ArticlePloS one2015
Clinical outcome and genetic differences within a monophyletic Dengue virus type 2 population.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Clinico-genomic study reveals association of dengue virus genome high frequency mutations with dengue disease severity.Scientific reports · 2025Article
- Inter-host diversity associated with age, sex, and menstrual cycle modulates clinical manifestations in DENV-2 patients.iScience · 2025Article
- Genomic hotspots in the DENV-2 serotype (E, NS4B, and NS5 genes) are associated with dengue disease severity in the endemic region of India.PLoS neglected tropical diseases · 2025Article
- The RNA Secondary Structure Analysis Reveals Potential for Emergence of Pathogenic Flaviviruses.Food and environmental virology · 2022Article
- Impaired NK cell activation during acute dengue virus infection: A contributing factor to disease severity.Heliyon · 2020Article
- Dengue Virus Infection of Blood-Brain Barrier Cells: Consequences of Severe Disease.Frontiers in microbiology · 2019Review
- In Vitro Infection with Dengue Virus Induces Changes in the Structure and Function of the Mouse Brain Endothelium.PloS one · 2016Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The exact mechanisms of interplay between host and viral factors leading to severe dengue are yet to be fully understood. Even though previous studies have implicated specific genetic differences of Dengue virus (DENV) in clinical severity and virus attenuation, similar studies with large-scale, whole genome screening of monophyletic virus populations are limited. Therefore, in the present study, we compared 89 whole genomes of DENV-2 cosmopolitan clade III isolates obtained from patients diagnosed with dengue fever (DF, n = 58), dengue hemorrhagic fever (DHF, n = 30) and dengue shock syndrome (DSS, n = 1) in Singapore between July 2010 and January 2013, in order to determine the correlation of observed viral genetic differences with clinical outcomes. Our findings showed no significant difference between the number of primary and secondary infections that progressed to DHF and DSS (p>0.05) in our study cohort. Despite being highly homogenous, study isolates possessed 39 amino acid substitutions of which 10 substitutions were fixed in three main groups of virus isolates. None of those substitutions were specifically associated with DHF and DSS. Notably, two evolutionarily unique virus groups possessing C-P43T+NS1-S103T+NS2A-V83I+NS3-R337K+ NS3-I600T+ NS5-P136S and NS2A-T119N mutations were exclusively found in patients with DF, the benign form of DENV infections. Those mutants were significantly associated with mild disease outcome. These observations indicated that disease progression into DHF and DSS within our patient population was more likely to be due to host than virus factors. We hypothesize that selection for potentially less virulent groups of DENV-2 in our study cohort may be an evolutionary adaptation of viral strains to extend their survival in the human-mosquito transmission cycle.
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