Aedes densonucleosis virus (family Parvoviridae, genus Brevidensovirus, AeDNV) is a mosquito pathogen that increases Aedes aegypti larval mortality and reduces adult life span. We conducted three laboratory population cage trials, each lasting 16–25 wk. We tested two broad hypotheses. First, Ae. aegypti raised in containers seeded with 10⁸ AeDNV genome equivaIents/ml (geq/ml), a concentration feasible for field application, increase AeDNV to concentrations that cause significant adult and larval mortality. Second, infected female mosquitoes disperse AeDNV to uninfected larval habitats. In hypothesis 1, we addressed the rate at which infected larvae secrete virus, how AeDNV titers change in seeded containers over time, whether AeDNV decays over time, and whether AeDNV exposed populations are reduced. In hypothesis 2, we monitored AeDNV concentrations in novel containers after oviposition by infected females. Both hypotheses were supported. Larvae increased AeDNV, secreting virus at a rate of 2.14 × 10⁶ geq/larva/d when exposed to 10⁸ geq/ml. AeDNV titers reached an asymptote of 10¹⁰ geq/ml by week 10 in seeded containers. AeDNV decayed by 1 log every 4 d as indicated by a reduction in larval mortality. Adult population size was reduced in treated populations. Infected females dispersed AeDNV to novel containers, with titers reaching 10⁸ geq/ml. The parameters were used in a Leslie-Lewis matrix model. This model predicted that AeDNV negatively affects Ae. aegypti densities and population structure and thus vectorial capacity.