IDentification of helper T cell epitopes of dengue virus E-protein
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Induction of virus-specific neutralizing immune response against West Nile and Japanese encephalitis viruses by chimeric peptides representing T-helper and B-cell epitopes
2012, Virus ResearchCitation Excerpt :This can be achieved by incorporating B-cell and T-helper epitopes in the form of a single chimeric peptide. T-helper epitopes have also been identified for many viruses (Kumar et al., 2004; Leclerc et al., 1993; Mathews et al., 1991; Roehrig et al., 1994). Earlier studies from author’ laboratory identified T-helper epitopes on JE, WN and DEN viruses (Kutubuddin et al., 1991).
Immunogenicity of novel Dengue virus epitopes identified by bioinformatic analysis
2010, Virus ResearchCitation Excerpt :However, these approaches have not been fully explored in the case of DENV. For example, initial studies focused on the prediction of epitopes from the E, prM or NS1 proteins allowed the identification of B and T cell epitopes in DENV-2 (Vázquez et al., 2002; Leclerc et al., 1993; Jiang et al., 2010). Analyzing proteins C, E and NS3 for CD4+ T cell epitopes, Wen et al. (2007) identified four new epitopes which stimulated IFN-γ production and proliferation of PBMC isolated from DF convalescent patients infected with DENV-1.
Secondary heterologous dengue infection risk: Disequilibrium between immune regulation and inflammation?
2010, Cellular ImmunologyCitation Excerpt :Written informed consent was obtained from each individual upon enrollment in the study. DENV antigens were prepared as previously described [21]. C636 cell lines from A. albopictus were grown to confluence, infected at a multiplicity of infection of 0.1 particle forming unit (pfu) per cell with the dengue strains DENV-1–113 Peru 1990, DENV-2 A15 Cuba 1981 and DENV-3 116 Cuba 2000, and cultured in Minimum Essential Medium (MEM) supplemented with 2% fetal calf serum.
Chapter 1 The History and Evolution of Human Dengue Emergence
2008, Advances in Virus ResearchCitation Excerpt :Due to the small sample size of DENV‐1 sequences, no positively selected sites were detected; however, weak positive selection was detected in both DENV‐3 (2 sites) and DENV‐4 (5 sites), and in the Cosmopolitan (2 sites) and lineage 2 of the Asian (17 sites) DENV‐2 genotypes. The majority of the selected sites (E‐169 of DENV‐3; E‐357 and E‐429 of DENV‐4; and E‐52, E‐85, E‐90, E‐122, E‐131, E‐144, E‐170, E‐330, E‐334, E‐342, E‐378, and E‐392 of DENV‐2) were located within or near potential B‐ or T‐cell epitopes (Aaskov et al., 1989; Innis et al., 1989; Kutubuddin et al., 1991; Leclerc et al., 1993; Megret et al., 1992; Roehrig et al., 1994), an association that suggests immune evasion as a selective factor (Twiddy et al., 2002). A number of selected sites were also located within functional domains involved in cell tropism (E‐380 of DENV‐3; E‐342, E‐378 and E‐392 of DENV‐2) or fusion (E‐108 and E‐131 of DENV‐4; E‐52, E‐98, E‐100, E‐105, E112 and E‐113 of DENV‐2), suggesting that cell tropism and/or virus‐mediated membrane fusion may also confer selective advantages by increasing fitness.
Antigenic Structure of Flavivirus Proteins
2003, Advances in Virus ResearchCitation Excerpt :The third peptide, DEN 2 aa 9–19, elicited a serotype-specific response that was also mouse haplotype dependent. A second study utilized the previously described trpE fusion proteins of DEN 2 virus and identified three large regions (aa 22–205, 267–354, and 366–424) that stimulated an in vitro blastogenic response of virus-primed lymphocytes (Leclerc et al., 1993; Megret et al., 1992). Four peptides (aa 135–157, 270–298, 295–307, and 337–359) capable of eliciting an in vitro blastogenic response of virus-primed lymphocytes were subsequently identified.