Abstract
Increased serum and mRNA levels of cytokines in patients with dengue virus (DV) infection suggest that cytokines are one of the key factors in the pathogenesis of disease caused by this virus. Here, we tested 211 serum and 56 mRNA samples from an equal number of dengue cases to determine the levels of interleukin-8 (IL-8), interferon gamma (IFN-γ), interleukin-10 (IL-10) and transforming growth factor beta (TGF-β). A total 70 serum and 15 mRNA samples from healthy individual were also tested for cytokines and served as controls. Serum and mRNA levels of IL-8 were highest in the earlier days of dengue infection. IFNγ levels peaked one or two days before defervescence. Levels of IL-10 and TGF-β were highest later in dengue infection, and TGF-β levels peaked on the day of defervescence. Mean levels of IFNγ, TGF β and IL-10 were higher in samples from dengue cases, irrespective of severity, than in healthy controls. In contrast, the level of IL-8 was significantly higher in samples from severe dengue cases and lower in cases of dengue without warning signs than in healthy controls. Children (82.2 % of 101 paediatric cases) commonly had severe dengue illness. Samples that were positive for anti-DV IgG antibody had higher levels of IL-8 and TGF β. DV-2 infections were associated with severe dengue illness. IL-8 and IFNγ levels were higher in the presence of warning signs of severe dengue. Levels of IL-8, IL-10 and TGF β were independently associated with disease outcome. These data provide evidence of an association of IL-8, IFNγ, TGF β and IL-10 levels with the severity of dengue illness. Especially, IL-8 levels can be used as a predictor of severe DV infection.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.