According to a new study, the coronavirus can infect insulin-producing cells in the pancreas, reducing their ability to secrete insulin and sometimes causing cell death. Damaging these insulin-producing cells, known as beta cells, can potentially worsen symptoms of diabetes, particularly type 1 diabetes. In addition, some studies suggest that severe COVID-19 may trigger diabetes in people with no previous history of the condition, again raising the possibility that the virus infects beta cells. This trend is still being investigated, but given the new data, the virus may sometimes induce diabetes by injuring beta cells.
People with either type 1 or type 2 diabetes — where the body makes some insulin but the tissue can’t take it up due to insulin resistance — face a greater risk of developing severe COVID-19 symptoms than the general population, according to the Centers for Disease Control and Prevention (CDC). In general, people with diabetes are more likely than those without the disease to experience complications when infected with any virus, since the condition can impair immune function. That said, no one knew whether SARS-CoV-2, the virus that causes COVID-19, can directly attack the pancreas, Jackson said.
Researchers ran experiments on pancreatic tissue from organ donors, nine of whom had died from severe COVID-19 infections and 18 who died of other causes and tested negative for the virus.
In the first group, they found SARS-CoV-2 had directly infected the beta cells of some individuals, and in several lab dish experiments, they found that the virus could infect, damage and kill beta cells drawn from the other donors who died from non-COVID-19 causes. The new study shows that pancreatic cells can be infected in a lab dish, but the same has not been definitively shown in humans, to reach a solid conclusion, scientists will need to examine many more pancreas samples from patients who died of COVID-19.
How the virus might break into beta cells?
The virus primarily uses a receptor protein called ACE2 to sneak into cells, but several other proteins on the cell surface appear to help prime the virus to plug into ACE2. For a recent study, researchers went hunting for ACE2 and one of these proteins, called transmembrane serine protease 2 (TMPRSS2), in beta cells, but found little of either.
In another independent study, published in the same journal, researchers reached the same conclusion, making it seem like SARS-CoV-2 had few doorways into beta cells.
As in previous studies, they found low levels of ACE2 and TMPRSS2 in beta cells from the donors, but interestingly, they found an abundance of neuropilin 1 (NRP1) and transferrin receptor (TFRC). Compared with alpha cells, another kind of pancreatic cell, beta cells expressed far more NRP1 and TRFC, hinting that the virus might show a selectivity for the beta cell if it does infect the pancreas. However, more research is needed to understand the mechanism of infection of pancreatic cells by SARS-CoV-2.
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