The ability of IFN pre-treatment to inhibit subsequent dengue replication has been previously reported [9, 40] , as has the importance of IFN in the anti-viral response [41] . Our results indicated that viperin was one of the most highly upregulated genes in all models following dengue infection. Viperin encodes for an IFN-inducible antiviral protein shown to be associated with the endoplasmic reticulum and redistributed to the Golgi apparatus and cytoplasmic vacuoles following human cytomegalovirus (HCMV) infection [26] . The induction of viperin has been suggested to be anti-viral in both HCMV [26] and hepatitis C (HCV) [27] infections, but this is its first association with dengue infection. The use of viperin overexpressing A549 cells demonstrated that, in addition to being significantly upregulated during infection, viperin is directly involved in the anti-viral response to dengue, as shown by the suppression of dengue replication in the presence of increased expression of viperin. This effect was not as significant as the effect of IFNb alone suggesting that viperin is only a part of the IFN-mediated response to dengue. The molecular mechanism of the action of viperin to counter dengue infection will need to be further studied.