Immunity：广州医科大学团队揭示铁代谢紊乱会损害新生儿抗病毒免疫并引发致命肝脏病变

Core Insights - The article discusses the significant impact of rotavirus infections on neonates, particularly highlighting the severe symptoms and systemic infections that can arise, which are not effectively prevented by existing vaccines [2][5] - A recent study reveals that dysregulation of the hepcidin-iron axis plays a critical role in impairing antiviral immunity and causing liver damage in neonates infected with rotavirus, providing new therapeutic targets for related diseases such as biliary atresia [3][11] Summary by Sections Rotavirus and Its Impact - Rotavirus is a major cause of life-threatening gastroenteritis in children under five, leading to severe symptoms in neonates, including blood in stool and unstable vital signs, with current vaccination strategies offering no protection [2][5] - The prevalence of biliary atresia (BA) is noted, affecting 1 in every 5,000 to 18,000 newborns, with its etiology linked to infections, immune dysregulation, and genetic susceptibility [5] Research Findings - The study published in the journal Immunity identifies iron metabolism dysregulation as a key mechanism in rotavirus-related systemic infections in neonates, suggesting new treatment avenues [3][11] - Single-cell RNA sequencing revealed that iron dysregulation is a driving factor for liver damage in rotavirus infections, with elevated hepcidin levels inhibiting iron export and leading to cellular damage [6][9] Clinical Implications - An open-label clinical trial demonstrated that preoperative folic acid supplementation significantly reduced the incidence of cholangitis from 74% to 21% and liver transplantation rates from 41.1% to 11.1% in biliary atresia patients [8] - The study emphasizes the importance of targeting the hepcidin-iron signaling pathway to mitigate liver damage and improve outcomes in neonates with rotavirus infections [9][11]