At a time when the world is slowly returning to normal after seeing an all-time decline in Covid-19 cases, scientists are wondering how SARS-CoV-2, the virus that causes Covid-19, can lead to long-term pain. Important insights are discovered. An advance that can lead to potential cure for the disorder.Also read – Booster shots mandatory for tourists: SII’s Poonawala explains India’s plans to face new covid recombinant variant
The experiments involved a hamster model of intranasal COVID-19 infection that closely reflects the symptoms experienced by humans. Also read – Why did people gain weight during the Kovid-19 epidemic? The new study explains
“A significant number of people with chronic COVID experience sensory abnormalities, including a variety of pains,” said Randall Serafini, a PhD candidate at the Icon School of Medicine at Mount Sinai in the US. Also read – Covid-19 Features: 9 new features added to the official list Check it out here
“We used RNA sequencing to get a snapshot of the biochemical mutations of the SARS-CoV-2 triggers in a pain-transmitting structure called the dorsal root ganglia,” said Serafini.
Using a hamster model of SARS-CoV-2 infection, the researchers found that the infection left a sign of gene expression in the dorsal root ganglia that remained after the virus was cleared.
The signature matching the gene expression pattern 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, April 2-5, in Philadelphia, USA.
“Our findings could potentially lead to new therapies for patients suffering from acute and chronic 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 a radically new way, and more emphatically explains why people should try to avoid infection,” said the scientist.
The researchers observed that SARS-CoV-2-infected hamsters showed a slight hypersensitivity to touch early after infection, which became more severe over a period of 30 days.
They then conducted similar experiments with the influenza A virus to determine if other RNA viruses stimulated similar responses.
Unlike SARS-CoV-2, influenza A causes early hypersensitivity which was more severe but faded four days after infection, according to the researchers.
Analysis of gene expression patterns in the dorsal root ganglia shows that SARS-CoV-2 causes more significant changes in expression levels of genes involved in neuron-specific signaling processes than in influenza, they said.
The researchers also found that four weeks after recovering from a viral infection, flu-infected hamsters showed no signs of long-term hypersensitivity while SARS-CoV-2-infected hamsters showed worsening hypersensitivity, reflecting chronic pain.
Hamsters recovered from SARS-CoV-2 had gene expression signatures that were affected by pain seen in the dorsal root ganglia of mice that were induced by inflammation or nerve injury.
The researchers also predicted that SARS-CoV-2 down-regulates the activity of some previously identified pain regulators and a protein called interleukin enhancer-binding factor 3 (ILF3).
This downregulation occurs at a time when the SARS-CoV-2-infected hamster had very mild pain behaviors despite severe systemic inflammation, they said.
The researchers speculated that mimicking the acute effects of ILF3 could serve as a new pain treatment strategy.
They administered a clinically tested anti-cancer drug that inhibited ILF3 activity, and found it to be very effective in treating pain in a mouse model of local inflammation.
“We think that therapeutic candidates derived from our gene expression data, such as ILF3 inhibitors, could potentially target pain mechanisms that are specific to covid patients, both acute and chronic,” Serafini added.
(PTI)
