Science uncovers why persistent COVID causes lasting pain | COVID-19 | Health | WORLD

The COVID Persistent infection can cause various forms of long-term pain, the explanation, according to one study, is that the infection leaves a pain-associated gene expression signature in a pain-transmitting structure that remains even after virus clearance.

A study carried out with mice, which has been presented at the congress Experimental Biology held in Philadelphia (USA), adds that that gene expression signature matches patterns seen in pain caused by other diseases.

“A significant number of people with persistent COVID experience sensory abnormalities, including various forms of pain”he pointed Randal Serafini from the Icahn School of Medicine at Mount Sinai Hospital in New York.

The team used sequencing of the ARN to get a snapshot of the biochemical changes that the SARS-CoV-2 triggers in the dorsal root ganglia, which is a pain-transmitting structure.

This finding, according to Serafini, could “lead to new therapies for patients with COVID-19 and persistent COVID, as well as other types of pain”.

The study also shows, he added, that SARS-CoV-2 causes long-term effects on the body “in drastically new ways, further underscoring why people should try to avoid getting infected”.

The experiments included a hamster model of intranasal infection by COVID-19which accurately reflects the symptoms experienced by people.

The researchers observed that the hamsters showed a slight hypersensitivity to touch at the beginning of the infection, which worsened over time, up to 30 days.

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

In contrast to SARS-CoV-2, influenza A caused an early hypersensitivity that was more severe, but disappeared four days post-infection.

Analysis of gene expression patterns in dorsal root ganglia revealed that coronavirus caused a more prominent change in the expression levels of genes involved in neuron-specific signaling processes compared to influenza.

Other experiments showed that, four weeks after recovering from the viral infection, hamsters infected with influenza showed no signs of long-term hypersensitivity, while those with SARS-Cov-2 showed aggravated hypersensitivity, reflecting chronic pain.

Hamsters that had recovered from COVID-19 had gene expression signatures similar to those seen in the dorsal root ganglia of mice affected by pain induced by inflammation or nerve injury.

To delve into the molecular machinery associated with altered sensitivity in SARS-CoV-2-infected hamsters, the researchers applied bioinformatic analysis to the gene expression data they had obtained.

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

This downregulation occurs at times when pain behaviors in SARS-CoV-2-infected hamsters were very mild, despite strong systemic inflammation. In contrast, influenza A-induced hypersensitivity was severe at the time.

ILF3 has not yet been studied in the context of pain, but it is a potent regulator of cancersay the researchers, who hypothesized that mimicking the acute effects of ILF3 could serve as a new pain management strategy.

To test this prediction, they administered a clinically proven anticancer drug that inhibits ILF3 activity and found that it was indeed “very effective” to treat pain in a mouse model of localized inflammation.

“We believe that therapeutic candidates derived from our gene expression data, such as ILF3 inhibitors, could target pain mechanisms that are specific to both COVID-19 and persistent patients,” Serafina said.

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