Transovarial transmission of St. Louis encephalitis virus by Culex pipiens complex mosquitoes
Francy, D.B.; Rush, W.A.; Montoya, M.; Inglish, D.S.; Bolin, R.A.
American Journal of Tropical Medicine and Hygiene 30(3): 699-705
1981
ISSN/ISBN: 0002-9637 PMID: 6266266 Document Number: 181014
Experiments were conducted to determine whether transovarial transmission of St. Louis encephalitis (SLE) virus occurs in mosquitoes of the complex of Culex pipiens L., the principal vectors of SLE virus in the central-eastern USA. In 1978, field-collected mosquitoes from Memphis, Tennessee and McLeansboro, Illinois, were used; during 1979, colonised mosquitoes from Chicago, Illinois and Memphis, Tennessee, were used. Mosquitoes were infected by feeding on viraemic chicks inoculated with an SLE virus strain isolated from C. pipiens complex mosquitoes collected from Memphis, Tennessee, in 1976. During the 1979 experiments, progeny larval and adult mosquitoes were held at 2 temperatures, 18 and 25 deg C. Progeny were tested for virus by plaque assay in duck embryo cell cultures and by inoculation of C6/36 cells of Aedes albopictus (Skuse) and examination by immunofluorescence. In 1978, most of the progeny tested were from the first ovarian cycle, and a single occurrence of transovarial transmission was documented. In 1979, a single transovarial transmission occurred from 46 856 progeny in the first ovarian cycle, whereas 7 of 9234 progeny of the second ovarian cycle were infected. The rate of transovarial transmission was higher for progeny of Memphis than Chicago mosquitoes, and for mosquitoes held at 18 than 25 deg C; however, these differences were not statistically significant. Four positive pools were of females, and 3 were fed on chicks for transmission attempts. The positive Chicago mosquito pool failed to transmit, but both Memphis pools successfully transmitted virus. The overall rates of transovarial transmission of SLE virus in progeny of the first and second ovarian cycle were, respectively, 1/45 151 and 1/1460. The significance of these results as they relate to the natural history of SLE virus is discussed.