Using a hamster model of SARS-CoV-2 infection, the research team found that the infection left a gene expression signature in the dorsal root ganglia that persisted after the virus was cleared. The signature matches the gene expression patterns seen in pain caused by other conditions.
“A significant number of people with chronic covid experience sensory abnormalities, including various forms of pain,” said researcher Randall (Alex) Serafini of the Icahn School of Medicine at Mount Sinai in New York City.
“We used RNA sequencing to obtain a snapshot of the biochemical changes SARS-CoV-2 triggers in the pain-transmitting structure, called the dorsal root ganglia,” said Serafini.
For the study, to be presented at the annual meeting of the American Society for Pharmacology and Experimental Therapeutics, the research team included a hamster model of intranasal COVID-19 infection that closely mirrors the symptoms experienced by people.
The researchers observed that SARS-CoV-2-infected hamsters showed slight hypersensitivity to touch early after infection, which became more severe over time, up to 30 days. They then conducted similar experiments with Influenza A viruses to determine whether other RNA viruses promote similar responses.
Unlike SARS-CoV-2, Influenza A caused an initial hypersensitivity that was more severe but faded after four days of infection.
Analysis of gene expression patterns in dorsal root ganglia revealed that SARS-CoV-2 caused a more prominent change in the expression levels of genes implicated in neuron-specific signaling processes than influenza.
Additional experiments showed that four weeks after recovery from the viral infection, flu-infected hamsters had no signs of long-term hypersensitivity, whereas SARS-CoV-2-infected hamsters showed poor hypersensitivity, reflecting chronic pain.
Hamsters that recovered from SARS-CoV-2 had gene expression signatures similar to those observed in the dorsal root ganglia of mice affected by pain that was induced by inflammation or nerve injury.