Many researchers now seem to think that not everyone is as susceptible to a COVID-19 infection. Although there is no empirical evidence to definitely suggest so, it is possible that some people are less vulnerable to SARS-CoV-2, the virus that causes COVID-19, due to previous exposure to other coronaviruses. If this is the case, there would be important implications for herd immunity. In a recent twitter thread, Francois Balloux, the Director of the Genetics Institute at the University College of London, highlighted a recent study published in pre-print, which found all 24 participants from Singapore infected with SARS-CoV-1 in 2003 also have immune cells against SARS-CoV-2. What’s striking is that 50% of the participants had no previous exposure to SARS-CoV-1, one of seven known coronaviruses to infect humans, which killed about one in 10 infected people, but ultimately disappeared somewhat mysteriously. In light of these findings, it may be possible that a proportion of the population may have pre-existing immunity to SARS-CoV-2, perhaps due to prior exposure to coronaviruses that cause the common cold. There are four such coronaviruses that we know of responsible for common colds. Most people pick up at least one of these congestion-inducing viruses in their lifetime, since they have been bouncing between humans for a long time. According to recent assessments performed by the World Health Organization (WHO), just 3% of the global population has antibodies against the new coronavirus. In order to attain herd immunity — the notion that a viral infection stops spreading in a community after a sufficient proportion develops antibodies after recovering from the illness — scientists estimate that at least 60% of a population needs to have antibodies against infection. But if there is indeed some cross-immunity from other coronaviruses, herd immunity could be reached earlier than thought. In a study published in May, Alessandro Sette and Shane Crotty of La Jolla Institute for Immunology, looked at the T cell response in blood samples that had been collected between 2015 and 2018 — before SARS-CoV-2 started circulating. Many of these individuals had significant T cell reactivity against SARS-CoV-2, although they had never been exposed to SARS-CoV-2. It is not at all clear, however, if this cross reactivity provides some level of preexisting immunity to SARS-CoV-2. But if it does, this could explain why there is so much variation in infection rates and disease outcomes between different geographical locations. “Given the severity of the ongoing COVID-19 pandemic, any degree of cross-reactive coronavirus immunity could have a very substantial impact on the overall course of the pandemic and is a key detail to consider for epidemiologists as they try to scope out how severely COVID-19 will affect communities in the coming months,” Crotty said in a statement. The two researchers also added that this is merely a hypothesis that requires validation by research. The WHO also expressed caution over this hypothesis. “There is certainly some evidence with regard to T cells, that if you have a previous coronavirus infection you may be able to mount a more rapid response to COVID-19,” said the WHO’s Michael Ryan at a press conference this week. “But there’s no empirical evidence that previous coronavirus infections protect you from infection with COVID-19. The jury is still very much out on that,” he added. Nevertheless, Ryan also expressed optimism. “It gives us hope that we are getting the kinds of immune responses that may be helpful to long-term protection,” he said. The threshold commonly accepted for achieving herd immunity is 60%-70%. But Gabriela Gomes, a researcher at the Liverpool School of Tropical Medicine, believes that individual variation — due to cross-immunity with other coronaviruses, as well as other pathogens — could lower this threshold. In fact, her mathematical models suggest that herd immunity could be reached with 10%-20% of the population getting infected. The study has yet to be peer-reviewed, though. Source
