A research study carried out by scientists from Boston University, Icahn School of Medicine at Mount Sinai, and New York University has revealed that SARS-CoV-2 infection can cause lasting damage to the dorsal root ganglia, resulting in signs of Post-COVID Conditions or Long COVID. The research study discovered that countless genes associated with neurodegeneration and pain-related paths were affected even after the viral infection had been cleared. The researchers observed a progressive boost in sensory sensitivity with time in an experimental design infected with SARS-CoV-2, highlighting the special method in which the virus causes long lasting pain.
New research study findings may add to the understanding of pathophysiology and help validate novel treatments for the prevention and treatment of COVID-19.
SARS-CoV-2 infection can cause enduring damage to sensory nerves, causing signs of Long COVID, according to a study by researchers from numerous institutions. The research study recognized gene expression modifications connected with neurodegeneration and pain-related paths, highlighting the requirement for targeted rehabs. The findings offer potential avenues for resolving somatosensory signs and developing new treatments.
For those with milder infections, COVID-19 can produce breathing infection symptoms (cough, blockage, fever) and sensory phenotypes such as headache and loss of sense of odor. In more extreme cases, SARS-CoV-2 infection can impact nearly every organ and result in strokes from vascular occlusion, cardiovascular damage and intense renal failure.
A study performed by scientists from Boston University, Icahn School of Medicine at Mount Sinai, and New York University has revealed that SARS-CoV-2 infection can lead to long lasting damage to the dorsal root ganglia, resulting in symptoms of Post-COVID Conditions or Long COVID. For those with milder infections, COVID-19 can produce breathing infection symptoms (cough, congestion, fever) and sensory phenotypes such as headache and loss of sense of odor. Utilizing a speculative design infected with SARS-CoV-2, the scientists studied the results of infection on sensitivity to touch, both during active infection and well after the infection had cleared. In the speculative model, they observed a sluggish but progressive boost in sensory sensitivity over time– one that differed substantially from viral control, influenza A virus, which caused fast hypersensitivity during active infection but returned to normal by the time infection was over.
In a new study, scientists from Boston University Chobanian & & Avedisian School of Medicine, Icahn School of Medicine at Mount Sinai (Icahn Mount Sinai) and New York University (NYU), have found that countless genes were impacted by SARS-CoV-2-mediated disease even after the viral infection had been cleared. These genes were associated with neurodegeneration and pain-related paths, recommending lasting damage to dorsal root ganglia (back nerves that carry sensory messages from different receptors) that might underlie symptoms of Post-COVID Conditions likewise called Long COVID.
” Several research studies have actually found that a high proportion of Long COVID clients experience abnormal understanding of touch, pressure, temperature, discomfort or tingling throughout the body. Our work recommends that SARS-CoV-2 might cause enduring pain in a rather distinct way, stressing the need for therapies that target molecular pathways specific to this virus,” explains matching author Venetia Zachariou, PhD, Edward Avedisian Professor and chair of pharmacology, physiology & & biophysics at BU Chobanian & & Avedisian School of Medicine. This work was performed in cooperation with Benjamin tenOever, PhD, teacher of microbiology and medicine at NYU, formerly at Icahn Mount Sinai.
Utilizing an experimental model contaminated with SARS-CoV-2, the researchers studied the effects of infection on sensitivity to touch, both during active infection and well after the infection had actually cleared. They then compared the effects of SARS-CoV-2 to those set off by influenza A virus infection. In the experimental model, they observed a progressive however sluggish increase in sensory level of sensitivity over time– one that varied considerably from viral control, influenza A virus, which triggered fast hypersensitivity throughout active infection but returned to typical by the time infection was over.
According to the researchers, this model can be used to get information on genes and pathways affected by SARS-CoV-2, offering novel information to the clinical neighborhood on gene expression changes in sensory ganglia numerous weeks after infection.
” We hope this research study will provide new avenues for resolving somatosensory signs of long COVID and ME/CFS (myalgic encephalomyelitis/chronic fatigue syndrome), which are only simply now starting to be attended to by mainstream medication. While we have begun utilizing this information by confirming one appealing target in this study, our company believe our now publicly offered data can yield insights into many brand-new therapeutic methods,” includes Zachariou.
These findings appear online in the journal Science Signaling.
Reference: “SARS-CoV-2 respiratory tract infection leads to the development of somatosensory irregularities in a hamster design” by Randal A. Serafini, Justin J. Frere, Jeffrey Zimering, Ilinca M. Giosan, Kerri D. Pryce, Ilona Golynker, Maryline Panis, Anne Ruiz, Benjamin R. tenOever and Venetia Zachariou, 9 May 2023, Science Signaling.DOI: 10.1126/ scisignal.ade4984.
This study was supported by National Institute of Neurological Disorders and Stroke NS086444S1 (R.A.S), the Zegar Family Foundation (B.T.) and the Friedman Brain Institute Research Scholars Program (V.Z., B.T., R.A.S., J.J.F.).
