EFFECT OF TEMPERATURE SURVIVAL AND RATE OF VIROGENESIS OF AFRICAN HORSE SICKNESS VIRUS IN CULICOIDES-VARIIPENNIS SONORENSIS (DIPTERA, CERATOPOGONIDAE) AND ITS SIGNIFICANCE IN RELATION TO THE EPIDEMIOLOGY OF THE DISEASE

Culicoides variipennis sonorensis Wirth & Jones and C. nubeculosus (Me igen) were orally infected with African horse sickness virus (AHSV) ty pe 9 and subsequently incubated at 10, 15, 20 and 25 degrees C (R.H. 3 0% +/- 10%). A time course of infection rates and virus titres was rec orded by assaying flies individually or in pools, and survival rates o f flies were also estimated. Survival rates at 10, 15 and 20 degrees C were very similar and 80-90% of flies remained alive after 14 days; a t 25 degrees C after the same period survival was reduced to 40%. None of the C. nubeculosus became persistently infected with AHSV, but the virus took longer to clear as the incubation temperature dropped. At temperatures of 10, 15, 20 and 25 degrees C virus was undetectable on days 12, 8, 5, and 4 days post infection (dpi), respectively. In C. v. sonorensis both the infection rate and rate of virogenesis were relat ed to temperature. At 25 degrees C a maximum mean titre of 10(4.3) TCI D50/fly was reached by 9 dpi and the infection rate remained between 6 0 and 80%. At 20 degrees C virogenesis was slower and a maximum mean t itre of 10(4.3) TCID50/fly was reached only after 23 days; the infecti on rate was also reduced to 50-70%. At 15 degrees C there was an overa ll decline in virus titre with time, although between 12 and 15 dpi so me pools of flies contained 10(3.0)-10(4.0) TCID50/fly, demonstrating that virogenesis can occur. The infection rate at this temperature dec reased dramatically to 0-15% after 9 dpi. At 10 degrees C there was no detectable virogenesis and all pools tested at 13 dpi were negative. The apparent infection rate dropped to 0-5% between 13 and 35 days pos t infection. However, when surviving flies were then returned to 25 de grees C for 3 days the infection rate increased to 15.5%. It therefore appears that at low temperatures the virus does not replicate but inf ectious virus may persist at a level below that detectable by the usua l assay systems. The implications of these findings for the epidemiolo gy of AHS are discussed.