An Indian population of the Aedes aegypti mosquito -- the carrier of dengue virus -- may be developing a resistance to alpha-cypermethrin, a common insecticide used for vector control worldwide, according to a new study.

Findings published in the Frontiers in Tropical Diseases journal show that despite early signs of resistance against alpha-cypermethrin, the mosquitoes have not developed lasting resistance, but this is a warning sign, researchers said.

"We show that an Indian Aedes aegypti mosquito population demonstrated a 97.91 per cent mortality rate when exposed to the recommended diagnostic dose of alpha-cypermethrin. This is an early sign these mosquitoes could be developing resistance to this insecticide," first author Rohit Lakhwani, a researcher at University of Delhi, said.

"Understanding the biological mechanisms that allow mosquitoes to survive this insecticide while resistance is still in its early stages is advantageous," senior author Sarita Kumar, a professor at the Department of Zoology, University of Delhi, said.

Insects are known to produce detoxification enzymes -- proteins to defend against toxic substances -- often within hours of exposure. "When an insecticide enters a mosquito's body, it activates a cellular alarm system. This triggers a cascade of responses within the insect's cells, and ramps up production of defensive proteins," Kumar said.

Detoxification enzymes bind to insecticide molecules, break molecular bonds, and leave behind less harmful compounds that can be excreted.

The team selected five detoxification enzymes that have been previously identified as primary detoxification mechanisms.

They found that beta-esterase -- an enzyme that specialises in breaking down compounds prevalent in insecticides like alpha-cypermethrin -- was most reactive in response to the insecticide.

Activity of beta-esterase was found to increase more than 21-fold following exposure, and it bound very strongly to insecticide molecules.

The result suggested that the enzyme is the primary mechanism through which mosquitoes defend against alpha-cypermethrin, researchers said.

Despite early signs of resistance against alpha-cypermethrin, the mosquitoes have not developed a lasting resistance. Instead, this is a warning sign, the team said.

It is especially true because mosquitoes can develop cross-resistance to insecticides that work similarly, they added.

"Because resistance develops at different speeds, it is not possible to predict when it will become so widespread that alpha-cypermethrin might not work anymore. Resistance at the biochemical level can also reverse if that particular insecticide is no longer used," Kumar said.

Researchers said there are varied ways to overcome detoxification enzymes, for example inhibitors that block defense systems.

Insecticide rotation can also limit resistance by not letting it develop in the first place. Elimination of mosquito breeding sites and biological control can help preserve the effectiveness of existing insecticides and improve long-term control, they said.

The team pointed out that the results are specific to a lab-bred population of Aedes aegypti at a specific point of time, and that resistance levels may be different in other populations, regions, or under natural conditions.

The study, nevertheless, consistently identified beta-esterase as the primary enzyme involved in alpha-cypermethrin detoxification, they said.

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