When a mosquito bites someone infected with dengue virus (DENV), the virus needs to complete its lifecycle in the mosquito's gut, eventually infecting its salivary glands, before it can infect another person.
Previous studies have shown that mosquitoes rely on a molecular pathway dubbed JAK/STAT to try to fight DENV infection and stop this cycle.
Proteins known as Dome and Hop are involved in turning on the JAK/STAT when the mosquito is infected with DENV.
Mosquitoes with engineered versions of Dome or Hop that were then infected with DENV had 78.18 per cent (Dome) and 83.63 per cent (Hop) fewer copies of the virus in their guts, as well as significantly less virus in their salivary glands.
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When the researchers repeated the experiments with Zika virus and chikungunya virus, no impact was seen on infection, suggesting that the importance of the JAK/STAT pathway in the fatbody tissue is unique to DENV.
"Recently developed powerful mosquito gene-drive systems, that are under development, are likely to make it possible to spread pathogen resistance in mosquito populations in a self-propagating fashion, even at a certain fitness cost," they said.
After decades of research and countless control attempts, dengue fever - a mosquito-borne viral disease - continues to infect an estimated 390 million people around the world each year.
The study appears in the journal PLOS Neglected Tropical Diseases.
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