A recent study by Johns Hopkins Children’s Center, has found that infection with cytomegalovirus (CMV), a common virus transmitted from mother to fetus during pregnancy, significantly worsens necrotizing enterocolitis (NEC), a life-threatening intestinal condition in premature babies.
NEC, is the most common emergency intestinal complication in preemies, affecting nearly 10% of premature infants. It causes severe inflammation that destroys intestinal tissue, with a mortality rate of about 30%. Despite its devastating effects, survival rates for NEC have remained unchanged for the past 30 years.
What the Study Found
The research, published on February 13 in Cellular and Molecular Gastroenterology and Hepatology, identifies CMV infection as a potential trigger for NEC. Dr. David Hackam, lead researcher at Johns Hopkins University, emphasized that the discovery could pave the way for better NEC treatments.
“NEC is a devastating disease that many people have never heard of until their loved one is diagnosed. By identifying CMV as a key factor in NEC severity, we’ve taken a critical step toward saving the lives of premature infants,” Hackam said.
CMV, a herpes virus affecting 40%-80% of the global population, typically remains dormant in healthy individuals. However, it can cause serious complications in newborns when transmitted during pregnancy, including hearing loss and birth defects. Fetuses acquire CMV from infected mothers in 30%-50% of cases, raising the risk of severe health issues.
How CMV Worsens NEC
In the study, researchers used neonatal mice to model NEC with CMV infection. The results showed that mice with CMV experienced more severe intestinal damage and higher mortality rates than those without the virus. Genetic analysis revealed that CMV infection activated inflammation-related pathways, disrupted metabolism, and increased the production of toll-like receptor 4 (TLR4) — a protein previously linked to NEC.
Further investigation found that CMV damaged mitochondria, the cell’s energy-producing structures, reducing adenosine triphosphate (ATP) production — a critical energy source. Mice engineered without TLR4 showed significantly lower NEC severity, suggesting TLR4 as a promising drug target for NEC treatment.
Additionally, researchers explored the potential of adenosine supplements, which boost ATP production. Administering adenosine to CMV-infected mice reduced NEC severity, offering a possible treatment option for future human studies.
The research was funded by the National Institutes of Health (NIH), mark a significant step toward understanding NEC’s underlying causes and developing new therapies. Future studies will focus on confirming the CMV-NEC link in humans and testing adenosine as a treatment option for preterm infants.
