Genome-wide Dengue conservation profile: implications for immunotherapy and vaccine design

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• Daniel Mansur is a Principal Investigator at the Federal University of Santa Catarina, Brazil.
• Thursday 08 December 2016, 10:00-11:00
• EE 611 Gabor Room.

If you have a question about this talk, please contact Pantelis Georgiou.

Despite several attempts and different vaccination strategies have achieved reasonable levels of protection, a vaccine that protects uniformly against the circulating serotypes is not available. Dengue is a mosquito-borne disease caused by a group of viruses collectively known as Dengue virus, belonging to the Flaviviridae family. It affects nearly 390 million people every year worldwide with symptoms ranging from mild fever to severe shock syndrome. Targeting regions of proteins that show a high degree of structural conservation has been proposed as a method of developing immunotherapies and vaccines that may bypass the wide genetic variability of RNA viruses. Despite several attempts, a vaccine that protects evenly against the four circulating Dengue virus (DV) serotypes remains elusive. To find critical conserved amino acids in dengue viruses, complete genomes of each serotype were selected at random and used to calculate conservation scores for nucleotide and amino acid sequences. Construction of a chimeric Junin-DENV virus-like participle was immunogenic and generated a neutralizing antibody response in mice. Hence, this study has identified a highly conserved, critical peptide in DV that is a target of antibodies in infected humans that could be used for vaccine design. Daniel Mansur is a Principal Investigator at the Federal University of Santa Catarina, Brazil. He studied biology and performed a PhD in microbiology at the Federal University of Minas Gerais, Brasil. After his studies, he moved to the UK and undertook a three-year postdoctoral position at Imperial College London where he described a new pattern recognition receptor for viral DNA that triggers an IRF3 dependent response upon infection and also uncovered novel mechanisms by which viruses evade innate immunity, describing a poxvirus protein that mimics a host E3 ubiquitin-ligase to evade the NF-κB pathway. diseases. His core expertise is in host/virus interactions.

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