Cytomegalovirus and Epstein–Barr virus may be associated with some cases of cerebral palsy

Abstract

Objective: Intrauterine infection is a risk factor for cerebral palsy. Previous work reported a high frequency of viral DNA in newborn screening cards from cerebral palsy cases and controls possibly due to contamination. Methods: Retrospective case-control study using improved methodologies to minimize contamination during PCR-based detection of viral DNA sequences. Newborn screening cards of 339 Caucasian children with cerebral palsy and 594 controls were examined. Viruses tested were herpes simplex viruses 1 and 2 (HSV1 and 2), varicella zoster virus (VZV), Epstein–Barr virus (EBV), cytomegalovirus (CMV), human herpes viruses 6, 7 and 8 (HHV6, HHV7 and HHV8), and parvovirus B19. Genotyping was performed on DNA extracted from dried blood spots. Results: CMV and EBV were detected in 5 (1.5%) and 3 (0.9%) of 339 cases, respectively, but not in controls (p = 0.047 and 0.006). Frequencies of detection of the other viruses examined were similar for cases and controls. DNA from at least one of the nine viruses tested was found in 4.4% of cases and 3.1% of controls [OR 1.4 95% CI (0.71–2.76)]. Conclusion: Evidence of congenital viral infection was uncommon in cases of cerebral palsy and controls. However, CMV and EBV were significantly associated with cerebral palsy.

Keywords::

• Cerebral palsy
• Epstein–Barr virus
• newborn screening cards
• cytomegalovirus

Acknowledgement

The authors would like to thank the Department of Microbiology, South Eastern Area Laboratory Service, Prince of Wales Hospital, New South Wales, Sydney, Australia, in particular Professor William Rawlinson and Dr Jonathan Howard for their most valued technical support and kind donation of DNA controls for HHV 6, 7 and 8 and parvovirus B19. We thank the staff of the South Australian Neonatal Screening Centre (Women’s and Children’s Hospital), South Australia, Australia, in particular Enzo Ranieri and Rosemary Gerace for their support in the collection of NBSC and the Department of Genetic Medicine, Children’s Hospital Westmead, New South Wales, Sydney, Australia in particular Professor Veronica Wiley for providing the NBSC. We particularly thank and acknowledge the families that kindly agreed to participate in this research. This work has been supported by the Cerebral Palsy Alliance Research Foundation and the University of Adelaide.

Declaration of Interest: The authors report no conflicts of interest.