ArticleJournal of virology2025
Pathogenic dengue virus TW2015 strain infection triggers anaerobic glycolysis and enhances mortality in diabetic mice.
Article in Journal of virology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07450833 (Assessing the Safety, Tolerability and Pharmacokinetics of Benfo-Oxythiamine), which is not on this map. Cited by 1 paper.
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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.
The trial behind it
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.
Assessing the Safety, Tolerability and Pharmacokinetics of Benfo-Oxythiamine (B-OT) in Healthy Volunteers - An Open Label, Phase I Study
Who cites it
1 citing paper in PubMed.
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Dengue virus (DENV) strains with high pathogenicity and transmissibility pose significant public health challenges, especially in tropical and subtropical regions. Underlying conditions such as diabetes mellitus and renal diseases significantly increase the risk of severe dengue. The DENV-2 strain, responsible for a severe outbreak in Taiwan in 2015, exhibits enhanced pathogenicity and transmissibility in a mosquito-mouse transmission model. In this study, we demonstrated that pathogenic DENV infection leads to elevated lactate levels and hypoglycemia in mice, correlating with increased mortality in streptozotocin-induced diabetic models. In infected cells, pathogenic DENV induces rapid eIF2α phosphorylation, extensive ER membrane aggregation, disrupted calcium transfer to mitochondria, and mitochondrial dysfunction, which may contribute to excessive lactate production. Notably, inhibition of lactate production reduced viremia and mortality in mice. These findings highlight the role of metabolic dysregulation in DENV pathogenesis and provide insights into the mechanisms driving severe dengue, particularly in patients with underlying comorbidities.IMPORTANCEDENV is a mosquito-borne virus that can cause severe illness, particularly in tropical and subtropical regions. In 2015, a strain of DENV-2 caused a major outbreak in Taiwan with high mortality rates. People with conditions like diabetes or kidney disease were more likely to develop severe dengue. In our study, we found that this highly pathogenic virus caused mice to have high levels of lactate and low blood sugar before death. In diabetic mice, the virus caused even higher death rates. The virus impairs cellular energy production by disrupting communication between the endoplasmic reticulum and mitochondria, potentially leading to excessive lactate accumulation. Blocking lactate production helped reduce viremia and death rate. These findings suggest that the virus's impact on metabolism may play a role in severe illness, especially for people with pre-existing health issues.
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Registered trials
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