Mosquitoes infected with the bacteria Wolbachia are more likely to become infected with West Nile virus and more likely to transmit the virus to humans, according to a team of researchers.
PLOS Neglected Tropical Diseases
“Previous research has shown that Wolbachia — a genus of bacteria that live inside mosquitoes — render mosquitoes resistant to pathogen infection, thereby preventing the mosquitoes from infecting humans with the pathogens,” said Jason Rasgon, associate professor of entomology, Penn State. “As a result, researchers are currently releasing Wolbachia-infected mosquitoes into the wild as part of a strategy to control Dengue virus. They also are investigating Wolbachia as a possible control strategy for malaria.”
Expecting to find that Wolbachia would block infection by West Nile virus in the same way that it blocks Dengue virus, Rasgon and his colleagues — which include researchers at the University of Maryland, the New York State Department of Health and the State University of New York at Albany — injected the Wolbachia bacteria into adult female Culex tarsalis mosquitoes. They then allowed the Wolbachia to replicate inside the mosquitoes and fed the mosquitoes a meal of blood that was infected with West Nile virus.
“We were surprised to find that Wolbachia infection did not block West Nile virus in this mosquito,” Rasgon said. “Instead, these mosquitoes had significantly higher West Nile virus infection rates seven days after they we fed them the infected blood. In other words, Wolbachia infection allowed the mosquitoes to become infected with West Nile virus faster than our controls.”
The results will appear in the July 7, 2014 issue of PLOS Neglected Tropical Diseases.
“Our results point to a previously unforeseen complication — the possibility that mosquitoes rendered resistant to one pathogen by Wolbachia infection might become better vectors of an alternative pathogen,” Rasgon said.
According to Rasgon, the team suspected that Wolbachia could enhance some pathogens within mosquitoes.
“Multiple studies suggest that Wolbachia may enhance some Plasmodium parasites in mosquitoes, thus increasing the frequency of malaria transmission to rodents and birds,” he said. “We recently published a paper in the journal PLOS Pathogens in which we summarized the current literature of Wolbachia-mediated pathogen enhancement with particular focus on Plasmodium parasites.”
But, he added, the team did not suspect that Wolbachia would enhance mosquito infection with the human pathogen West Nile virus.
“In this study, we were surprised to find that Wolbachia infection enhances, rather than suppresses, mosquito infection by West Nile virus,” Rasgon said.
The team also found that West Nile virus enhancement in the Wolbachia-infected mosquitoes occurred in conjunction with the suppression of genes associated with the mosquitoes’ anti-viral immune response. According to Rasgon, the researchers plan to conduct additional experiments to determine the exact mechanism of Wolbachia-based West Nile virus enhancement in Culex tarsalis.
“This is the first study to demonstrate that Wolbachia can enhance a human pathogen in a mosquito,” Rasgon said. “The results suggest that caution should be used when releasing Wolbachia-infected mosquitoes into nature to control vector-borne diseases of humans.”
The National Institutes of Health supported this research.
Other authors on the paper include Brittany Dodson, graduate student in entomology, Penn State; Grant Hughes, research associate in entomology, Penn State; Oluwatobi Paul, researcher in biological sciences, University of Maryland, Baltimore County; Amy Matacchiero, researcher, New York State Department of Health; and Laura Kramer, director, Arbovirus Laboratories, New York State Department of Health and University at Albany-SUNY.
Dodson BL, Hughes GL, Paul O, Matacchiero AC, Kramer LD, et al. (2014) Wolbachia Enhances West Nile Virus (WNV) Infection in the Mosquito Culex tarsalis. PLoS Negl Trop Dis 8(7): e2965. doi:10.1371/journal.pntd.0002965, http://dx.PLOS.org/10.1371/journal.pntd.0002965
Jason Rasgon is available at firstname.lastname@example.org or 814-863-3668
This research was funded by NIH grants R01AI067371, R21AI070178 and R21AI111175 to JLR. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
The authors have declared that no competing interests exist.