New research raises the possibility that some of us may be partially protected due to past encounters with “common cold” coronaviruses. COVID19
providing evidence the T cell responses may derive in part from memory of “common cold” coronaviruses.“The immune system is basically a memory machine,” he said. “It remembers and fights back stronger.
” Interestingly, the researchers noted in their paper, the strongest reaction they saw was against the spike proteins that the virus uses to gain access to cells — suggesting that fewer viral copies get past these defenses. “The current model assumes you are either protected or you are not — that it’s a yes or no thing,” Sette added. “But if some people have some level of preexisting immunity, that may suggest it’s not a switch but more continuous.”Nearly 2,000 miles away, at the Mayo Clinic in Rochester, Minn., Andrew Badley was zeroing in the possible protective effects of vaccines. Teaming up with data experts from nference, a company that manages their clinical data, he and other scientists looked at records from 137,037 patients treated at the health system to look for relationships between vaccinations and coronavirus infection.They knew that the vaccine for smallpox, for example, had been shown to protect against measles and whooping cough. Today, a number of existing vaccines are being studied to see if any might offer cross-protection against SARS-CoV-2. The results were intriguing: Seven types of vaccines given one, two or five years in the past were associated with having a lower rate of infection with the new coronavirus. Two vaccines in particular seemed to show stronger links: People who got a pneumonia vaccine in the recent past appeared to have a 28 percent reduction in coronavirus risk. Those who got polio vaccines had a 43 percent reduction in riskVenky Soundararajan, chief scientific officer of nference, remembers when he first saw how large the reduction appeared to be, he immediately picked up his phone and called Badley: “I said, ‘Is this even possible?’” The team looked at dozens of other possible explanations for the difference. They adjusted for geographic incidence of the coronavirus, demographics, comorbidities, even whether people had had mammograms or colonoscopies under the assumption that people who got preventive care might be more apt to social distance. But the risk reduction still remained large. “This surprised us completely,” Soundararajan recalled. “Going in we didn’t expect anything or maybe one or two vaccines showing modest levels of protection.” The study is only observational and cannot show a causal link by design, but Mayo researchers are looking at a way to quantify the activity of these vaccines on the coronavirus to serve as a benchmark to the new vaccines being created by companies such as Moderna. If existing vaccines appear as protective as new ones under development, he said, they could change the world’s whole vaccine strategy.Genetics and biology At NIH headquarters in Bethesda, Md., meanwhile, Alkis Togias has been laser-focused on one group of the mildly impacted: children. He wondered if it might have something to do with the receptor known as ACE2, through which the virus hitchhikes into the body. In healthy people, the ACE2 receptors perform the important function of keeping blood pressure stable. The novel coronavirus latches itself to ACE2, where it replicates. Pharmaceutical companies are trying to figure out how to minimize the receptors or to trick the virus into attaching itself to a drug so it doesn’t replicate and travel throughout the body. Was it possible, Togias asked, that children naturally expressed the receptor in a way that makes them less vulnerable to infection? He said recent papers have produced counterintuitive findings about one subgroup of children — those with a lot of allergies and asthma. The ACE2 receptors in those children were diminished, and when they were exposed to an allergen such as cat hair, the receptors were further reduced. Those findings, combined with data from hospitals showing that asthma did not seem to be a risk factor for the respiratory virus, as expected, have intrigued researchers. “We are thinking allergic reactions may protect you by down-regulating the receptor,” he said. “It’s only a theory of course.” Togias, who is in charge of airway biology for the National Institute of Allergy and Infectious Diseases, is looking at how those receptors seem to be expressed differently as people age, as part of a study of 2,000 U.S. families. By comparing those differences and immune responses within families, they hope to be able to better understand the receptors’ role. Separately, a number of genetic studies show variations in genes associated with ACE2 with people from certain geographic areas, such as Italy and parts of Asia, having distinct mutations. No one knows what significance, if any, these differences have on infection, but it’s an active area of discussion in the scientific community.Before the pandemic, Gandhi, the University of California researcher, specialized in HIV. But like other infectious-disease experts these days, she has spent many of her waking hours thinking about the coronavirus. And in scrutinizing the data on outbreaks one day, she noticed what might be a pattern: People were wearing masks in the settings with the highest percentage of asymptomatic cases. The numbers on two cruise ships were especially striking. In the Diamond Princess, where masks weren’t used and the virus was likely to have roamed free, 47 percent of those tested were asymptomatic. But in the Antarctic-bound Argentine cruise ship, where an outbreak hit in mid-March and surgical masks were given to all passengers and N95 masks to the crew, 81 percent were asymptomatic. Similarly high rates of asymptomatic infection were documented at a pediatric dialysis unit in Indiana, a seafood plant in Oregon and a hair salon in Missouri, all of which used masks. Gandhi was also intrigued by countries such as Singapore, Vietnam and the Czech Republic that had population-level masking.The scientific literature on viral dose goes back to around 1938 when scientists began to find evidence that being exposed to one copy of a virus is more easily overcome than being exposed to a billion copies. Researchers refer to the infectious dose as ID50 — or the dose at which 50 percent of the population would become infected. While we don’t know what that level might be for the coronavirus , previous work on other nonlethal viruses showed that people tend to get less sick with lower doses and more sick with higher doses. A published in late May involving hamsters, masks and SARS-CoV-2 found those given coverings had milder cases than those who did not get them., Gandhi noted that in some outbreaks early in the pandemic in which most people did not wear masks, 15 percent of the infected were asymptomatic. But later on, when people began wearing masks, the rate of asymptomatic people was 40 to 45 percent. She said the evidence points to masks not just protecting others — as U.S. health officials emphasize — but protecting the wearer as well. Gandhi makes the controversial argument that while we’ve mostly talked about asymptomatic infections as terrifying due to how people can spread the virus unwittingly, it could end up being a good thing. “It is an intriguing hypothesis that asymptomatic infection triggering immunity may lead us to get more population-level immunity,” Gandhi said. “That itself will limit spread.”
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