Vector Incompetency: Its Implication in the Disappearance of Epizootic Venezuelan Equine Encephalomyelitis Virus from Middle America1

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Abstract
Mesenteronal infection and transmission thresholds for several Middle American epizootic and enzootic Venezuelan equine encephalomyelitis (VEE) viruses were evaluated in field-collected (Guatemala) and colonized individuals of the enzootic vector mosquito Culex (Melanoconion) taeniopus. Approximate thresholds for 3 epizootic, hemagglutination-inhibition (HI) subtype I-AB strains were 104.0 chick embryo cell (CEC) plaque-forming units (pfu) per blood meal. Infection rates never exceeded 33%, despite oral doses as high as 105.4 CEC pfu. Mosquitoes were incapable of transmitting epizootic viruses to hamsters even after oral doses of 105.4 CEC pfu and 21 days of extrinsic incubation. In contrast, infection thresholds for 3 enzootic, HI subtype I-E viruses were less than 100.7 CEC pfu, as were transmission thresholds. Mesenteronal 50% infectious doses were also less than 100.7 for all enzootic strains evaluated. The possibility of transovarial transmission of VEE viruses was evaluated by rearing progeny from Aedes taeniorhynchus mosquitoes infected with a Middle American epizootic VEE virus strain. No virus was recovered from 1,037 fourth-instar larvae reared at 20 or 27 °C. Culex taeniopus mosquitoes were also infected with enzootic viruses and progeny from 2nd and subsequent ovarian cycles tested for infectious virus. Vertical transmission was not detected despite assays of 5,077 fourth-instar larvae reared at 20 or 27 °C. Epidemiological implications of these findings related to postepizootic survival of HI subtype I-AB viruses in Middle America are discussed.

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