Chapter 1 Molecular Virology of Rubella Virus

Abstract

Publisher Summary Rubella virus is a potent, infectious, teratogenic agent that continues to cause devastating epidemics of congenital rubella syndrome (CRS) in much of the world Viruses isolated from CRS cases are identical to viruses from postnatal rubella cases. There is significant sequence variation among the currently circulating rubella viruses; although a specific antigenic site in the E2 protein recognized a monoclonal antibody in western blots is not conserved, overall there is only one serotype of rubella viruses. There is sufficient variability in currently circulating rubella viruses to allow the molecular epidemiology of rubella viruses to support rubella control and elimination activities. Some rubella virus genotypes are geographically restricted, allowing sporadic cases caused by these genotypes in other locations to be considered importations. In addition, p90 has been shown to interact with both the retinoblastoma tumor suppressor protein and the cytokinesis regulatory protein, citron-K kinase. There is evidence that a balance between cellular survival signals and normal proliferative signals is needed for optimal virus growth. It is noted that molecular evidence for the mechanism(s) of teratogenesis are lacking in humans or animal models. These works in cell lines suggest that interactions between rubella proteins (e.g. p90) with cellular proteins that regulate cell growth may be the reason why rubella virus is a potent human teratogen.