The study suggests that undetected viral infections may explain some cases of SIDS. (Image courtesy of Oscar Wong via Getty Images)
A small study suggests that infections and inflammation of the brain may explain some cases of sudden infant death syndrome (SIDS).
The study identified a specific virus, known as human parechovirus 3 (HPeV3), as potentially linked to the death of one child included in the study; HPeV3 is known to cause both mild respiratory infections and serious nervous system infections. At this time, the virus cannot be definitively confirmed as the cause of the child's death, but the study highlights the possibility that some cases of SIDS may be caused by viral infections, a concept that requires further study.
“Our results provide proof of concept that undetected infections may increase the risk of SIDS and that increased surveillance for HPeV3 in particular may be warranted,” study co-author Ben Okati, a geneticist at Harvard Medical School, said in an email to Live Science. The team reported their findings Monday (Jan. 29) in the journal JAMA Neurology.
“There is a possibility that there could be other similar cases,” particularly involving the HPeV3 virus, said Dr. Avindra Nath, clinical director of the National Institute of Neurological Disorders and Stroke, who was not involved in the study. “Patients should be evaluated for this possibility,” he added in an email to Live Science.
SIDS refers to the sudden death of a baby younger than 1 year of age that has no clear explanation even after a thorough postmortem investigation. The causes of SIDS vary widely from case to case, but often death occurs during sleep. The incidence of SIDS dropped significantly in the 1990s in the United States due to a government campaign to raise awareness of safe sleep practices for infants.
However, since then, SIDS rates have remained relatively stable, suggesting that there are factors other than sleep-related factors at play.
Researchers have identified potential differences in genetics, nervous system function, and enzyme activity in babies who died from SIDS compared with those who died from known causes or those who survived infancy. Some studies have also pointed to neuroinflammation, which is inflammation in the brain or spinal cord, as potentially linked to some cases of SIDS.
To further explore the inflammatory processes in SIDS, the study authors analyzed clinical samples from 64 infants who died from SIDS and 20 infants who died from known causes. They examined the clear fluid surrounding the brain and spinal cord for signs of immune activation and inflammation.
A compound known as neopterin, which is produced by immune cells when activated in response to infection, is one sign of inflammation; it can be found in various body fluids but does not indicate a specific pathogen, just a general activation of the immune system. Six babies with SIDS had high levels of neopterin in their samples, indicating inflammation in their nervous systems.
To find out what causes this inflammation, the researchers used a technique called next-generation metagenomic sequencing.
“This type of screening is not performed in a standard autopsy,” study co-author Dr. Prashant Ramachandran, an associate professor of neurology at the University of California, San Francisco, told Live Science in an email.
Autopsies typically look at shape and microscopic details of cell structure, Nath said. Pathologists also sometimes test for specific pathogens in tissue samples, but those tests are aimed at identifying known viruses and bacteria. The screening method used in the study allowed the scientists to look for pathogens blindly — “it provides an objective analysis,” he added.
This screening found HPeV3 in fluid samples from one child, as well as in liver tissue and several brain regions, including the brainstem. HPeV3 can cause fairly mild
Sourse: www.livescience.com
