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An Interspecific Mosquito Model for the Mesenteronal Infection Barrier to Western Equine Encephalomyelitis Virus (Culex Tarsalis and Culex Pipiens)
Edward J. Houk
Edward J. Houk
Naval Biosciences Laboratory and Department of Biomedical and Environmental Sciences, School of Public Health, University of California, Berkeley, California 94720
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Laura D. Kramer
Laura D. Kramer
Naval Biosciences Laboratory and Department of Biomedical and Environmental Sciences, School of Public Health, University of California, Berkeley, California 94720
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James L. Hardy
James L. Hardy
Naval Biosciences Laboratory and Department of Biomedical and Environmental Sciences, School of Public Health, University of California, Berkeley, California 94720
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Sally B. Presser
Sally B. Presser
Naval Biosciences Laboratory and Department of Biomedical and Environmental Sciences, School of Public Health, University of California, Berkeley, California 94720
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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 cells 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.
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