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Rubella virus replication and links to teratogenicity.

J Y Lee¹, D S Bowden

¹Research and Molecular Development Division, Victorian Infectious Diseases Reference Laboratory, North Melbourne, Victoria 3051, Australia. jia-yee.lee@mh.org.au

Clinical Microbiology Reviews

|October 12, 2000

Summary

Rubella virus (RV) causes German measles, a mild childhood illness. However, RV infection during pregnancy can lead to congenital rubella syndrome (CRS), causing birth defects.

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Area of Science:

Virology
Immunology
Teratology

Background:

Rubella virus (RV) causes German measles, a globally endemic human disease.
While typically mild, rubella complications include polyarthralgia and rare serious sequelae.
The primary public health concern is rubella's teratogenicity, leading to congenital rubella syndrome (CRS).

Purpose of the Study:

To elucidate the mechanisms of rubella virus teratogenesis.
To investigate rubella virus replication and virus-host interactions in fetal tissues.
To understand how RV infection leads to congenital defects.

Main Methods:

Analysis of cytopathology in RV-infected fetal tissues.
Observation of RV replication in cell culture.

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Investigation of mitochondrial abnormalities and cytoskeletal disruption during RV infection.

Main Results:

RV infection in fetal tissues suggests necrosis, apoptosis, and inhibited cell division.
Cell culture studies reveal unusual RV replication features, including mitochondrial and cytoskeletal abnormalities.
These cellular disruptions are hypothesized to contribute to RV teratogenesis.

Conclusions:

The exact pathway of RV teratogenesis remains unclear.
Observed cytopathology and replication anomalies likely play a role in causing congenital defects.
Further research into RV replication and host interactions is crucial for understanding and preventing CRS.