SARS-CoV-2, the virus that causes COVID-19, binds to a receptor on a cellular receptor called angiotensin-converting enzyme 2 (ACE2) to enter the cell and replicate. This process markedly impairs ACE2 receptor function. Findings from a recent study suggest that antibodies for the ACE2 receptor develop after COVID-19 illness, driving long-term complications.
Most people recover from COVID-19 illness within a few weeks of symptom onset. Some, however, experience long-term complications that last several weeks or months, a phenomenon previously referred to as “long COVID” and now known as “Post-Acute Sequelae after SARS-CoV-2 infection,” or PASC.
Many of the acute symptoms of COVID-19 arise from overactivation of the body’s immune system following loss of ACE2 function. A key player in this overactivation is the renin-angiotensin-system, an important regulator of blood pressure, inflammation, and body fluid homeostasis. Disturbances in this system in the setting of SARS-CoV-2 infection can drive poor outcomes, such as acute respiratory distress syndrome and death in COVID-19.
The authors of the study analyzed blood samples for the presence of ACE2 antibodies in 67 people who had a history of previous SARS-CoV-2 infection and 13 people with no history of infection. They also measured ACE2 levels and activity in the participants' blood.
Whereas 81 percent of the participants with previous infection had antibodies against ACE2, none of the participants who had never been infected had antibodies. Even though ACE2 levels were comparable in both infected and non-infected participants, ACE2 activity was lower among participants with antibodies compared to those without antibodies.
These findings suggest that following SARS-CoV-2 infection, antibodies against the ACE2 receptor can be detected in the blood. These antibodies, which likely form early in the disease process, impair ACE2 function, providing a potential mechanism for PASC. One limitation of this study is that the blood samples were de-identified, meaning that they carried no identifiers or information about whether the samples were from people who experienced long-term complications of COVID-19.
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