J. Chinsangaram et al., Ability of foot-and-mouth disease virus to form plaques in cell culture isassociated with suppression of alpha/beta interferon, J VIROLOGY, 73(12), 1999, pp. 9891-9898
A genetic variant of foot-and-mouth disease virus lacking the leader protei
nase coding region (A12-LLV2) is attenuated in both cattle and swine and, i
n contrast to wild-type virus (A12-IC), does not spread from the initial si
te of infection after aerosol exposure of bovines, We have identified secon
dary cells from susceptible animals, i.e., bovine, ovine, and porcine anima
ls, in which infection with A12-LLV2, in contrast to A12-IC infection, does
not produce plaques; this result indicates that this virus cannot spread f
rom the site of initial infection to neighboring cells. Nevertheless, A12-L
LV2 can infect these cells, but cytopathic effects and virus yields are sig
nificantly reduced compared to those seen with A12-IC infection. Reverse tr
anscription-PCR analysis demonstrates that both A12-LLV2 and A12-IC induce
the production of alpha/beta interferon (IFN-alpha/beta) mRNA in host cells
, However, only supernatants from A12-LLV2-infected cells have significant
antiviral activity. The antiviral activity in supernatants from A12-LLV2-in
fected embryonic bovine kidney cells is IFN-alpha/beta specific, as assayed
with mouse embryonic fibroblast cells with or without IFN-alpha/beta recep
tors, The results obtained with cell cultures demonstrate that the ability
of A12-IC to form plaques is associated with the suppression of IFN-alpha/b
eta expression and suggest a role for this host factor in the inability of
A12-LLV2 to spread and cause disease in susceptible animals.