ReviewCurrent topics in microbiology and immunology2026
Innate Immune and Inflammatory Responses to Dengue Virus Infection.
Review in Current topics in microbiology and immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Authors and funding
3 authors.
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Abstract
Dengue is the most common arboviral infection in the world, causing up to 400 million cases per year. Although most cases are asymptomatic, the virus can cause a wide range of symptoms varying from high fever and pain, common to several arbovirus infections, to hemorrhagic fever and shock syndrome, which can often be fatal. Despite the association of some genotypes with disease severity, most symptom varieties can be traced to the interaction of the virus with the immune system. As early as viral entry, Dengue virus co-evolved with humans to evade the innate immune system, especially the antiviral response triggered by type I and III interferons, posing a strict bottleneck to its host range. This directly affects our ability to study the virus interaction with the innate immune system. Here, we will explore how dengue virus is recognized by pattern recognition receptors and triggers an immune response and how cells associated with innate immunity influence the course of infection, culminating with the inflammatory response, key to understanding the spectrum of dengue disease.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.