SARS-CoV-2 Needs Cholesterol to Invade Cells and Form Mega Cells

Amazing stuff! Good news!

"... To cause COVID-19, the SARS-CoV-2 virus must force its way into people’s cells – and it needs an accomplice. Cholesterol, the waxy compound better known for clogging arteries, helps the virus open cells up and slip inside ... Without cholesterol, the virus cannot sneak past a cell’s protective barrier and cause infection ...
“Cholesterol is an integral part of the membranes that surround cells and some viruses, including SARS-CoV-2. ...
These experiments and others suggested that if SARS-CoV-2’s membrane lacks cholesterol, the virus cannot enter its target cell. ...
This isn’t the first evidence implicating cholesterol. The previous study ... found that the body’s immune response to the virus produces a compound that depletes cholesterol – but in this case from the cell’s own membrane, not the virus’s. ...
The interesting thing is that cholesterol’s role in viral entry varies a lot between viruses.” It’s not clear exactly how cholesterol aids SARS-CoV-2, but understanding that process could offer clues about the biology of infection ...

“People already knew that the COVID-19 virus will create syncytia, but the researchers were able to visualize the process beautifully,” ... “Cell-cell fusion is itself a really under-studied area in biology.”

The experiments likely illustrate how mega cells found in patients’ lungs form ... “The formation of syncytia can be very injurious in the case of COVID, where it can destroy lung tissues and lead to death.” ... it’s not clear yet whether or not syncytia play a major role in the progression of COVID-19. ..."

"Many enveloped viruses induce multinucleated cells (syncytia), reflective of membrane fusion events caused by the same machinery that underlies viral entry. These syncytia are thought to facilitate replication and evasion of the host immune response. ...
Together with cell biological and biophysical approaches, the screen reveals an essential role for membrane cholesterol in spike-mediated fusion, which extends to replication-competent SARS-CoV-2 isolates. Our findings provide a molecular basis for positive outcomes reported in COVID-19 patients taking statins, and suggest new strategies for therapeutics targeting the membrane of SARS-CoV-2 and other fusogenic viruses. ..."

SARS-CoV-2 Needs Cholesterol to Invade Cells and Form Mega Cells | HHMI.org People taking cholesterol-lowering drugs may fare better than others if they catch the novel coronavirus. A new study hints at why: the virus relies on the fatty molecule to get past the cell’s protective membrane.

Here is the link to the underlying research paper:

SARS-CoV-2 Requires Cholesterol for Viral Entry and Pathological Syncytia Formation

Researchers engineered cells to carry either a protein (green) from SARS-CoV-2 or its human target ACE2 (magenta). When near each other, the cells’ membranes fused. Researchers think a similar process lets the virus slip into cells.