An international study of long covid symptoms by the Stanford University School of Medicine in cooperation with scientists from the University of Basel and the University Hospital there fuels the initial suspicion that the SARS-CoV-2 virus not only reduces lung function but also attacks the pancreas of seriously ill hospital patients.
Using tissue samples from seven corona deaths, the research collaboration analyzed the mechanism. According to this, the coronavirus can attack, infect and destroy the beta cells in the islets of Langerhans of the pancreas. Tissue samples showed infection of insulin-producing beta cells with disintegration. This means that a severe Covid 19 course is a risk factor for developing diabetes because the virus has chosen a protein called neuropilin 1 as its port of entry. According to the study, the virus not only invades lung tissue and uses the so-called ACE2 protein there but can also suppress insulin-producing cells in the pancreas and cause them to die; the researchers have now found. Fifteen percent of the patients admitted appearing to have newly diagnosed diabetes, the symptoms of which can last for weeks to months, perhaps even a lifetime.
How then can the pancreas protect itself from the coronaviruses? There are indications that an inhibitor can block the entry port, neuropilin 1, so that the virus can penetrate the beta cells much more poorly. However, it is still unclear whether the sugar metabolism will completely return to normal in all patients. Further analyses must determine whether permanent damage is to be expected and how it can be prevented. In any case, the team of scientists will try to develop methods and options to prevent long-term negative effects, explains the study’s co-leader, Dr. Matthias Matter.
Source: www.focus.de