Scientists have found important information about how the SARS-CoV-2the virus that causes COVID-19May cause long term paina breakthrough that could lead to a possible therapy for the disorder.
They discover how COVID-19 can cause long-term pain
The experiments involved a hamster model of intranasal COVID-19 infection which closely mirrors the symptoms experienced by people.
“A significant number of long-term COVID sufferers 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 US.
“We used RNA sequencing to get a snapshot of the biochemical changes that SARS-CoV-2 triggers in a pain-transmitting structure called the dorsal root ganglion,” Serafini said.
Using a hamster model of SARS-CoV-2 infectionthe researchers found that the infection left a signature of gene expression in dorsal root ganglia that remained even after the virus was eliminated.
The signing coincided with gene expression patterns seen in pain caused by other conditions, they said.
This finding could lead to new therapies for patients suffering from acute and prolonged COVID
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 suffering from acute and prolonged COVID-19. as well as other pain conditions,” Serafini said.
“Our study also shows that SARS-CoV-2 causes long-term effects on the body in dramatically new ways, further underscoring why people should try to avoid becoming infected,” said the scientist.
The researchers observed that the hamsters infected with SARS-CoV-2 showed slight hypersensitivity to touch shortly after infection, which became more severe over time, up to 30 days.
They then performed similar experiments with the influenza A viruses to determine if other RNA viruses promote similar responses.
Unlike SARS-CoV-2, influenza A caused early hypersensitivity that was more severe but disappeared four days after infection. This, according to the researchers.
SARS-CoV-2 downregulates the activity of several pain regulators
The analysis of the patterns of gene expression in dorsal root ganglia showed that SARS-CoV-2 caused a more prominent change. This, in the expression levels of genes involved in signaling processes specific to neurons compared to influenza, they said.
The researchers also found that four weeks after recovering from the viral infection. Influenza-infected hamsters had no signs of long-term hypersensitivity. While the hamsters infected with SARS-CoV-2 showed worsening hypersensitivity, reflecting chronic pain.
Hamsters that recovered from SARS-CoV-2 had gene expression signatures similar to those seen in dorsal root ganglial of mice affected by pain induced by inflammation or nerve injury.
The researchers also predicted that SARS-CoV-2 downregulates the activity of several pain regulators previously identified and a protein called interleukin-enhancer binding factor 3 (ILF3).
Mimicking the acute effects of ILF3 could serve as a new pain management strategy
This downregulation occurs at times when pain behaviors in hamsters infected with SARS-CoV-2 they were very mild. Despite strong systemic inflammation, they said.
The researchers hypothesized that mimicking the acute effects of ILF3 might serve as a new treatment strategy from pain.
They administered a anticancer drug clinically proven to inhibit ILF3 activity. And they found that it was very effective for treat pain in a mouse model with localized inflammation.
“We believe that therapeutic candidates derived from our gene expression data, such as inhibitors of ILF3. They could potentially point to pain mechanisms that are specific to COVID patients, both acutely and chronically,” added Serafini.
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