Covid, Josh Fishman, Tanya Lewis discussed on 60-Second Science
We bring you up to speed on the science behind the most urgent questions about the virus and the disease. We demystify the research and help you understand what it really means. I'm Josh fishman, scientific American senior health editor. Tanya Lewis usually here with me has the day off. Today, new research shows how old coal viruses may help protect you against the coronavirus causing the pandemic. And vaccine makers are not rushing out shots against the Akron variant, even though the original shots have lost some effectiveness. What's the hold up? We'll explain. From early in the pandemic, it's been clear that not everyone is equally vulnerable to SARS CoV-2, the coronavirus that causes COVID. Some people get really sick while others have mild symptoms or none at all. And this was true before any of us were protected by vaccines. Overall, about 80% of infected people get a mild illness. The virus is so wildly infectious, though, that the 20% of serious cases have been a global catastrophe. 5 and a half million people dead, 850,000 of them in the U.S.. But in people who don't get very ill, what's protecting them? We hear a lot about neutralizing antibodies, but this is a new virus to us. You don't get antibodies until after you've been exposed or vaccinated. Well, it turns out that some people might be getting help from another part of the immune system. T cells, which were triggered years ago, by exposure to different but related coronaviruses. These microbes have been with us forever, and they cause sneezing and runny noses, a common cold. The cold coronavirus and the pandemic coronavirus are distantly related, but they do share similar proteins. Early in the pandemic, scientists noticed that T cells that reacted to the cold virus also reacted to the pandemic virus. These are called cross reactive T cells. But since researchers saw this in test tubes, they had no idea what this meant for immunity in real life. Ajit levonian infectious disease physician at imperial college London decided to find out. England has a really good contact tracing system. It allowed Lal vani and his colleagues to find 52 people who lived with individuals who tested positive for COVID. These 52 started out negative themselves. Within about three days, half of that group or 26 turned positive. The other 26 stayed negative. Taking a closer look at the negative people who didn't get COVID while vani's team found that 7 of them had a lot of these cross reactive T cells. None of the people who got COVID had such cells. Zero. Lalvani told me this is a very substantial protective effect, and his team just published the results in the journal nature communications. The T cells primed by that older cold virus recognized the new pandemic virus because it has those similar proteins, and they work to fight it off. Immunologist Alex city from the la Jolla institute for immunology told me he thinks this research is on the right track. Other studies have linked recent exposure to these cold viruses with less severe COVID, says SETI, who is not involved in la vani's work. Research has also tied preexisting T cells to a stronger immune response to a COVID vaccine. The important thing about the T cells is that they point to new targets to add to second generation vaccines. The proteins these T cells reacted to went beyond the well-known spike protein at the heart of the first gen shots. The cells respond to other proteins called N and ORF, for instance. Adding those to a new vaccine formula both lalvani and SETI suggest could widen the protection of vaccines against variance. The proteins do seem to trigger a broader immune response to different forms of the coronavirus. And a few companies have such T cell enhanced vaccines in the works. Grit stone and immunity bio BioTech firms in California are two that have started clinical trials, including more of these proteins in a shot could create a vaccine capable of boosting your immunity against whatever variant comes along. The variant that has come along right now is, of course, a, and it is exhibit a for the case that vaccines rolled out a year ago have lost a bit of their edge. Remember, the original vaccine trials showed that Pfizer and Moderna shots were 90 to 95% effective at stopping infection. Now, two shots of the Pfizer vaccine are only 33% effective at stopping a infection. Scientists looking at cases in South Africa found. A booster shot does increase the amount of Akron neutralizing antibodies, and the Moderna and Pfizer vaccines with that booster are tremendously effective at preventing hospitalization and serious illness. Still, I'm a crown's wild spread has many people asking why we don't have a specific shot to stop it. mRNA vaccine makers have been saying that they could roll out new formulas fast if needed. But my colleague Charlie Schmidt did some reporting on this for scientific American, and he found out that really fast may not be fast enough. Designing a variant vaccine then testing and mass producing it can take four to 6 months. But now we know that variants can burst out in shorter time periods, followed by other variants. That makes companies reluctant to change all of their production over to a shot that may be irrelevant by the time it reaches your arm. As long as the current shots keep hospitalizations down, we should stick with them, says Paul offit vaccine specialist at children's hospital in Philadelphia. Right now, hospitalizations are running at about 2% of cases. Office says that if that number climbs to 15%, then it's time to change to a new shot. Not everyone agrees. Ralph barrack of virologist at the university of North Carolina told Schmidt that aron could be the backbone for the next set of variants since it's so good at spreading. So vaccines designed around a could offer more protection against future waves. What barrack would really like to see is a more universal vaccine that covers more variants. So we're not constantly playing catch up. The T cell stimulating shots I mentioned are one way to get there. So are vaccines that incorporate proteins from several closely related coronaviruses. Researchers at the University of Washington are working on one of those, using proteins that don't mutate much, so they should work from variant to variant. Other groups are trying related approaches, but it might be two years before those are ready. So companies may have to bite the bullet and roll out.