Cytomegalovirus infection and pathogenesis in the human placenta
Lenore Pereira A B , Takako Tabata A and Matthew Petitt AA Department of Cell and Tissue Biology, University of California San Francisco, San Francisco, CA 94143, USA
B Tel: 415 476 8248
Email: Lenore.Pereira@UCSF.edu
Microbiology Australia 36(4) 171-174 https://doi.org/10.1071/MA15061
Published: 27 October 2015
Abstract
Human cytomegalovirus (HCMV) is the most common cause of congenital viral infection. Affected children can have permanent neurological complications, including hearing loss, visual impairment and mental retardation1–3. In Australia, 57% of women are seronegative and at risk for primary infection and transmission of virus to the fetus during pregnancy4. Despite its public health significance, the specific molecular and cellular basis of HCMV replication in the human placenta and pathogenesis associated with poor clinical outcome are unknown. Direct fetal infection is involved in severe cases of neuropathology and infection of the placenta can impair its development and functions resulting in a hypoxic environment5–8 and stillbirth6,9,10. Gestational age at the time of infection is an important determinant of outcome. The rates of virus transmission increase from 30% in first trimester to over 70% in third trimester suggesting different mechanisms for overcoming the placental barrier2. Remarkable insights into viral pathogenesis factors that function in the tissue environment have been gained by studying congenitally infected placentas and explants infected by clinical strains
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