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Coronavirus can transform pancreas cell function; certain genes may protect an infected person’s spouse By Reuters

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© Reuters. FILE PHOTO: The ultrastructural morphology exhibited by the 2019 Novel Coronavirus (2019-nCoV), which was identified as the cause of an outbreak of respiratory illness first detected in Wuhan, China, is seen in an illustration released by the Centers for

By Nancy Lapid

(Reuters) – The following is a summary of some recent studies on COVID-19. There are some research results that require further analysis to verify the findings, and others that still need to be approved by peer review.

Coronavirus transforms pancreas cell function

When the coronavirus infects cells, it not only impairs their activity but can also change their function, new findings suggest. Researchers found that coronavirus causes pancreas beta cells, insulin-producing, to not only make less insulin but also produce more glucose and other digestive enzymes. This is not the normal function of these cells. This is what we call a “change of cell fate”, said Dr. Shuibing Ch, the study leader. He presented the findings at the European Association for the Study of Diabetes’ annual meeting, which was held virtual this year. The researchers reported earlier in Cell Metabolism, that the change in cell fate may be permanent or reverseable. Chen also noted that COVID-19 victims have experienced diabetes in the days following infection. She stated that it was worth looking into the incidence of diabetes in COVID-19 survivors. Her group has experimented with coronavirus using clusters of cells that were engineered to produce mini-organs (or organoids) that closely resemble the lungs and liver. Chen of Weill Cornell Medicine in New York stated that the findings indicate loss in cell function and fate may also be occurring in lung tissues.

Certain genes may protect an infected patient’s spouse

A study of couples in which both partners were exposed to the coronavirus but only one person got infected is helping to shed light on why some people may be naturally resistant to the virus. Researchers had assumed such cases would be rare but an appeal for volunteers led to the discovery of approximately a thousand people. They ultimately took blood samples of 86 people for further analysis. They found that more resistant partners have genes that are capable of activating natural killer (NK), cells more efficiently. This is part of our immune system’s initial reaction to germs. Infected cells can be destroyed and recognized by NKs, which prevents the disease developing. The research was published in Frontiers in Immunology on Tuesday. “Our hypothesis is that the genomic variants most frequently found in the susceptible spouse lead to the production of molecules that inhibit activation of NKs,” study leader Mayana Zatz of the University of São Paulo, Brazil, said in a statement. This is not supported by the present study, she said. Researchers said that even if these findings were confirmed by more research, other immune mechanisms will need to also be examined.

Experimental pill shows promise against coronavirus variants

Laboratory (NYSE:) studies show that Merck & Co’s experimental oral COVID-19 antiviral drug, molnupiravir, is likely to be effective in patients infected with any of the known variants of the coronavirus, including the dominant, highly transmissible Delta, researchers said on Wednesday in a presentation during IDWeek 2021, the virtual annual meeting of infectious disease organizations. Molnupiravir is not designed to target the spike protein that the virus uses, as this target for all COVID-19 vaccinations. It targets the enzyme that virus uses to create copies of itself. This drug works by inserting errors into the virus’s genetic code. Merck noted that early treatment is the best way to get the drug’s effectiveness. Two large-scale late-stage drug trials are currently underway by Merck – one in treatment for COVID-19, and the other as a preventive.

Click for a Reuters graphic https://tmsnrt.rs/3c7R3Bl on vaccines in development.

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