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All attempts at controlling the spread of diseases by transgenic mosquitoes are ineffective, inefficient, costly, and hazardous to varying degrees

Considerable controversy has been aroused by Oxitec, a UK company based in Oxford, over its releases of transgenic mosquitoes designed to control the spread of dengue fever, which at the same time, highlighted the gross inadequacy of the regulation of transgenic insects releases worldwide (Regulation of Transgenic Insects Highly Inadequate and Unsafe, SiS 54).

More important than the adequacy of regulation is whether transgenic insects are a solution to the problem of disease control. 

Population reduction by introducing dominant lethal gene

Transgenic mosquitoes such as those created by Oxitec are designed to reduce or eradicate natural populations of disease vectors, whereas newer approaches are designed instead to replace natural populations with the minimum of ecological disturbance.

For far too long, the extermination of the insect vector has been the preferred option to controlling the spread of infectious disease, starting with DDT and other toxic insecticides.  Not surprisingly, the first efforts in creating transgenic mosquitoes followed the same path, and Oxitec was no exception. It consisted in the ‘release of insects with a dominant lethal’ (RIDL) intended to reduce natural populations (see Terminator Mosquitoes to Control Dengue? SiS 39). Oxitec’s transgenic mosquitoes were created with the transposon (jumping gene) piggyBac, the dominant lethal gene incorporated is tTA, coding for the tetracycline-repressible transcription activator protein, which when expressed at high levels kills the developing embryo, for reasons still unknown (Can GM Mosquitoes Eradicate Dengue Fever, SiS 50). When expressed, the tTA protein binds to the tetO operator upstream of the tTA transgene and drives more synthesis of tTA in a positive feedback loop. In the presence of tetracycline, however, tetracycline binds to the tTA protein, and prevents it from binding to tetO, thereby turning off the synthesis of more tTA, allowing the insect embryo to survive.