Whereas iminosugars did not affect surface expression of any of the receptors examined, DENV infection significantly reduced surface IFNγ receptor amongst other changes to total receptor expression.
We have also used ex vivo IFNγ ELISpot assays to determine the functionality of T cell responses in those who were previously naturally infected with dengue and we have determined the frequency of DENV-specific memory T cells responses in relation to past clinical disease severity.
Correction: Peripheral Organs of Dengue Fatal Cases Present Strong Pro-Inflammatory Response with Participation of IFN-Gamma-, TNF-Alpha- and RANTES-Producing Cells.
Severity of Plasma Leakage Is Associated With High Levels of Interferon γ-Inducible Protein 10, Hepatocyte Growth Factor, Matrix Metalloproteinase 2 (MMP-2), and MMP-9 During Dengue Virus Infection.
This research identifies the association of the IFNG (+874 A/T), TNFA (-308G/A), IL-10 (-819 C/T) genotypes as a factor for protection, susceptibility and severity to dengue.
The purpose of the present study was to evaluate the methylation status of the IFN-γ and TNF-α promoters in DNA extracted from dengue infected patients using methylation-specific polymerase chain reaction.
However, Phase 1 clinical evaluation of a prototype monovalent dengue 1 DNA vaccine expressing prM and E genes revealed anti-dengue T cell IFNγ responses, but poor neutralizing antibody responses.
However, while DENV-NS3 specific T cells of those with mild/sub clinical dengue infection were more likely to produce only granzyme B (p=0.02), those who were hospitalized were more likely to produce both TNFα and IFNγ (p=0.03) or TNFα alone.
This study was undertaken to determine the prevalence of dengue clinical symptom persistence during 60days of disease follow up, in patients of Espírito Santo state (ES)-Brazil and to evaluate the relation of single nucleotide polymorphisms (SNPs) in FcγRIIa, CD209, VDR, TNF-α, IL-4, IL-6 and IFN-γ genes with symptom persistence.
In contrast, IFN-gamma receptor-mediated responses seem to act at later stages of DEN disease by restricting viral replication in the periphery and eliminating virus from the CNS.