Oral Presentation 8th Australasian Virology Society Meeting and 11th Annual Meeting of the Australian Centre for Hepatitis & HIV Virology Meeting 2015

Diagnosis and epidemiology of congenital infections – Human cytomegalovirus infection (CMV) (#37)

Stuart Hamilton 1 , Beverley Hall 1 , Zin Naing 1 , Gillian Scott 1 , Antonia Shand 1 , Wendy van Zuylen 1 , William Rawlinson 2
  1. Virology Research Laboratory, SAViD, SEALS Microbiology and UNSW, Sydney, NSW, Australia
  2. Prince of Wales Hospital, Virology Division,, RANDWICK, NSW, Australia

CMV is under-recognised, despite being the leading infectious cause of congenital malformation, affecting 0.3 - 0.7% of Australian live births. Congenital CMV infection may cause clinical manifestations including jaundice, hepatosplenomegaly, petechiae, microcephaly, intrauterine growth restriction, and severe long-term sequelae including progressive sensorineural hearing loss and developmental delay in 40-58% of symptomatic neonates, and ~14% of initially asymptomatic infected neonates. Up to 50% of maternal CMV infections have non-specific clinical manifestations, and most remain undetected unless specific serological testing is undertaken. The serology tests for CMV-specific IgM, IgG, and IgG avidity provide improved distinction between primary and secondary maternal infections, although such distinction is not possible in all women. Appropriate tests for congenital CMV infection at birth or in the first three weeks of an infant’s life provide a definitive diagnosis of infection, and can lead to appropriate investigations. Importantly, this may prompt interventions for delayed-onset hearing loss and neurodevelopmental delay in affected infants. Increased maternal awareness and hygiene measures may reduce maternal infection, with consequent reduced risk to the fetus. Our studies of CMV pathogenesis in trophoblast cells and placental explant models (GS, ZN, SH, BH) have shown CMV induces a Th1 bias in placentae that are naturally infected, placental trophoblasts infected in vitro, and in placental explants infected in vitro. We (WVZ) have recently shown CMV infection inhibits Wnt5a-stimulated migration of human SGHPL-4 trophoblasts through transwells, and that inhibition of the pathway restores normal migration of CMV-infected cells. These observations, combined with our data on CMV inhibition by siRNAs (SH, WVZ) show new targets for intervention exist and may be utilised in preventing and/or treating congenital CMV during pregnancy.
Recognition of the importance of CMV in pregnancy and in neonates is increasingly needed, particularly as novel therapeutic and preventive interventions at different times of pregnancy are developed.