Researchers at Swansea University Medical School are helping to drive forward understanding of the virus that causes Covid-19 and how it can be tackled.
The novel severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), the etiological agent of Covid-19, has swept across the world with unprecedented speed. Since it was initially identified there have been more than 72 million infections and 1.61 million deaths worldwide.
The Swansea scientists have contributed to a multicentre study led by Washington University School of Medicine which reveals one of the molecular mechanisms of host innate immune defence against SARS-CoV-2 and how it restricts virus entry into a cell.
Upon SARS-CoV-2 infection, the virus enters a cell and releases its RNA by a process called membrane fusion. In their study, a cholesterol derivative, 25-hydroxycholesterol, was given to cells and found to prevent viral replication by trapping the virus and its RNA in a vesicular structure called a late-endosome.
Their findings have just been published online in the journal Proceedings for the National Academy of Science (PNAS).
Professor Siyuan Ding, who led the study in Washington University, said: “Understanding the virus-host interaction is important for the development of an antiviral strategy. The results of this study highlight one possible antiviral mechanism of 25-hydroxycholesterol and provide a basis for drug development based on this natural compound.”
Professor Yuqin Wang, from Swansea, commented: “25-Hydroxycholesterol is a close relative of cholesterol formed by the enzyme cholesterol 25-hydroxylase in response to viral infection. 25-Hydroxycholesterol and its derivatives have multiple effects on the host inflammatory response. ”
Professor William Griffiths added: “The level of 25-hydroxycholesterol in SARS-CoV-2 infected patients and its role in the body’s defence against COVID-19 diseases warrant further investigation.”
Cholesterol 25-hydroxylase suppresses SARS-CoV-2 replication by blocking membrane fusion
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