We've updated our Privacy Policy to make it clearer how we use your personal data. We use cookies to provide you with a better experience. You can read our Cookie Policy here.


RSV Can Infect Nerve Cells

Credit: iStock.
Listen with
Register for free to listen to this article
Thank you. Listen to this article using the player above.

Want to listen to this article for FREE?

Complete the form below to unlock access to ALL audio articles.

Read time: 2 minutes

Respiratory syncytial virus (RSV) is a common respiratory virus that infects mostly children and senior adults. In mild cases of RSV, people recover from symptoms such as coughing, sneezing and fever after one to two weeks. In more severe cases, symptoms can worsen and lead to the development of pneumonia or bronchiolitis.

In the United States, RSV causes 6,000–10,000 deaths in patients aged 65 years and older, and 100-300 deaths in children under 5 each year.

“This is the most common respiratory virus in the first years of life as well as an impactful virus among the elderly,” Dr. Giovanni Piedimonte, Tulane University vice president for research and professor of pediatrics, biochemistry and molecular biology, said.

While RSV typically infects respiratory cells, there is growing evidence that it can also cause neurological symptoms. The virus has been detected in the spinal fluid of children experiencing seizures, and approximately 40% of RSV-positive children aged two years and under present with acute encephalopathy.

What is encephalopathy?

Encephalopathy is a group of conditions that lead to brain dysfunction, which may present as memory loss, confusion, personality changes or comas in severe cases.


Piedimonte is the lead author of a new study demonstrating RSV’s capacity to infect nerve cells and trigger inflammation in vitro. The first-of-its-kind research is published in The Journal of Infectious Diseases.

RSV can infect nerve cells and enter the spinal cord

Piedimonte and team used 3D peripheral nerve cell cultures, grown from stem cells and rat embryos, for the study. This approach enables scientists to explore research questions that are hard to address in humans or existing laboratory models.

The virus was able to penetrate the nerve cells, leading to the release of chemokines and inflammation. “Low-level infection was transient, primarily involved macrophages, and induced moderate chemokine release with transient neural hypersensitivity,” the authors described. “Infection with higher viral loads was persistent, infected neuronal cells in addition to monocytes, and induced robust chemokine release followed by progressive neurotoxicity.”

Want more breaking news?

Subscribe to Technology Networks’ daily newsletter, delivering breaking science news straight to your inbox every day.

Subscribe for FREE

“Until this study, the theory was that the inflammatory response was indirectly activating the nerves,” Piedimonte said. “This study shows that not only does that happen, but the virus can penetrate directly into the nerves.”

The researchers also discovered that, despite RSV being unable to enter spinal neurons directly, the virus could enter the spinal cord via peripheral nerves. Piedimonte hypothesized that this helps RSV to overcome the blood–brain barrier, which might explain the link between RSV and neurological/ neurodevelopmental disorders. More research will be required to confirm that theory.

“If indeed it’s confirmed in future studies that viruses like this are able to access the central nervous system, that opens a huge Pandora’s box,” Piedimonte said.

While 3D cell cultures create new possibilities for researching disease mechanisms in the laboratory, they do not reflect the total anatomical landscape of cells, tissues and organs in vivo. This is a limitation to the study that would need to be addressed to validate its translation to humans.

Reference: Pollard KJ, Traina-Dorge V, Medearis SM, et al. Respiratory syncytial virus infects peripheral and spinal nerves and induces chemokine-mediated neuropathy. J Infect Dis. 2023:jiad596. doi: 10.1093/infdis/jiad596

This article is a rework of a press release issued by Tulane University. Material has been edited for length and content.