Inside the body, the coronavirus is even more sinister than scientists had realized.

An electron microscopy image of a cell infected by the coronavirus that causes COVID-19. <span class=(UC San Francisco)TABLE “https: //yyg/ny/api/res/1.2/_4EBMH7C.4xwUm8XiV6o_g–/YXBwaWQ9aGlnaGxhbmRlcjt3PTcwNTtoPTUyOC41MTQwNTYyMjQ4OTk2 / HTps.
An electron microscopy image of a coronavirus-infected cell that causes COVID-19. (UC San Francisco)

The new coronavirus’s reputation for messing with scientists’ assumptions has taken a really creepy turn.

Researchers exploring the interaction between the coronavirus and its hosts have found that when the SARS-CoV-2 virus infects a human cell, it triggers a macabre transformation. Obeying the virus’s instructions, the newly infected cell sprouts with multiple tentacles dotted with viral particles.

These disfigured zombie cells appear to be using those flux filaments, or filopodia, to reach neighboring cells that are still healthy. The bumps appear to pierce the cells ‘bodies and inject their viral venom directly into those cells’ genetic command centers, thereby creating another zombie.

The authors of the new study, an international team led by researchers at the University of California, San Francisco, say that the coronavirus appears to be using these newly germinated dendrites to increase their efficiency in capturing new cells and establishing infections in their victims. human.

Their research was published Friday in the journal Cell.

Scientists also believe they have identified several drugs that could disrupt viral absorption by cells and slow the process by which COVID-19 takes hold. It seems likely that these compounds, many of which were designed as cancer treatments, work because they block the chemical signals that trigger filopodia production in the first place.

Among the seven drugs they identified as potentially useful against COVID-19 are Silmitasertib, a drug still experimental in early clinical trials as a treatment for bile duct cancer and a form of childhood brain cancer; ralimetinib, an anticancer drug developed by Eli Lilly; and gilteritinib (marketed as Xospata), a medicine already used to treat acute myeloid leukemia.

The new research stems from an ambitious effort to identify promising COVID-19 treatments using the science of “proteomics,” interactions between proteins. The scientists set out to identify the chemical signals and cascading chain of events that take place when a virus encounters and overcomes a host cell. Then they look for drug compounds that can encode those chemical signals and interrupt the infection process.

Until now, the process by which the coronavirus was thought to infect cells was fairly common for a virus: it found receptors on the surface of cells that line the mouth, nose, airways, lungs, and blood of humans. humans. glasses

Like space invaders in a science fiction story, the tiny virus was known to dock on the surface of the much larger cell. A viral landing party boarded the ship and hijacked the cell’s normal function, turning it into a factory for replication.

Tendrils reach out from a coronavirus-infected cell. <span class=(UCSF)“src =” “data-src =”–/YXBwaWQ9aGlnaGxhbmRlcjt3PTcw44_5_5_4_5_5_5_5_5_times_times_times_5_5_5_5
The tendrils extend from a coronavirus-infected cell. (UCSF)

The discovery that the coronavirus initiates the filopodia outbreak in infected cells suggests that, at some point in its evolution, it has developed more than one way to ensure that it is transmitted rapidly from one cell to another.

Generally, a rapid increase in infected cells will raise the victim’s viral load, make her feel sick, and promote transmission of the virus to others. Nevan Krogan of UC San Francisco, one of the paper’s lead authors, said there is a lot about the coronavirus that doesn’t match scientists’ expectations.

But the discovery of filopodia in coronavirus-infected cells suggests that this virus has developed more than one way to make its way into the cells and establish itself as a force to be reckoned with.

“It is so sinister that the virus uses other mechanisms to infect other cells before killing them,” said Krogan. Other researchers include scientists from the bush. Sinai in New York, Rocky Mountain Labs in Montana (where these electron microscopy images were made), the Pasteur Institute in Paris, and the University of Freiburg in Germany.

Another cell infected by the coronavirus. <span class=(UC San Francisco)“src =” “data-src =”–/YXBwaWQ9aGlnaGxhbmRlcjt3PTc09_5_7_times_b0_times_e_5_7_times_times_times_times_times_times_times_7_times_a
Another cell infected by the coronavirus. (UC San Francisco)

Cells that sprout filopodia don’t just look creepy. They also maintain a rather unpleasant company.

Vaccinia, a member of the poxvirus family that causes smallpox, uses filopodia that sprouts from infected cells to “navigate” to those cells and inject them with more viral particles, a 2008 study he found. HIV and some influenza viruses are known to use filopodia to improve their ability to break down and enter cells. Many viruses alter the exoskeleton of the cells they infect, and filopodia induction is one way to do this, said Columbia University virologist Angela L. Rasmussen. And while improving infection is a role they often play, there are many others.

But Krogan said that even those viruses don’t appear to cause the prolific growth of filaments their colleagues saw in cells infected with coronaviruses. The branched tentacles protruding from those cells were very unusual, he said.

A coronavirus-infected cell reaches out to new hosts. <span class=(UC San Francisco)“src =” “data-src =”–/YXBwaWQ9aGlnaGxhbmRlcjt3PTcwNTtoPTUyOC43NQ//ttttps://la.zen_53 53 51256e5423769fe2a44363b9f744a90e “/>
A coronavirus-infected cell reaches new hosts. (UC San Francisco)

Columbia University microbiologist Stephen P. Goff called for caution in assuming that filopodia necessarily behave as a second way of infecting cells with viruses.

“It’s intriguing and a really cool observation,” said Goff. The striking images from the study show that filopodia contain many viruses and that inhibiting their growth in the laboratory appears to reduce viral replication. This strongly suggests that filopodia are somehow amplifying the virus’s ability to infect cells, he acknowledged.

“But we still don’t know at what stage [of infection] it’s affected ”by the strange bumps, he said. “It will be a lot of fun to find out.”