Culex tarsalis, a putative mosquito vector of
western equine encephalomyelitis (WEE) virus, is susceptible to peroral
infection by WEE virus. The nonvector mosquito, Culex pipiens, has a very high peroral threshold of
infection and is considered to be refractory. By parenteral inoculation, both mosquito species are equally susceptible. Thus, Cx. tarsalis and Cx. pipiens represent an excellent model system to examine the mechanisms for the mesenteronal
infection barrier to WEE virus. Diethylaminoethyl (
DEAE)-dextran (1.6 mg/ml), when added to a pledget bloodmeal that contained high concentrations of WEE virus, enhanced peroral
infection rates of Cx. pipiens. In Cx. tarsalis, a reduction in
infection rates was observed when low WEE concentrations of virus were ingested.
DEAE-dextran had no apparent effects on the dissemination of WEE after
infection of either mosquito species. It is suggested that the peroral enhancement of WEE
viral infection observed with Cx. pipiens may be related to random, nonspecific mechanisms of
infection, since it requires high titers of ingested WEE virus. Interference with specific binding of WEE virus to cellular receptor sites is suggested to explain the reduction in WEE
viral infection rates in Cx. tarsalis. Altering the pH of the ingested infectious bloodmeal did not affect the WEE
viral infection rate of Cx. pipiens, within the range of 6.0-8.5. Cx. tarsalis was optimally infected when the infectious bloodmeal was pH 8.0, and the
infection rate was significantly reduced when the infectious blood was at either extreme of the pH range tested. This is again interpreted to indicate that different mechanisms control the peroral
infection of Cx. tarsalis and Cx. pipiens with WEE virus. The mesenteronal
infection barrier to WEE virus in Cx. pipiens is associated with an inability of the virus to adsorb and/or penetrate mesenteronal epithelial when administered perorally. The barrier is not related to an inability of the Cx. pipiens mesenteronal epithelial cells to support viral multiplication since these cells become infected when the virus is administered parenterally.