Phenotypic analysis of dengue virus isolates associated with dengue fever and dengue hemorrhagic fever for cellular attachment, replication and interferon signaling ability.

摘要

Eighteen dengue viruses (DENVs) representing all four serotypes, isolated from pediatric patients at children's hospital, Queen Sirikit National Institute of Child Health, Bangkok, Thailand exhibiting a diverse spectrum of disease ranging from uncomplicated dengue fever (DF) to severe dengue hemorrhagic fever (DHF), were tested for their ability to attach to host cells, replicate and interfere with the IFNalpha signaling pathway by interfering with signal transducer and activator of transcription 1 (STAT-1) function. Although most isolates suppressed IFNalpha-induced STAT-1 phosphorylation, our results showed no difference between DENV strains associated with DF and those associated with DHF. However, the DHF isolates tended replicate to higher titers in dendritic cells (DCs) than the DF isolates, but this ability was independent of their cell-binding capability. Our results suggest that the emergence early in infection of viruses with a high degree of replication fitness may play an important role in DENV pathogenesis.