A recent study entitled “Trained immunity in newborn infants of HBV-infected mothers” revealed that newborns’ exposure to hepatitis B virus (HBV) while in the womb is not associated with an immune tolerance but rather with the development of a more mature immune system that could be effective at fighting later infections. The study was published in the journal Nature Communications.

Infants are known to exhibit higher susceptibility to severe infections when compared to adults, since their immune system is less mature. HBV infection is commonly passed from infected mothers to babies at birth and as such, HBV is thought to hijack the newborns’ immune system to establish a persistent infection. In the study, authors challenged this dogma by showing HBV exposure in utero actually promotes innate immune cells’ maturation and development, resulting in an enhanced immune response to bacterial infection.

Researchers investigated the impact of HBV exposure on the newborn immune system by performing a comprehensive analysis of immune cells in the umbilical cord blood of neonates born from HBV chronically infected mothers. The team discovered that contrary to what was previously thought, newborns exposed to HBV exhibited a more mature immune system, with higher numbers of activated immune cells (from both the innate and adaptive immune system). Furthermore, HBV exposure in utero induced a state of trained immunity in vitro — where HBV infection acted as a trigger, activating the innate immune system. Even though this initial innate immune response declines over time, it “alerts” the immune system so that when a new pathogen infects these infants, their immune responses are more potent.

The mechanisms behind the observed trained immunity included changes in cytokine (a large group of proteins, peptides, or glycoproteins secreted by specific cells of the immune system) secretion, specifically a lower IL-10 secretion and higher  IL-12p40 and IFN-α2 secretion.

These findings suggest that HBV infection in utero enhances the plasticity of the fetal immune system, giving babies a selective advantage when facing a second new infection.