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Published on: January 30, 2017
Molecular aspects of the teratogenesis of rubella virus
Suji George1, Rajlakshmi Viswanathan1, Gajanan N Sapkal2
1Diagnostic Virology Group, ICMR-National Institute of Virology, 20-A, Dr. Ambedkar Road, Pune, Maharashtra, 411001, India.
Abstract:
Rubella or German measles is an infection caused by rubella virus (RV). Infection of children and adults is usually characterized by a mild exanthematous febrile illness. However, RV is a major cause of birth defects and fetal death following infection in pregnant women. RV is a teratogen and is a major cause of public health concern as there are more than 100,000 cases of congenital rubella syndrome (CRS) estimated to occur every year. Several lines of evidence in the field of molecular biology of RV have provided deeper insights into the teratogenesis process. The damage to the growing fetus in infected mothers is multifactorial, arising from a combination of cellular damage, as well as its effect on the dividing cells. This review focuses on the findings in the molecular biology of RV, with special emphasis on the mitochondrial, cytoskeleton and the gene expression changes. Further, the review addresses in detail, the role of apoptosis in the teratogenesis process.
Insights
Rubella virus (RV) causes mild illness in children but severe birth defects in infants. This review explores RV's molecular mechanisms, focusing on mitochondrial, cytoskeleton, and gene expression changes in fetal development.
Area of Science:
- Molecular Biology
- Virology
- Developmental Biology
- Teratology
Background:
- Rubella virus (RV) causes German measles, a generally mild illness in children and adults.
- However, RV infection during pregnancy is a significant teratogen, leading to congenital rubella syndrome (CRS) and fetal death.
- Over 100,000 CRS cases are estimated annually, highlighting a major public health concern.
Purpose of the Study:
- To review molecular biology findings on rubella virus (RV) teratogenesis.
- To elucidate the mechanisms by which RV damages the developing fetus.
- To emphasize the roles of mitochondrial function, cytoskeleton integrity, gene expression, and apoptosis in RV-induced birth defects.
Main Methods:
- Literature review of molecular biology studies on rubella virus.
- Analysis of research on RV's impact on cellular processes in fetal development.
- Focus on mitochondrial, cytoskeleton, gene expression, and apoptotic pathways.
Main Results:
- RV teratogenesis is multifactorial, involving cellular damage and effects on dividing cells.
- Molecular insights reveal RV's disruption of mitochondrial function and cytoskeleton.
- Alterations in gene expression and the induction of apoptosis are key mechanisms of fetal damage.
Conclusions:
- Understanding RV's molecular biology is crucial for addressing congenital rubella syndrome (CRS).
- Targeting mitochondrial, cytoskeletal, and apoptotic pathways may offer strategies to prevent RV-induced teratogenesis.
- Further research into RV's molecular interactions can inform public health interventions.
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