The reputation of the new coronavirus in connection with the assumptions of scientists has taken a really eerie turn.
Researchers studying the interaction between coronavirus and its hosts have found that when the SARS-CoV-2 virus infects a human cell, it triggers a monstrous transformation. Obeying the instructions of the virus, a recently infected cell sprouts multifaceted tentacles, strewn with viral particles.
These mutilated zombie cells seem to use these streaming threads, or filopodia, to reach still healthy neighboring cells. The bulges seem to penetrate the bodies of cells and inject their viral poison directly into the genetic command centers of these cells, creating another zombie.
The new study, an international group led by researchers from the University of California at San Francisco, says coronavirus appears to be using these recently sprouted dendrites to increase the uptake of new cells and detect infections in their human victims.
Their study was published Friday in the journal Cell.
Scientists also believe that they have identified several drugs that can disrupt the viral uptake of cells and slow down the process by which COVID-19 is fixed. These compounds, many of which have been developed for the treatment of cancer, probably work because they block the chemical signals that primarily activate the production of filopodia.
Among the seven drugs that they identified as potentially useful against COVID-19, Silmitasertib– another experimental drug in early clinical trials for the treatment of bile duct cancer and forms of brain cancer in children; ralimetiniba cure for cancer developed by Eli Lilly; and gilteritinib (marketed as Xospata), a drug that is already being used to treat acute myeloid leukemia.
The new study is the result of ambitious efforts to identify promising treatments for COVID-19 using the science of “proteomics,” the interaction between proteins. Scientists intend to identify chemical signals and a cascading chain of events that occur when the virus meets and overtakes the host cell. Then they look for drug compounds that can encrypt these chemical signals and disrupt the infection process.
Until now, the process by which coronavirus was supposed to infect cells was pretty common for the virus: it found receptors on the surface of cells that line the human mouth, nose, airways, lungs, and blood. ships.
Like space invaders in science fiction, a tiny virus has been known to dock on the surface of a much larger cell. A viral landing group appeared on board, which stole the usual function of the camera, making it a factory for its replication.
The discovery of the fact that coronavirus initiates the germination of filopodia in infected cells suggests that at some point in its development more than one method was developed to ensure its rapid transmission from cell to cell.
As a rule, a rapid increase in the number of infected cells increases the victim’s viral load, makes her feel ill, and helps transmit the virus to other people. UC San Francisco Nevan KroganOne of the newspaper’s senior authors said that much about coronavirus does not meet the expectations of scientists.
But the detection of filopodia in cells infected with a coronavirus suggests that this virus has developed several methods of penetration into cells and has established itself as a force to be reckoned with.
“It’s so ominous that the virus uses other mechanisms to infect other cells before killing them,” Krogan said. Other researchers include scientists from Mt. Sinai in New York, Rocky Mountain Laboratory in Montana (where these images were taken using electron microscopy), the Pasteur Institute in Paris and the University of Freiburg in Germany.
The cells of germinating filopodia not only look creepy. They also keep a pretty nasty company.
The vaccine, a member of the poxvirus family of smallpox viruses, uses filopodia that sprout from infected cells to “travel” to these cells and inject more viral particles into them. study found. HIV and some influenza viruses are known to use filopodia to enhance their ability to break down and enter cells. According to a virologist at Columbia University, many viruses alter the exoskeleton of the cells they infect, and inducing filopodia is one way to do this. Angela L. RasmussenAnd although the increase in infection is one of the roles they often play, there are many others.
But Krogan said that even these viruses do not seem to cause the prolific filament growth that was seen by his colleagues on cells infected with coronavirus. According to him, the branching tentacles protruding from these cells were very unusual.
Microbiologist at Columbia University Stephen P. Goff I strongly recommended that caution be advised that filopodia necessarily behave as a second way to infect cells with the virus.
“This is an intriguing and really cool observation,” said Goff. The striking snapshots of the study show that filopodia contain a lot of viruses and that in the laboratory, inhibition of their growth appears to reduce viral replication. This convincingly indicates that filopodia somehow enhances the ability of the virus to infect cells, he admitted.
“But we still do not know at what stage [of infection] influenced by weird ledges, he said. “It will be very fun to find out.”