These genes were associated with pathways related to neurodegeneration and pain, suggesting permanent damage to the dorsal root ganglia (spinal nerves that carry sensory messages from various receptors) may underlie symptoms of post-Covid conditions known as Also called long covid.
The findings, which appear online in the journal Science Signalling, may contribute to the understanding of the pathophysiology and help validate novel therapies for the prevention and treatment of Covid.
Venetia Zachariau, chair of pharmacology, physiology and biophysics at Boston University, said, “Several studies have found that a high proportion of long-term COVID patients experience abnormal perception of touch, pressure, temperature, pain or tingling throughout the body.” suffers.”
“Our work shows that SARS-CoV-2 can cause chronic pain in a unique way, emphasizing the need for therapeutics that target molecular pathways specific to this virus,” Zachariau said.
COVID-19, the disease resulting from SARS-CoV-2 infection, is associated with highly variable clinical outcomes ranging from asymptomatic illness to death.
For people with mild infection, Covid-19 can cause symptoms of respiratory infection (cough, congestion, fever) and sensory phenotypes such as headache and loss of sense of smell. In more severe cases, SARS-CoV-2 infection can affect nearly every organ and result from vascular occlusion, heart damage, and stroke from acute kidney failure.
A significant number of actively infected patients with both mild and severe infections experience sensory-related symptoms, such as headache, visceral pain, Guillain-Barre syndrome, nerve pain, and inflammation. These symptoms subside in most patients after the infection clears up, but may persist in other patients.
Using an experimental model infected with SARS-CoV-2, the researchers studied the effects of infection on sensitivity to touch, both during active infection and after infection had recovered. They then compared the effects of SARS-CoV-2 to those triggered by infection with the influenza A virus.
In experimental models, they observed a slow but progressive increase in sensory sensitivity over time – one that was quite different from the viral control, influenza A virus, which caused a quick hypersensitivity during active infection, but returned to normal by the time the infection was over. .
According to the researchers, this model can be used to obtain information about the genes and pathways affected by SARS-CoV-2, providing the scientific community with new information on gene expression changes in sensory ganglia several weeks after infection. provides.
“We hope this study will provide new avenues to address somatosensory symptoms of long-lasting COVID and ME/CFS (myalgic encephalomyelitis/chronic fatigue syndrome), which are just beginning to be addressed by mainstream medicine.” While we have just begun to use this information. While validating a promising target in this study, we believe that our now publicly available data may provide insight into many new therapeutic strategies,” Zacharias said.