Rubella virus is a single-stranded, plus-sense RNA virus belonging to
the Togaviridae family. Rubella virus infection causes a benign diseas
e known as rubella or German measles, however infection during early p
regnancy can lead to severe birth defects known as congenital rubella
syndrome (CRS). Sequelae of rubella virus infection include three dist
inct neurological syndromes: a postinfectious encephalitis following a
cute infection, a spectrum of neurological manifestations following co
ngenital infection, and an extremely rare neurodegenerative disorder,
progressive rubella panencephalitis (PRP), that can follow either cong
enital or postnatal infection. The pathogenesis of all three of these
syndromes is incompletely understood. Virus invasion and replication i
n the brain has only been definitively demonstrated in CRS and appears
to account for the majority of neurological lesions observed in this
disease. Immune-mediated pathology is particularly evident in PRP and
may be autoimmune in nature, possibly triggered by molecular mimicry b
etween viral and host epitopes, considering the apparent lack of virus
in the brain. The pathogenesis of rubella encephalitis following acut
e infection has not been determined.