Pathogenesis, Clinical Findings and Immunity in Rubella


Rubella affects unvaccinated individuals. The infection is transmitted via airborne route. Transmission rate for non-vaccinated exceeds 80-90%.

Vertical “mother-to-child” transmission results in congenital rubella syndrome.

Rubella is anthroponotic disease – the source of infection is solely human.

The upper respiratory tract and nasopharyngeal lymphoid tissue are the first sites of viral replication. Next the virus migrates to regional lymph nodes.

Incubation period of the disease lasts 2-3 weeks.

The clinical manifestations of RV infection in adults are generally mild, and many infections are asymptomatic.

The first clinical sign of rubella is usually the appearance of a macropapular rash. Other symptoms typically include low-grade fever, lymphadenopathy, sore throat, etc. Lymphadenopathy is typical, involving the posterior cervical and occipital nodes. Rubella can cause complications with joint involvement such as transitory arthritis.

However, the main threat for public health is the teratogenicity of rubella virus.

Maternal infection early in pregnancy results in congenital rubella syndrome (CRS) in infants. The time the infection affects women during gestation can influence CRS outcome. The earlier in gestation the maternal infection occurs, the more severe is the damage to the fetus. Maternal infection during the first 8 weeks inevitably results in fetus disease. In this condition up to 100% of infected fetuses develop congenital defects.

The virus penetrates all fetal tissues. RV is supposed to affect mitochondria, interfering cell respiration, and can cause apoptosis of infected cells.

The risk of fetal infection and the severity of congenital abnormalities decreases after the first trimester; after 17 weeks gestation, the risk of developing any defects is low.

The clinical manifestations of CRS vary significantly. The deafness is the most common. Other clinical features include cardiac disease, mental retardation, and ocular impairments such as cataracts and glaucoma. Non-inflammatory necrosis is observed in affected organs due to viral action.

After disease lifelong humoral IgG-mediated immunity arises. Maternal antibodies protect the newborns against rubella within 4-6 months after birth.