The Dengue virus contains discretely folded RNA structures that confer the ability to resist a powerful host cell enzyme and produce a disease-inducing noncoding RNA.
Talaromyces (Tsp_PR) fungus render Aedes aegypti mosquitoes more susceptible to dengue virus infection through secreted molecules that impair midgut digestive enzyme transcription and activity.
Proteins produced by mast cells modulate the permeability of blood vessels, and may determine whether patients infected with dengue virus develop life-threatening complications.
Despite size heterogeneity, an epitope-resurfaced mature-form dengue VLP has the potential to induce quaternary structure-recognizing broad cross-reactive neutralizing antibodies.
Investigation of antibody responses to variant Dengue virus proteins demonstrate new mechanisms that could increase the potential for vaccines to protect against mutable pathogens such as Flu, Dengue and HIV.
Building on previous work (St John et al., 2013), we explain why secondary infection by dengue virus is associated with more severe vascular disease than primary infection.
In vivo study of arbovirus infections reveals the dominant role of pDC IRF7-signaling in directing both type I and II IFN responses, and leading to viral control.
