https://pubmed.ncbi.nlm.nih.gov/20015551/
Annexin A2 on lung epithelial cell surface is recognized by severe acute respiratory syndrome-associated coronavirus spike domain 2 antibodies
Yi-Ting Fang 1 , Chiou-Feng Lin, Pao-Chi Liao, Yu-Min Kuo, Shuying Wang, Trai-Ming Yeh, Chi-Chang K Shieh, Ih-Jen Su, Huan-Yao Lei, Yee-Shin Lin
>The target of this autoimmune attack is Annexin A2, a phospholipid-binding protein, which acts as a cofactor for tPA, ensuring integrity of the pulmonary vasculature and promoting lung elasticity. Antagonism of Annexin A2 would cause lung blood clots, pulmonary edema, and ARDS.
>n essence, anti-Annexin A2 would cause all the hallmark pulmonary pathology already identified on autopsy among severe cases of acute COVID-19. Autoantibodies to this lung protective protein were already identified among hospitalized SARS patients.
>Furthermore, Annexin A2 is also expressed in the vasculature of the brain. Therefore, antagonism of Annexin A2 can cause microvascular stroke and damage to the blood-brain barrier, which would result in neuro-inflammation and long-term neurological injury.
>The implications for acute COVID-19 are enormous. Not only would it explain why steroids work in this disease, but it would suggest that we should be treating the disease more like other autoimmune diseases of the lung.
>We have misdiagnosed severe cases of acute COVID-19 as a viral pneumonia, which disregards the established evidence that shows viral load of SARS-CoV-2 is markedly diminished by the time patients develop the respiratory distress that only occurs in second stage of the disease.
>We are also misdiagnosing Long COVID, which is also characterized by lung perfusion deficits, pulmonary fibrosis, and various neurologic sequelae. Our next studies will establish whether these autoantibodies are also present among patients with persistent post-COVID symptoms.
Annexin A2 on lung epithelial cell surface is recognized by severe acute respiratory syndrome-associated coronavirus spike domain 2 antibodies
Yi-Ting Fang 1 , Chiou-Feng Lin, Pao-Chi Liao, Yu-Min Kuo, Shuying Wang, Trai-Ming Yeh, Chi-Chang K Shieh, Ih-Jen Su, Huan-Yao Lei, Yee-Shin Lin
>The target of this autoimmune attack is Annexin A2, a phospholipid-binding protein, which acts as a cofactor for tPA, ensuring integrity of the pulmonary vasculature and promoting lung elasticity. Antagonism of Annexin A2 would cause lung blood clots, pulmonary edema, and ARDS.
>n essence, anti-Annexin A2 would cause all the hallmark pulmonary pathology already identified on autopsy among severe cases of acute COVID-19. Autoantibodies to this lung protective protein were already identified among hospitalized SARS patients.
>Furthermore, Annexin A2 is also expressed in the vasculature of the brain. Therefore, antagonism of Annexin A2 can cause microvascular stroke and damage to the blood-brain barrier, which would result in neuro-inflammation and long-term neurological injury.
>The implications for acute COVID-19 are enormous. Not only would it explain why steroids work in this disease, but it would suggest that we should be treating the disease more like other autoimmune diseases of the lung.
>We have misdiagnosed severe cases of acute COVID-19 as a viral pneumonia, which disregards the established evidence that shows viral load of SARS-CoV-2 is markedly diminished by the time patients develop the respiratory distress that only occurs in second stage of the disease.
>We are also misdiagnosing Long COVID, which is also characterized by lung perfusion deficits, pulmonary fibrosis, and various neurologic sequelae. Our next studies will establish whether these autoantibodies are also present among patients with persistent post-COVID symptoms.
