ArticleApplied microbiology and biotechnology2015
Replacement of pr gene with Japanese encephalitis virus pr using reverse genetics reduces antibody-dependent enhancement of dengue virus 2 infection.
Article in Applied microbiology and biotechnology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Global Epidemiology of Dengue Outbreaks in 1990-2015: A Systematic Review and Meta-Analysis.Frontiers in cellular and infection microbiology · 2017Pooled it
- Antibody dependent enhancement: Unavoidable problems in vaccine development.Advances in immunology · 2021Article
- Adaptive Immunity to Dengue Virus: Slippery Slope or Solid Ground for Rational Vaccine Design?Pathogens (Basel, Switzerland) · 2020Review
- Epidemiology and characteristics of the dengue outbreak in Guangdong, Southern China, in 2014.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2016Article
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Authors and funding
9 authors.
Funding
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Abstract
Severe dengue is more likely found during secondary heterologous dengue virus (DENV) infection or primary infection of infants born to dengue-immune mothers and led to the hypothesis of antibody-dependent enhancement (ADE). It has been reported that pre-membrane (prM)-reactive antibodies do not efficiently neutralize DENV infection but instead potently promote ADE infection. Meanwhile, these enhancing anti-prM antibodies mainly react with the precursor (pr) peptide. To evaluate the effect of pr gene substitution on neutralization and ADE of DENV infection, a novel chimeric dengue virus (JEVpr/DENV2) was rationally constructed by replacing the DENV pr gene with Japanese encephalitis virus (JEV) pr gene, based on the full-length infectious complementary DNA (cDNA) clone of DENV2 ZS01/01. We found that chimeric JEVpr/DENV2 showed reduced virulence and good immunogenicity. In addition, anti-JEVpr/DENV2 sera showed broad cross-reactivity and efficient neutralizing activity with all four DENV serotypes and immature DENV2 (ImDENV2). Most importantly, compared with anti-DENV2 sera, anti-JEVpr/DENV2 sera showed significantly reduced enhancing activity of DENV infection in K562 cells. These results suggest that the ADE activities could be reduced by replacing the DENV pr gene with JEV pr gene. These findings may help us better understand the pathogenesis of DENV infection and provide a reference for the development of a vaccine against DENV.
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