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SARS-CoV-2 requires cholesterol to invade cells and form megacells


Cell fusion
Researchers have manipulated cells to carry either the protein from SARS-CoV-2 (green) or its human target, ACE2 (magenta). As they approached each other, the cell membranes fused. Researchers believe that a similar process causes the virus to slip into cells. Credit: D. Sanderset al./

To cause COVID-19, the SARS-CoV-2 virus must invade human cells and requires an accomplice.Cholesterol, a waxy compound well known for arterial blockage, helps the virus open cells and slide inside, a researcher at the Howard Hughes Medical Institute. Clifford Brangwin’s Lab report.

Without cholesterol, the virus cannot sneak through the protective barrier of cells and cause infection, The team writes in a preprint posted on on December 14, 2020. The work of reproducing the early stages of infection of cells grown in the laboratory has not yet undergone a peer-reviewed scientific review process.

“Cholesterol is an integral part of the membrane that surrounds cells containing SARS-CoV-2 and some viruses. It makes sense that it is very important for infection,” said a biophysical engineer at Princeton University. One Brangwynne says.

The survey results are Better health outcomes seen in COVID-19 patients taking cholesterol-lowering drugs known as statins, He adds.Scientists have not yet established a responsible mechanism, but with this study Another published last fall We propose that the drug prevent SARS-CoV-2 from entering cells by denying cholesterol.

This discovery of the importance of cholesterol may help scientists develop new temporary measures to treat COVID-19 until most people are vaccinated, says Brangwynne. The study may also shed light on the strange feature of the disease: the formation of large complex cells found in the lungs of COVID-19 patients. In their experiments, scientists saw similar megacells appear under the microscope.

Mimicking a virus infection

Usually, Brangwynne’s team studies the physical forces that organize molecules inside cells. However, in the spring of 2020, his lab, like many other labs around the world, shifted focus and trained in biological expertise on SARS-CoV-2. They began investigating how viral and human proteins interact and how that interaction causes SARS-CoV-2 to enter cells. “We are not a virology lab. We have never worked in this area before, so we started thinking about the tools and approaches we could use,” he says.

Brangwin’s labs often work with cells grown in the lab. To mimic SARS-CoV-2 infection, his team designed such cells to play either of the two molecules of the viral “peplomer” or the human ACE2 protein. (To cause an infection, the virus must fuse its membrane to the cell’s membrane. This process begins when the peaplomer reaches the cell’s target, ACE2.)

In the lab, researchers observed the interaction of these proteins with cells grown in the lab. First, small tentacles emerged from ACE2 cells and attached to peplomer proteins in nearby cells. At these points, the two cell membranes fuse to form an opening and the cell contents are mixed. Eventually, the two cells merged. This is the same as scientists expect the virus to fuse with cells and infect.

Researchers such as Princeton’s David Sanders, Chanel Jumper, and Paul Ackerman have sought to prevent this cell fusion. Using an automated system, we tested the effects of about 6,000 compounds and more than 30 adjustments to peplomer. These and other experiments suggested that if the SARS-CoV-2 membrane lacks cholesterol, the virus cannot invade its target cells.

This is not the first evidence related to cholesterol.The· Previous researchAccording to a group at the University of California, San Diego, the body’s immune response to the virus has been found to produce cholesterol-depleting compounds, but in this case from the cell’s own membrane, not the virus.

“Cholesterol is very well studied as an important factor in many viral infections,” he said. Peter Casson, A scientist at the University of Virginia, studying the physical mechanisms of viral disease. “Interestingly, the role of cholesterol in virus invasion varies greatly between viruses.” It is not clear exactly how cholesterol helps SARS-CoV-2, but the process is the biology of infection. Understanding that it may provide clues about, says Kason, who was not involved in the study.

The obvious beneficial effects of statins extend to other viral infections. Some studies suggest that these drugs damage the flu virus by depriving it of cholesterol, Kasson says. But that may not be the only way drugs can change the course of a viral infection, he says. “Statins also alter the immune response, so it’s a bit complicated.”

Mysterious mega cell

When the Brangwin experiment was conducted, his team noticed something strange. The cells continued to swallow each other and spilled the contents together so that the eggs would break into a bowl. The complex cells known as syncytium that appear under a microscope are similar to those found in healthy tissues such as muscle and placenta and in some viral diseases.

“People already knew that the COVID-19 virus causes syncytium, but researchers were able to visualize the process beautifully,” he says. Jennifer Lippincott-SchwartzHe was a senior group leader at HHMI’s Janelia Research Campus and was not involved in the research. “Cell-cell fusion is an area that is not really well studied in biology in itself.”

The experiments are likely to show how the megacells found in the patient’s lungs are formed, she says. “The formation of syncytium can be very detrimental in the case of COVID, as it can destroy lung tissue and cause death.”

Brangwin says it is not yet clear whether syncytium will play a major role in the progression of COVID-19. But his team writes that the discovery of cholesterol contributions may help scientists fight the disease. “Our findings highlight statins and other potential benefits. [similar] Treatment. “



David W. Sanders et al. , “SARS-CoV-2 requires cholesterol for viral invasion and pathological syncytium formation.. Posted on on December 14, 2020. doi: 10.1101 / 2020.12.14.422737


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