No Bite, No Disease

Researchers identify an evolutionary transformation that stops mosquitos from biting, providing the basis for a new strategy to control the spread of mosquito-borne diseases

A Wyeomyia smithii mosquito whirrs about the forest, darting under tree branches at the edge of a murky pond in rural Maine. A hiker, sitting with feet in the water, hears the distinct high-pitched tone of the mosquito whizzing by her ear before landing on her bare arm. She would swat the pest away, but this hiker knows that Wyeomyia smithii mosquitos in the north of the United States don’t bite. Only the southern ones, down in places like Florida, are known to take a blood meal. 

Until recently, evolutionary changes accounting for the difference in biting behavior between these two mosquito populations were unknown. In a study published November 28, 2017, in the Proceedings of the National Academy of Sciences, researchers identified distinct evolutionary changes in non-biting mosquitos' metabolism and sensory systems. This finding provides a launchpad to uncover universal nonbiting genes that scientists can manipulate to control mosquito-borne diseases. 

“Hundreds of laboratories have been employing heroic means to eradicate pathogens of humans transmitted by mosquitoes,” says scientist William Bradshaw, the study's lead author. “All these efforts assume that a bite will occur. However, what if there is no bite? If there is no bite, there is no disease transmission.” 

Vector-borne diseases are a significant world health issue and are responsible for over 700,000 deaths per year, according to the World Health Organization. Mosquitos are the number one culprit of vector-borne disease spread, killing more people than any other animal. They are invasive in many parts of the world, rapidly spreading through human activities. Most methods to reduce the transmission of vector-borne diseases have focused on reducing mosquito populations, preventing transmission of disease between mosquitos, or treating the diseases once the human host is already infected. 

Biologists William Bradshaw and Christina Holzapfel wanted to try something different: manipulating mosquito bite behavior to control the spread of disease. The first step was identifying the genetic differences between the biting and nonbiting populations.

Bradshaw and Holzapfel bred three populations of mosquitos: Florida mosquitos with a low propensity to bite, Florida mosquitoes with a high propensity to bite, and Maine mosquitos that are obligate non-biters, meaning they do not bite at all. This allowed them to compare Florida biting and non-biting mosquitos from the same genetic background and Maine nonbiting mosquitos with a different genetic background. Using a technique called differential gene expression analysis, the researchers identified specific sets of genes that differ between the biting and nonbiting populations. By comparing the genetic backgrounds, they were able to eliminate other sets of genes unrelated to biting behavior. 

They found that biting mosquitos had increased expression of genes related to smell, breakdown of proteins, cell proliferation, and ovarian development. These processes help the female to find a host, turn the blood meal into usable material, and reproduce. But each of these processes come at a cost. It is energetically expensive to find a host and to break down the proteins in the blood. “Blood feeding is not a free lunch” says Bradshaw. “The added nutritional benefits of blood feeding are balanced by both extrinsic and intrinsic costs“ of finding a host and breaking down its blood.  

Now that the researchers have identified that there are distinct physiological changes associated with a non-biting lifestyle, the important remaining question is what genes control this shift. Their long term goal is to develop new stategies to reduce or completely stop biting behavior in disease-carrying mosquitos. 

Other authors include Joshua Burkhart and Rudyard Borowczaka of the University of Oregon, John K. Colbournec of the University of Birmingham, Jacqueline Lopez and Michael E. Pfrender of the University of Notre Dame, and David L. Denlinger and Julie A. Reynolds of Ohio State University.

This work was supported by National Science Foundation Grants IOS-1255628 (to W.E.B.) and DEB-1455506 (OPUS) (to W.E.B. and C.M.H.).

DOI: 10.1073/pnas.1717502115

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