patients confirms the susceptibility of granulocytes, monocytes, B cells, natural killer cells, and T cells to infection, further validating the clinical relevance of our model. Additionally, we observed dynamic changes in circulating blood cell populations during acute dengue, potentially reflecting both direct virus-mediated effects and immune responses. This whole-blood model offers a valuable tool for investigating the complex interplay between DENV and host factors, facilitating a deeper understanding of dengue pathogenesis and ultimately contributing to the development of novel therapeutic strategies.\n            <\/jats:p>\n            <jats:sec>\n              <jats:title>IMPORTANCE<\/jats:title>\n              <jats:p>\n                Dengue virus (DENV) infection is a significant global health threat, with increasing incidence in endemic regions and expanding geographic range due to factors like global warming. Current models for studying DENV pathogenesis often lack the complexity of the human immune system, hindering the development of effective therapies and vaccines. To address this, we have established the first\n                <jats:italic>in vitro<\/jats:italic>\n                whole-blood model using hirudin, preserving critical immune components and cellular interactions. This model reveals granulocytes as previously unrecognized targets of productive DENV infection, challenging existing paradigms of viral tropism. Our\n                <jats:italic>ex vivo<\/jats:italic>\n                analysis of patient blood samples confirms the clinical relevance of this finding and validates our model\u2019s utility. This unique model offers a powerful platform for future studies to dissect the complex interactions between DENV and the host immune system, including the roles of different leukocyte populations, ultimately informing the development of novel therapeutic strategies to combat this devastating disease.\n              <\/jats:p>\n            <\/jats:sec>\n          <\/jats:sec>","DOI":"10.1128\/mbio.01505-24","type":"journal-article","created":{"date-parts":[[2024,11,14]],"date-time":"2024-11-14T14:03:47Z","timestamp":1731593027000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":5,"title":["Whole-blood model reveals granulocytes as key sites of dengue virus propagation, expanding understanding of disease pathogenesis"],"prefix":"10.1128","volume":"15","author":[{"given":"Hansa","family":"Praneechit","sequence":"first","affiliation":[{"name":"Graduate Program in Immunology, Department of Immunology, Faculty of Medicine 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