Impact of Covid 19: how COVID-19 can cause long-term pain

Scientists have found important insights into how SARS-CoV-2, the virus that causes COVID-19, can lead to long-term pain, a breakthrough that could lead to a potential therapy for the disorder. The experiments involved a hamster model of intranasal COVID-19 infection that closely mirrors the symptoms people experience.

“A significant number of people with long-term COVID experience sensory abnormalities, including various forms of pain,” said Randal Serafini, a doctoral candidate at the Icahn School of Medicine at Mount Sinai in the United States.

“We used RNA sequencing to get a snapshot of the biochemical changes triggered by SARS-CoV-2 in a pain-transmitting structure called the dorsal root ganglia,” Serafini said.

Using a model of SARS-CoV-2 infection in hamsters, the researchers found that the infection left behind a gene expression signature in the dorsal root ganglia that remained even after the virus disappeared.

The signature matched gene expression patterns seen in pain caused by other conditions, they said.

The research was presented at the annual meeting of the American Society for Pharmacology and Experimental Therapeutics held April 2-5 in Philadelphia, USA.

“Our findings could potentially lead to new therapies for patients with acute and long-lasting COVID, as well as other pain conditions,” Serafini said.

“Our study also shows that SARS-CoV-2 causes long-term effects on the body in radically new ways, further highlighting why people should try to avoid getting infected,” the scientist said.

Researchers observed that hamsters infected with SARS-CoV-2 exhibited mild hypersensitivity to touch early after infection, which worsened over time, up to 30 days.

They then performed similar experiments with the Influenza A virus to determine whether other RNA viruses promote similar responses.

Unlike SARS-CoV-2, influenza A caused more severe early hypersensitivity but subsided four days after infection, the researchers said.

Analysis of gene expression patterns in dorsal root ganglia showed that SARS-CoV-2 caused a greater change in expression levels of genes involved in neuron-specific signaling processes compared to SARS-CoV-2. flu, they said.

Researchers also found that four weeks after recovering from viral infection, influenza-infected hamsters showed no signs of long-term hypersensitivity, while SARS-CoV-2-infected hamsters showed worsened hypersensitivity. , reflecting chronic pain.

Hamsters that recovered from SARS-CoV-2 had gene expression signatures similar to those seen in the dorsal root ganglia of mice affected by pain induced by inflammation or nerve injury.

The researchers also predicted that SARS-CoV-2 downregulates the activity of several previously identified pain regulators and a protein called interleukin-binding factor 3 (ILF3).

This downregulation occurs at times when pain behaviors in SARS-CoV-2-infected hamsters were very mild, despite strong systemic inflammation, they said.

The researchers hypothesized that mimicking the acute effects of ILF3 could serve as a novel pain treatment strategy.

They administered a clinically tested cancer drug that inhibits ILF3 activity and found it to be highly effective in treating pain in a mouse model of localized inflammation.

“We believe that therapeutic candidates derived from our gene expression data, such as ILF3 inhibitors, could potentially target pain mechanisms specific to COVID patients, both acute and chronic,” Serafini added.

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