We are investigating the molecular mechanisms of rubella
virus (RV) pathogenesis. RV, the causative agent of German
measles, can cause human fetal death or multisystem birth
defects and is associated with arthropathy in persistently
infected individuals (11). RV, a member of Togaviridae,
possesses a (+)-stranded RNA genome, and little is known
about the molecular events occurring during its life cycle
(12-14). We have shown (15) that an inverted repeat sequence
of 12 nt, located at the 3' end of genomic RNA and capable
of forming a stem-loop (SL) structure, is necessary for
initiation of (-)-strand synthesis. In Vero 76 cells, permissive
for viral replication, the existence of a host protein (=60 kDa)
that interacts specifically with the 3' (+)-SL RNA has been
demonstrated (5). An increase in the affinity of host protein
binding activity is observed after RV infection (5), coinciding
temporally with the appearance of (-)-strand RNA synthesis