An article in Science recently generated a lot of interest by providing a possible explanation as to why COVID-19 may be lethal for some to some, but virtually unnoticed in others.
Scientists at the La Jolla Institute for Immunology in California have shown that infection with common cold coronaviruses can generate an immune response that is similar to important pieces of the immune response generated by SARS-CoV-2 – the virus that causes COVID-19. This raises the possibility that previous infection with one of the milder coronaviruses could make COVID-19 less severe. But how likely is this? And how does this relate to what we already know about coronaviruses?
A few weeks ago, another article was at the center of the SARS-CoV-2 immunity debate. This showed that the antibody response to SARS-CoV-2 may decrease over time.
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The findings made it clear that SARS-CoV-2 could infect a person many times over and that a vaccine might not generate lasting protection. But the article focused on only one arm of the immune response, the B cells, which produce antibodies that help clear an infection.
T cells are also key to the immune response against viruses. They play a variety of roles, including helping B cells grow into disease-fighting machines. The article by Jose Mateus and colleagues at La Jolla Institute of Immunology is important because it shows that people love T cells from the milder coronaviruses long enough to potentially interact with a new challenge of SARS-CoV-2 and that those T cells may even recognize SARS-CoV-2 and help clear the infection.
The case for cross-immunity
For epidemiologists, the evidence of declining immunity and cross-immunity did not come as a surprise. A 1990 study found that soldiers infected with one of the milder coronaviruses did not retain immunity for more than a year. Also, the boom-bust cycle that the milder coronaviruses undergo from year to year can be explained by a mix of declining immunity and cross-immunity.
The milder coronaviruses can generate similar antibodies as those generated by the coronaviruses that cause Sars and Mers. These antibodies are so similar that they almost cheated a British Columbia healthcare facility into thinking they had an outbreak of Sars after the Sars epidemic was declared. In fact, the outbreak was caused by OC43, one of the coronaviruses that causes the cold.
However, infections that generate structurally similar antibodies do not necessarily provide cross-protection in a medically meaningful way.
We’re just not sure yet
Evidence for cross-protection among all but the most related coronaviruses is poor.
It is difficult to say whether the milder coronaviruses protect against SARS-CoV-2 in part because we have done so little oversight of them. Ideally, we could look at historical data to identify which communities have experienced significant outbreaks of each milder coronavirus strain in recent years and then see if there is a link with less severe COVID-19 cases.
Challenge studies, in which a person is intentionally infected with a milder coronavirus strain and then exposed to SARS-CoV-2, could also address the question, but are dangerous and ethically questionable. For now, we can only say that the possibility that the common coronaviruses can protect against SARS-CoV-2 remains just that – a possibility. Indeed, Matthew and colleagues describe this theory as “highly speculative.”
This article was republished from The Conversation by Stephen Kissler, Postdoctoral Researcher, Immunology and Infectious Diseases, University of Cambridge under a Creative Commons license. Read the original article.
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