Mary Wilson
Well-known member
Published 21 October 2024
DOI https://doi.org/10.1038/s44298-024-00064-y
Ng, W.H., Tang, P.C.H. & Mahalingam, S.
Rheumatic symptoms such as joint inflammation and pain are known features of SARS-CoV-2 infection, though the mechanisms remain unclear. Au and colleagues identified the interaction between the viral spike protein and the endothelin-1 (ET-1) signaling pathway as a cause of osteochondral damage. Their study showed that macitentan, an FDA-approved ET-1 receptor antagonist, reduced joint damage and inflammation in a hamster model, suggesting ET-1 as a potential therapeutic target for viral-induced osteoarthritis (OA).
A number of viruses, including alphaviruses, human immunodeficiency virus, hepatitis viruses, Epstein-Barr virus, herpes simplex virus, cytomegalovirus, and dengue, are known to cause rheumatic disease characterized by joint and muscle inflammation, such as arthritis, myositis, as well as associated pain, including arthralgia and myalgia[SUP]1[/SUP]. Among the most prominent are arthritogenic alphaviruses, such as Chikungunya virus and Ross River virus, both of which infect joint and muscle cells, leading to acute and chronic arthritis[SUP]2,3,4[/SUP]. Similarly, several clinical studies have linked SARS-CoV-2 infection to musculoskeletal inflammation and pain[SUP]5,6[/SUP]. Although viral-induced inflammatory arthritis and OA are less commonly reported compared to the overall burden of COVID-19, arthralgia and myalgia remain frequent symptoms[SUP]7[/SUP]. Whether arthritis and myositis are triggered by the direct presence of the virus in joint and muscle tissue remains unknown. Interestingly, no virus was detected in the joint tissues of cadavers from individuals who died of SARS-CoV-2 infection[SUP]8[/SUP], while viral nucleic acids have been found in the joint of a living patient[SUP]9[/SUP], suggesting that viral presence in tissues may vary depending on disease stage or individual factors. ...
https://www.nature.com/articles/s44298-024-00064-y#citeas
DOI https://doi.org/10.1038/s44298-024-00064-y
Ng, W.H., Tang, P.C.H. & Mahalingam, S.
Rheumatic symptoms such as joint inflammation and pain are known features of SARS-CoV-2 infection, though the mechanisms remain unclear. Au and colleagues identified the interaction between the viral spike protein and the endothelin-1 (ET-1) signaling pathway as a cause of osteochondral damage. Their study showed that macitentan, an FDA-approved ET-1 receptor antagonist, reduced joint damage and inflammation in a hamster model, suggesting ET-1 as a potential therapeutic target for viral-induced osteoarthritis (OA).
A number of viruses, including alphaviruses, human immunodeficiency virus, hepatitis viruses, Epstein-Barr virus, herpes simplex virus, cytomegalovirus, and dengue, are known to cause rheumatic disease characterized by joint and muscle inflammation, such as arthritis, myositis, as well as associated pain, including arthralgia and myalgia[SUP]1[/SUP]. Among the most prominent are arthritogenic alphaviruses, such as Chikungunya virus and Ross River virus, both of which infect joint and muscle cells, leading to acute and chronic arthritis[SUP]2,3,4[/SUP]. Similarly, several clinical studies have linked SARS-CoV-2 infection to musculoskeletal inflammation and pain[SUP]5,6[/SUP]. Although viral-induced inflammatory arthritis and OA are less commonly reported compared to the overall burden of COVID-19, arthralgia and myalgia remain frequent symptoms[SUP]7[/SUP]. Whether arthritis and myositis are triggered by the direct presence of the virus in joint and muscle tissue remains unknown. Interestingly, no virus was detected in the joint tissues of cadavers from individuals who died of SARS-CoV-2 infection[SUP]8[/SUP], while viral nucleic acids have been found in the joint of a living patient[SUP]9[/SUP], suggesting that viral presence in tissues may vary depending on disease stage or individual factors. ...
https://www.nature.com/articles/s44298-024-00064-y#citeas