Abstract
Human cytomegalovirus (HCMV) is shed into breast milk in nearly every seropositive woman during lactation. This reactivation shows mostly a self-limited, unimodal course. The dynamics and functional role of HCMV-specific-IgG in breast milk and in plasma during reactivation are unknown. Milk whey viral loads were monitored with real-time PCR in 18 HCMV-seropositive mothers over two months postpartum. HCMV-antibody binding assays (ECLIA) and antigen-specific immunoblotting were performed from plasma and corresponding milk samples. Epithelial-cell-specific neutralization was used to analyze functional antibodies in plasma- and whey-pools. Viral loads in milk whey showed unimodal courses in 15 of 18 mothers with peak viral loads around one month postpartum. HCMV-specific-IgG-antibodies increased significantly in plasma and milk whey during reactivation. The mean levels of plasma IgG were about 275-fold higher than in whey. Only antibodies against tegument protein p150 were continuously expressed in both compartments. Anti-glycoprotein-B1 IgG-antibodies were variably expressed in whey, but continuously in plasma. Neutralization assays showed 40-fold higher NT-50 values in plasma compared to whey at two months postpartum. During reactivation, HCMV-specific-IgG reactivities and neutralizing capacities are much lower in whey than in plasma. Therefore, their specific role in the decrease and discontinuation of virus-shedding in milk remains unclear.
Highlights
Human cytomegalovirus (HCMV) belongs to the β-herpesvirus family and plays a major role in immunosuppressed patients in the transplant setting and in the context of congenital and postnatal HCMV-infection [1]
To find a better understanding of these mechanisms, we inaugurated the BlooMil study in which we simultaneously evaluated blood and breast milk during the first 8 weeks postnatally at defined time ranges in a cohort of HCMV-seronegative and -seropositive breastfeeding mothers of mostly preterm infants
The frequency of viral reactivation in breast milk of HCMV-IgG-positive mothers is nearly equal to their serostatus [30]
Summary
HCMV belongs to the β-herpesvirus family and plays a major role in immunosuppressed patients in the transplant setting and in the context of congenital and postnatal HCMV-infection [1]. Restricted HCMV-reactivation during lactation can be studied by viral DNA (DNAlactia), as well as by infectious virions isolated from breast milk in microculture (virolactia) [2]. The mechanism of postnatal HCMV-reactivation in the mammary gland without viral systemic infection (DNAemia) is still unknown. Virus-shedding into breast milk of immunocompetent healthy breastfeeding mothers occurs in nearly every seropositive mother at any time point during lactation, but usually ends 2–3 months after birth [3,4]. Transmission via breastfeeding can lead to severe symptomatic HCMV-infection in preterm infants, with increased risk with birth weight below 1500 g or less than 32 weeks of gestational age [2]. A first case report on immunohistochemically proven manifestation of postnatally acquired
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