After infection one can approximate the novel gene regulation to be a combination of the host wild type gene regulation, perturbed by the Wolbachia gene regulatory network.
The metabolic rate of the Wolbachia will be a function of genome variations in the wild type population. The population (even if fully infected) thus has access to a whole bunch of knobs (promoter region binding affinities) and can continuously shed the metabolic burden of the parasite by natural selection, since 2 infected mosquitos, with differing levels of Wolbachia metabolism / reproduction, will have more energy and amino acids available for flight, healinig / repair, eggs, ... so that over a number of generations the Wolbachia incidence rate falls back to equilibrium levels. Then its a matter of time until a dormant virus or a one of the many virus particles scattered in nature and a mosquito meet again.
lets say on the order of 1 billion, and let's assume the effectivity doesn't change when considering the 30% unaffected population
it would need to be applied to the surviving 30% repeatedly:
0.3 ^ N = 1 / 1B
so N = log(1B)/log(10/3) = ~17.2 times.
I predict nature protects itself with diversity: some of the male and female wild type will have natural aversion from, attraction to or neutral stance the modified Wolbachia carriers.
I predict that those mosquito family lines that happen to be more Wolbachia-carrier averse become enriched over time.
There is an energetic cost to maintaining a parasitic lifeform, and that energetic term will always favor immunity against the parasite.