Recent research suggests that some cases of sudden infant death syndrome (SIDS) could be connected to undiagnosed brain infections in infants. A study published in JAMA Neurology sheds light on this possibility, indicating that unnoticed inflammation and hidden infections may contribute to SIDS and the brainstem pathology observed in certain infants.
Conducted by researchers from Boston Children’s Hospital and Harvard Medical School, the study analyzed autopsy samples from 71 infants who tragically succumbed to SIDS along with 20 control subjects. By employing advanced molecular tools, the team initially screened cerebrospinal fluid samples for neopterin, a biomarker of cellular immune activation. Among the 64 infants with SIDS who were screened, six exhibited significantly elevated neopterin levels, suggesting the presence of brain inflammation.
Subsequently, samples from these six infants underwent metagenomic sequencing to detect DNA from any potential microbes. In one case, a viral pathogen known as human parechovirus 3 (HPeV3) was identified in an 11-day-old infant who showed no signs of encephalitis prior to succumbing to SIDS, besides displaying fussiness and a slight fever.
Further analysis utilizing single-nucleus RNA sequencing of brainstem tissue from the HPeV3-infected infant, alongside samples from three SIDS infants without brainstem inflammation, unveiled variations in gene expression across different brain cell types and vascular cells. Notably, genes associated with interferon signaling and the innate immune response were prominently upregulated in cells from the medulla, particularly in serotonergic neurons crucial for regulating breathing and heart rate, which are believed to be abnormal in SIDS cases.
While the study only identified a pathogen in a single infant, the researchers are exploring non-infectious causes of neuroinflammation, such as hypoxia, which has links to established SIDS risk factors like bed sharing and prone sleep positions. The complex nature of SIDS suggests a multifaceted interplay of brainstem infections, inflammation, genetic predispositions, and environmental factors like infant sleep position. Technological advancements are now enabling a comprehensive examination of these contributing elements all at once.
The study’s authors emphasize the importance of collaborations with medical examiners, who often lack access to these innovative resources for autopsy investigations. Dr. Haynes, who leads the CJ Murphy Laboratory for SIDS Research at Boston Children’s, collaborates with Robert’s Program on Sudden Unexpected Death in Pediatrics, providing diagnostic services and support to families affected by sudden and unexplained child deaths.
The emerging insights into the potential role of brain infections in SIDS underscore the need for further research and collaboration among experts in the field to better understand the intricate factors contributing to this heartbreaking phenomenon.
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1. Source: Coherent Market Insights, Public sources, Desk research
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