This paper shows that both the infection rate and the rate of virogene
sis of African horse sickness virus (AHSV) within vector Culicoides ar
e temperature dependent. As temperature is reduced from permissive lev
els the lifespan of the vector itself is extended but the rate of viro
genesis decreases and infection rate falls dramatically so that at 10
degrees C virtually all midges are free from virus by 13 days post inf
ection (dpi). When vectors that had been kept at this temperature for
35 days were moved to a permissive temperature for 3 days; however, th
e apparent zero infection rate increased to 15.5%. It therefore appear
s that at low temperature (less than or equal to 15 degrees C) AHSV do
es not replicate bur virus may persist in some vectors at a level belo
w that detectable by traditional assay systems and when the temperatur
e later rises to permissive levels virus replication is able to commen
ce. On the basis of this information an overwintering mechanism for AH
SV is suggested. The temperature at which the immature stages of Culic
oides are reared may also influence infection with AHSV. A 5-10 degree
s C rise in larval developmental temperature resulted in an increase i
n oral infection rate of a normally non-vector species of Culicoides,
from < 1% to > 10%. A mechanism is suggested.