![]() So, unlike CCR5, you can't simply knock out the ACE2 receptor, he says. "The receptor regulates your blood pressure," Landau explains. Instead of using CCR5 to "open the cell's door," SARS-CoV-2 uses the ACE2 receptor. And inspired by the story of CCR5, they went looking for mutations in the genes required for SARS-CoV-2 to enter and infect cells.įor COVID superdodgers, the situation appears to be more complex than for people resistant to HIV, Landau says, because the way SARS-CoV-2 infects cells is different from that of HIV. "So when SARS-CoV-2 came along, of course, many labs looked to see if the same might be true for this virus," Landau says. One mutation in their genes could make them a true superdodger. But it did something else: It showed scientists that one mutation could make a person completely resistant to an infection. It led to the first - and only - way to cure a person of HIV and suggested a new route, using gene editing with CRISPR. The finding completely shifted the field of HIV. "So in the case of resistance to HIV, the story was very clear." "You can put as many virus particles as you want onto those cells, and they will not get infected," he says. Remember, without CCR5, HIV can't infect the cell. It completely cripples the molecule so that it doesn't appear on the cells' surface, the group reported in the journal Cell. Lo and behold! Both people had the same mutation in the gene - and it's a powerful mutation. In collaboration with a research group down the hall, Landau and his colleagues sequenced the CCR5 gene in two people completely resistant to HIV. "We were quite amazed that it all happened so quickly," Landau says. Then only a few short weeks later, Landau and his colleagues made another huge discovery, and in the process solved the final piece of the HIV puzzle. "That was the moment where we could say, 'We found something that had never been seen before.' " "That was what we call a eureka moment," Landau says. "It's kind of like the virus is knocking at the door, but nobody's opening the door. ![]() Without CCR5, the virus only sticks to the cell's surface but can't enter. Specifically, HIV needs a specific molecule, called CCR5, on the surface of the cell to "open the door" and let the virus enter, Landau says. Instead it needed a little bit of extra help. It showed that HIV didn't enter cells the way scientists had believed. The experiment garnered spectacular results. The night before, they had set up an experiment to test which molecules HIV needed to infect a human cell. In 1996, his team was getting really close to solving that puzzle. The ones Landau and his colleagues were studying back in the early 1990s. However, over the past decade, further studies have clarified that these superdodgers actually do become infected with the parasite, they simply don't show symptoms.)īy far, the most famous virus superdodgers are people protected against HIV. (In 1995, researchers in France figured out why some people appeared to never be infected with a species of malaria, known as Plasmodium vivax. The researchers found that one mutation in their genes prevents them from making a molecule the virus needs to infect the cell. In 2003, a team in London showed how some people never get a stomach bug, called norovirus, which causes vomiting and diarrhea. So that it slides off their cells, "like water sliding off a glass window," as Casanova puts it. That is, where a specific mutation in their genes makes people completely resistant to a virus. ![]() Over the course of human history, scientists have identified only two instances of true virus superdodgers. What does it take to be a true superdodger? Turns out, stopping an infection altogether is an extremely tough nut for our bodies to crack. Hollenbach and her team have found a genetic mutation doesn't prevent the virus from infecting cells - that's what Landau was searching for - but still does something remarkable: It prevents a person from having COVID symptoms. It's all stuff that's been happening this summer." "These findings are like hot off the presses," says immunogeneticist Jill Hollenbach, who led this research. Some say it's now less risky than fluĪfter two years of hunting, a team at the University of California, San Francisco has come pretty close to answering the question. Shots - Health News Scientists debate how lethal COVID is.
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