A Science article recently generated a great deal of interest providing a possible explanation for why COVID-19 can be fatal for some and go virtually unnoticed by others.
Scientists at the La Jolla Institute for Immunology in California have shown that infection with the common cold coronavirus can generate an immune response that resembles key parts of the immune response generated by SARS-CoV-2 – the virus that causes COVID-19. This raises the possibility that a previous infection with one of the milder coronaviruses could make COVID-19 less severe. But what is the probability? And how does that relate to what we already know about coronaviruses?
A few weeks ago, a different 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 results raised concerns that SARS-CoV-2 could infect a person multiple times and that a vaccine may not generate lasting protection. But the article focused on just one arm of the immune response, B cells, which produce antibodies that help clear an infection.
T cells are also essential for the immune response against viruses. They play various roles, one of which is helping B cells to become disease fighting machines. The article by Jose Mateus and his colleagues at the La Jolla Institute of Immunology is important because it shows that people keep the T cells of the milder coronaviruses long enough to potentially interact with a new SARS-CoV challenge. 2 and that these T cells might even recognize SARS-CoV-2 and help clear the infection.
The case of cross-immunity
For epidemiologists, the evidence for decreased immunity and cross-immunity came as no surprise. A 1990 study showed that soldiers infected with one of the milder coronaviruses did not retain immunity for well over a year. In addition, the boom-bust cycle that milder coronaviruses undergo from year to year can be explained by a mixture of waning immunity and cross-immunity.
The mildest coronaviruses can generate antibodies similar to those generated by the coronaviruses responsible for Sars and Mers. These antibodies are so similar that they almost fooled a British Columbia healthcare facility into believing there was a Sars outbreak after the Sars outbreak was declared over. In fact, the outbreak was caused by OC43, one of the coronaviruses that cause the common cold.
However, infections which generate structurally similar antibodies do not necessarily provide medically meaningful cross-protection.
We are still not sure
Evidence of cross-protection between all but the most closely related coronaviruses is scarce.
It’s hard to say whether the milder coronaviruses protect against SARS-CoV-2 in part because we’ve done so little monitoring on them. Ideally, we would be able to examine historical data to identify communities that have experienced major outbreaks of each milder strain of coronavirus in recent years, and then see if there is a link to any cases of COVID-19. less serious.
Challenge studies, in which a person is intentionally infected with a milder strain of coronavirus and then exposed to SARS-CoV-2, could also answer the question but are dangerous and ethically burdensome. For now, all we can say is that the possibility that common coronaviruses may protect against SARS-CoV-2 remains just that – a possibility. Indeed, Mateus and his colleagues describe this theory as “highly speculative”.
This article is republished from The Conversation by Stephen Kissler, Postdoctoral Fellow, Immunology and Infectious Diseases, University of Cambridge under a Creative Commons license. Read the original article.
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