Most infants with congenital cytomegalovirus (CMV) infection are born to seropositive women as a result of maternal CMV non-primary infection (reinfection or reactivation). Although infected children are known to transmit CMV to their seronegative mothers, the frequency and magnitude of non-primary maternal CMV infection after exposure to viral shedding by children in their household has not been characterized.
A cohort of Ugandan newborns and their mothers were tested weekly for CMV by quantitative PCR of oral swabs. Infant primary infection and maternal non-primary infection were defined by the onset of persistent high-level oral CMV shedding. Strain-specific antibody testing was used to assess maternal reinfection. Cox regression models with time-dependent covariates were used to evaluate risk factors for non-primary maternal infection.
Non-primary CMV infection occurred in 15 of 30 mothers, all following primary infection of their infants by a median of 6 weeks (range 1 to 10) in contrast to none of the mothers of uninfected infants. The median duration of maternal oral shedding lasted 18 weeks (range: 4 - 42) reaching a median maximum viral load of 4.69 log copies/ml (range 3.22 - 5.64). Previous-week infant CMV oral quantities strongly predicted maternal non-primary infection (hazard ratio 2.32 per log10 DNA copies/swab increase; 95% CI 1.63, 3.31). Maternal non-primary infections were not associated with changes in strain-specific antibody responses.
Non-primary CMV infection was common in mothers following primary infection in their infants, consistent with infant-to-mother transmission. Since infants frequently acquire CMV from their mothers, e.g. through breast milk, this suggests the possibility of “ping-pong” infections. Additional research is needed to characterize the antigenic and genotypic strains transmitted among children and their mothers.
1. Université de Montréal, CHU Sainte-Justine, Montréal, Canada
2. Fred Hutchinson Cancer Research Center, Seattle, Washington, USA
3. Institute for Medical Immunology, Université libre de Bruxelles, Charleroi, Belgium
4. University of Alabama Hospital, Birmingham, USA
5. University of Washington, Seattle, Washington, USA
6. Infectious Disease Research Institute, Seattle, Washington, USA
7. University of British Columbia, BC Children’s Hospital, Vancouver, Canada
Sources of support/funding: This work was supported by grants from the NIH – Roadmap KL2 Clinical Scholar Training Program KL2-RR025015-01 (SG), University of Washington Center for AIDS Research New Investigator Award P30-AI027757 (SG), P01-AI 030731 (LC, AW, SS, JTS, MLH); R01-CA138165 (CC), and P30-CA015704 (CC and LC) – and by a Child & Family Research Institute Salary Award (SG).
Correspondence: S. Gantt, BC Children’s Hospital Research Institute, 950 W 28th Ave, Rm A5-144, Vancouver, BC V5Z 4H4, Canada (email@example.com).