Dengue virus (DENV) is the causative agent of the world’s most prevalent arboviral disease. A new biocontrol has been developed based on infection of Aedes aegypti vector mosquitoes with the intracellular bacteria Wolbachia. We used experimental evolution in cell lines to test the hypothesis that DENV-2, an RNA virus with large population sizes and high mutation rates, may adapt to counteract the anti-viral effect of Wolbachia. We did not find any significant differences in titer from virus experimentally evolved in the presence of Wolbachia (wMelPop strain) versus controls. Oral challenges of mosquitoes did not indicate consistently higher infection rates or virus titers, in either wildtype or Wolbachia-infected mosquitoes, by virus evolved in the presence of the bacteria versus controls. Regardless of the presence of Wolbachia, virus evolved in alternating insect and vertebrate cell line passage consistently produced higher titers compared to virus evolved only in insect cells. Alternating passage also resulted in greater stochastic loss of virus replicates that were evolved in the presence of Wolbachia versus controls. Our results indicate a lack of adaptation in DENV-2 to counter Wolbachia, at least over the short term. The results may be useful in predicting the evolutionary consequences and thus long term utility of Wolbachia-based biocontrol.