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In spite of the availability of a safe and effective vaccine against rubella, recent worldwide estimates are that more than 100,000 infants are born with CRS annually.<\/jats:p><\/jats:sec><jats:sec><jats:title>RECENT PROGRESS<\/jats:title><jats:p>Recently, several significant findings in the field of cell biology, as well as in the RV replication and virus\u2010cell interactions, have originated from the authors' laboratory, and other researchers have provided insights into RV teratogenesis. It has been shown that 1) an RV protein induces cell\u2010cycle arrest by generating a subpopulation of tetraploid nuclei (i.e., 4N DNA) cells, perhaps representative of the tetraploid state following S phase in the cell cycle, due to its interaction with citron\u2010K kinase (CK); 2) RV infection induces apoptosis in cell culture, and 3) CK functional perturbations lead to tetraploidy, followed by apoptosis, in specific cell types.<\/jats:p><\/jats:sec><jats:sec><jats:title>CONCLUSIONS<\/jats:title><jats:p>Based on several similarities between known RV\u2010associated fetal and cellular manifestations and CK deficiency\u2013associated phenotypes, it is reasonable to postulate that P90\u2010CK interaction in RV\u2010infected cells interferes with CK function and induces cell\u2010cycle arrest following S phase in a subpopulation, perhaps representative of tetraploid stage, which could lead to subsequent apoptosis in RV infection. Taking all these observations to the fetal organogenesis level, it is plausible that P90\u2010CK interaction could perhaps be one of the initial steps in RV infection\u2013induced apoptosis\u2010associated fetal birth defects in utero. Birth Defects Research (Part A), 2004. \u00a9 2004 Wiley\u2010Liss, Inc.<\/jats:p><\/jats:sec>","DOI":"10.1002\/bdra.20045","type":"journal-article","created":{"date-parts":[[2004,6,25]],"date-time":"2004-06-25T16:01:34Z","timestamp":1088179294000},"page":"431-437","source":"Crossref","is-referenced-by-count":56,"title":["Rubella virus and birth defects: Molecular insights into the viral teratogenesis at the cellular 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