SARS-CoV-2 Nucleocapsid Protein Found to Worsen Chronic Pain in Those Exposed to COVID-19
Nikhil Prasad Fact checked by:Thailand Medical News Team Nov 03, 2024 1 day, 13 hours, 42 minutes ago
Medical News: A recent study has revealed that the nucleocapsid (N) protein of SARS-CoV-2, the virus responsible for COVID-19, may be more dangerous than previously understood. Scientists from Guangdong Provincial People's Hospital, Sun Yat-sen University, and the Guangdong Academy of Medical Sciences have discovered that this protein not only contributes to the virus's infectious capabilities but also promotes severe and lasting pain in affected patients. This
Medical News report discusses how the research team identified the link between the N protein and increased pain sensitivity in patients, especially those with conditions like cancer, chemotherapy-induced pain, and inflammatory pain.
SARS-CoV-2 Nucleocapsid Protein Found to Worsen Chronic Pain in Those Exposed to COVID-19
Study Overview and Methodology
The study was conducted using mouse models designed to simulate conditions of pathological pain. These models included mice injected with bone cancer cells, mice undergoing chemotherapy, and mice with inflammatory pain. Using these models, researchers injected the mice with a SARS-CoV-2 N protein viral vector, observing significant increases in pain sensitivity. Tests involved both mechanical and thermal pain sensitivity assessments, including tail flick, Hargreaves, and hot plate tests at different temperatures.
One key finding in the study was that the N protein interacts specifically with the sodium ion channel Nav1.7, a crucial element in pain perception. By modulating Nav1.7 function, the N protein increases pain sensitivity, making affected neurons more responsive to painful stimuli. This discovery helps to clarify how COVID-19 might contribute to lingering pain symptoms.
Key Findings
The research yielded several notable findings:
-Increased Pain Sensitivity: Mice injected with the N protein showed heightened pain responses, especially to thermal and mechanical stimuli. In tests involving temperatures above 46°C, these mice displayed markedly decreased withdrawal times, indicating increased sensitivity to heat.
-Chronic Pain Promotion: The study observed that N protein significantly prolonged the duration of pain in various models. For example, in mice with bone cancer, the presence of N protein extended the period of pain sensitivity beyond what was observed in the control group. Chemotherapy-induced pain, too, lasted longer in N protein-exposed mice, with pain levels remaining high even after normal recovery times.
-Nav1.7 Interaction: Using proximity ligation assays and co-immunoprecipitation, researchers confirmed a specific interaction between the SARS-CoV-2 N protein and the Nav1.7 channel. In normal conditions, the Nav1.7 channel enables sensory neurons to transmit pain signals; however, the N protein amplifies this transmission by delaying the channel's inactivation phase, resulting in prolonged pain signaling.
-Broader Implications<
;/strong>: Beyond animal models, the study also suggested that this interaction might affect humans. By examining DRG (dorsal root ganglion) neurons from both nonhuman primates and humans, the researchers noted similar Nav1.7 modulation, indicating that patients with certain types of pre-existing pain conditions may be especially vulnerable to severe and persistent pain following COVID-19 infection.
Conclusion
The findings offer critical insights into one mechanism by which COVID-19 worsens or prolongs pain in affected individuals. SARS-CoV-2's N protein, by modulating Nav1.7 function, plays a significant role in increasing both the intensity and duration of pain. For patients with conditions like bone cancer, undergoing chemotherapy, or those with pre-existing inflammatory pain, COVID-19 may trigger chronic pain or exacerbate existing symptoms.
This study highlights the need for pain management strategies for COVID-19 patients, particularly those with pre-existing conditions. The insights gathered here also open new avenues for therapeutic research, including targeted treatments that may alleviate COVID-19-induced pain by focusing on Nav1.7 modulation.
The study findings were published on a preprint server and are currently being peer reviewed.
https://papers.ssrn.com/sol3/papers.cfm?abstract_id=4997931
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