Are antiviral effects of arsenic trioxide in coxsackievirus B3 infection associated with NFκB and IFN-γ expression in infected mouse tissues?
(English)Manuscript (preprint) (Other academic)
Today, efficient antiviral drugs targeting acute RNA virus infections, such as coxsackievirus B3 (CVB3) are lacking. Arsenic trioxide (As2O3) was recently found to impair the replication of CVB3 in vitro and in vivo, but it is unknown whether this antiviral effect of As2O3 involves immune-mediated effects. In this study CVB3-infected Balb/c mice were intraperitoneally treated daily with 1 mg As2O3/kg bw for 3, 5 or 7 days. The expression of two genes mediating host defence reactions, nuclear factor κB (NFκB) and interferon γ (IFN-γ), was measured by real-time PCR in the liver, brain and pancreas. In the infected brain As2O3 treatment resulted in an earlier response of IFN-γ, i.e. mice were positive 2 days earlier in the treatment group, but the treatment had no effect on NFκB. In the infected pancreas and liver the expression of both IFN-γ and NFκB remained unaffected by As2O3 treatment. To conclude, As2O3 treatment during infection did not affect NFκB or IFN-γ, except for IFN-γ in the brain. Thus, a reasonable conclusion is that As evolves its antiviral effects mainly by a direct effect on the replication process and to a lesser extent through general host defence-mediated mechanisms.
NFκB; IFN-γ; arsenic trioxide; coxsackie B3 infection
Research subject Infectious Diseases
IdentifiersURN: urn:nbn:se:uu:diva-112045OAI: oai:DiVA.org:uu-112045DiVA: diva2:284472