Skip directly to site content Skip directly to page options Skip directly to A-Z link Skip directly to A-Z link Skip directly to A-Z link
Volume 22, Number 10—October 2016
Letter

Culex pipiens and Aedes triseriatus Mosquito Susceptibility to Zika Virus

Cite This Article

To the Editor: Zika virus, genus Flavivirus, has spread nearly uncontrolled since its introduction into the Western Hemisphere; autochthonous spread has occurred in >39 countries and territories, including several US territories. Transmission of Zika virus is usually by the bite of infected mosquitoes, and potential for emergence in areas with competent mosquito vectors is high (1). Future spread of Zika virus is unpredictable; however, eventual local spread in the United States is possible. As of July 13, 2016, a total of 1,306 travel-associated cases had been reported (ArboNET, https://www.cdc.gov/zika); substantial populations of Aedes (Stegomyia) aegypti (Linnaeus) mosquitoes exist in >16 states in the eastern, southeastern, and southwestern United States; and Ae. (Stegomyia) albopictus (Skuse) mosquitoes inhabit >28 states and continued expansion throughout the northern United States is probable (2). Mosquitoes of these 2 species have demonstrated the ability to transmit Zika virus (1).

The recent epidemic spread of Zika virus suggests that Ae. aegypti mosquitoes are the main vector; however, information about the role of other species in driving and maintaining Zika virus transmission is lacking. Of particular concern this summer (2016) is emergence and establishment of Zika virus in previously unaffected geographic areas; with the advent of mosquito season commencing in most of the continental United States, the likelihood of mosquitoborne transmission of Zika virus in states without populations of Ae. aegypti and Ae. albopictus mosquitoes remains unknown. To understand the potential risk for spread of Zika virus in temperate US states, we compared the relative abilities of Culex pipiens and Ae. triseriatus mosquitoes to transmit Zika virus in the laboratory. We used Ae. aegypti and Ae. albopictus mosquitoes as positive controls.

Laboratory colonies of mosquitoes used in this study were maintained at the University of Wisconsin–Madison, and vector competence for Zika virus was evaluated by using established procedures (3,4). Mosquitoes from each group were incapacitated (exposed to trimethylamine); legs were removed and collected. Salivary secretions were collected in capillary tubes containing a 1:1 ratio of fetal bovine serum and 50% sucrose. Mosquitoes were then placed in individual tubes; their bodies and legs were homogenized, clarified by centrifugation, and screened for virus infection. Dissemination was indicated by virus-positive legs, and transmission potential was indicated by virus-positive salivary secretions. All samples were screened by plaque assay on Vero cells. Mosquitoes were exposed to Asian lineage Zika virus strain PRVABC59 (GenBank accession no. KU501215) (5) by feeding on Zika virus-infected Ifnar−/− mice (4). Mice (n = 4/replicate) yielded infectious blood meal concentrations of 6.02 log10 PFU/mL ± 0.67 (mean ± SD; biological replicate no. 1), 4.74 log10 PFU/mL ± 0.06 (replicate no. 2), and 6.83 log10 PFU/mL ± 0.45 (replicate no. 3). Blood meal concentrations in mice were consistent with viremia concentrations of humans in the field (4).

All samples from Cx. pipiens mosquitoes and all replicates were negative for Zika virus by plaque assay (Table). In contrast, Ae. triseriatus mosquitoes were susceptible to infection when exposed to mice with the highest viremia concentrations (Table). However, none of these infected mosquitoes disseminated virus and none were capable of transmitting the virus. Data from Ae. albopictus and Ae. aegypti mosquitoes that had been exposed to the same mice demonstrated that the viremia concentrations used could productively infect mosquitoes. Of note, Ae. albopictus mosquito infection rates were dose dependent (i.e., infection rates increased with blood meal titer). Furthermore, data generated from exposure to the same mice demonstrated productive mosquito infection with these viremia concentrations (4). It therefore seems likely that if Zika virus circulation in the United States occurs, it will be driven by Ae. albopictus or Ae. aegypti mosquitoes (6). However, we cannot rule out that anthropophilic mosquitoes of other species in this country could be competent vectors.

These data argue for continued studies (experimental and epidemiologic) assessing interactions between differing mosquito–Zika virus combinations in the United States because of geographic variations that may exist in oral susceptibility of mosquitoes of the same or different species. The few vector competence studies conducted to date have focused primarily on Ae. aegypti and Ae. albopictus mosquitoes (8), but mosquitoes of other species may be vectors, depending on geographic location. We focused on Cx. pipiens mosquitoes because they are ubiquitous (7), they are considered one of the principal vectors of West Nile virus in the northern half of the United States, and a recent report from Brazil suggests Cx. quinquefasciatus mosquitoes as potential Zika virus vectors (8). We chose Ae. triseriatus mosquitoes because they are the natural vector and overwintering host of La Crosse virus, they are extremely tolerant to a range of temperatures, they are distributed from Florida to eastern Canada (9), and they have been implicated as potential enzootic vectors for West Nile virus (10). To determine the risk for Zika virus transmission in the United States, surveillance of different human-biting mosquito species will be paramount. Although we expected that Cx. pipiens and Ae. triseriatus mosquitoes would not be competent Zika virus vectors, our experimental verification helps exclude uncertainties surrounding the potential vectors of this emerging pathogen.

Top

Matthew T. AliotaComments to Author , Stephen A. Peinado, Jorge E. Osorio, and Lyric C. Bartholomay

Author affiliations: University of Wisconsin, Madison, Wisconsin, USA

Top

References

  1. Musso  D, Gubler  DJ. Zika virus. Clin Microbiol Rev. 2016;29:487524. DOIPubMed
  2. Kraemer  MU, Sinka  ME, Duda  KA, Mylne  AQ, Shearer  FM, Barker  CM, The global distribution of the arbovirus vectors Aedes aegypti and Ae. albopictus. Elife. 2015;4:e08347.DOIPubMed
  3. Aliota  MT, Walker  EC, Uribe Yepes  A, Dario Velez  I, Christensen  BM, Osorio  JE. The wMel strain of Wolbachia reduces transmission of chikungunya virus in Aedes aegypti. PLoS Negl Trop Dis. 2016;10:e0004677. DOIPubMed
  4. Aliota  MT, Peinado  SA, Velez  ID, Osorio  JE. The wMel strain of Wolbachia Reduces Transmission of Zika virus by Aedes aegypti. Sci Rep. 2016;6:28792 .DOIPubMed
  5. Lanciotti  RS, Lambert  AJ, Holodniy  M, Saavedra  S, Signor  LDCC. Phylogeny of Zika virus in Western Hemisphere, 2015. Emerg Infect Dis. 2016;22:9335. DOIPubMed
  6. Chouin-Carneiro  T, Vega-Rua  A, Vazeille  M, Yebakima  A, Girod  R, Goindin  D, Differential susceptibilities of Aedes aegypti and Aedes albopictus from the Americas to Zika virus. PLoS Negl Trop Dis. 2016;10:e0004543. DOIPubMed
  7. Farajollahi  A, Fonseca  DM, Kramer  LD, Marm Kilpatrick  A. “Bird biting” mosquitoes and human disease: a review of the role of Culex pipiens complex mosquitoes in epidemiology. Infect Genet Evol. 2011;11:157785. DOIPubMed
  8. Franca  RFO, Neves  MHL, Ayres  CFJ, Melo-Neto  OP, Filho  SPB. First International Workshop on Zika Virus held by Oswaldo Cruz Foundation FIOCRUZ in Northeast Brazil March 2016—a meeting report. PLoS Negl Trop Dis. 2016;10:e0004760. DOIPubMed
  9. Darsie  RF, Ward  RA. Identification and geographical distribution of the mosquitoes of North America, North Mexico. Gainesville (FL): University Press of Florida; 2005.
  10. Erickson  SM, Platt  KB, Tucker  BJ, Evans  R, Tiawsirisup  S, Rowley  WA. The potential of Aedes triseriatus (Diptera: Culicidae) as an enzootic vector of West Nile virus. J Med Entomol. 2006;43:96670. DOIPubMed

Top

Table

Top

Cite This Article

DOI: 10.3201/eid2210.161082

Related Links

Top

Table of Contents – Volume 22, Number 10—October 2016

Comments

Please use the form below to submit correspondence to the authors or contact them at the following address:

Address for correspondence Matthew T. Aliota, Department of Pathobiological Sciences, University of Wisconsin-Madison, 1656 Linden Dr, Madison, WI 53706, USA

Send To

character(s) remaining.

Comment submitted successfully, thank you for your feedback.

Top

Page created: September 20, 2016
Page updated: September 20, 2016
Page reviewed: September 20, 2016
The conclusions, findings, and opinions expressed by authors contributing to this journal do not necessarily reflect the official position of the U.S. Department of Health and Human Services, the Public Health Service, the Centers for Disease Control and Prevention, or the authors' affiliated institutions. Use of trade names is for identification only and does not imply endorsement by any of the groups named above.
file_external