Most common colds are caused by rhinoviruses — a different family — but about 15% are caused by coronaviruses. “Cross-immunity” is where past infection (and acquired immunity) against one virus in a family gives you partial or complete immunity against other viruses in the family (e.g., because your immune system got “trained” to a part of the virus common to the entire family, such as the coronavirus “spikes”).
DIE WELT has a long interview (in German) with a pulmonologist at the Charité Hospital in Berlin. Below are some highlights in (very slightly edited) machine translation, thanks to the awesome DeepL.com.
[…]WELT: In April, they made a very astonishing discovery in the laboratory: 40 percent of the volunteers they tested who had never come into contact with the corona virus before had cells in their blood that the virus was able to fend off. What exactly does this mean?
Leif Sander: At first, we were amazed by the findings ourselves. But apparently a previously experienced infection with related corona viruses activates the immune system in such a way that it also reacts to sars-CoV-2.
WELT: What does this activation look like?
Sander: The immune system consists of two systems: In one system antibodies are produced, i.e. proteins that can recognize an invading pathogen and eliminate it if possible. The second system is the cellular immune response. This produces so-called T-cells, which can either help other cells to render the pathogen harmless, or which can also attack it directly. In further experiments we have now been able to show that these T-cells apparently originate from previous cold corona infections. The common cold has given people immune cells that also recognise the new corona virus.
WELT: Does this mean that people who previously had a cold are now protected from Covid-19?
Sander: Unfortunately, we do not know. Based on our findings and similar studies from other laboratories, we have put forward the hypothesis that 30 or 40 percent of all people have cross-immunity. But this is only a hypothesis. In the laboratory we see that the activated T-cells are able to recognise sars-CoV-2 viruses. Do you think this also leads to protection against infections in living humans? In order to prove that, one has to do large studies. At the beginning of the study, the blood of volunteers would have to be searched for T-cells from previous coronavirus infections. And then it would have to be observed whether people with this existing immune trait become infected less frequently or at least become less seriously ill. Such a study was initiated by my colleague Andreas Thiel at the Charité. The study will, for example, examine the immune status of educators, residents of nursing homes and other institutions.
WELT: With the rhinitis corona viruses the immune protection does not last very long.
Sander: That is true, recently a large study has shown that a reinfection with these viruses is possible after only one or two years. The antibody concentrations in the body decrease rapidly. Maybe this is also due to the fact that rhinitis corona viruses do not make people particularly ill, which means that the immune system is not activated as strongly.
WELT: Could this also be the case with infections with the new corona virus? So that only those who are seriously ill – those who have no symptoms or only mild symptoms but no protection – build up good immune protection?
Sander: That could be, yes.
WELT: Does cross-reactivity mean that we have less to fear about the further course of the pandemic? After all, a part of the population would then be a little bit protected …
Sander: No, the basic assessment does not change at first. Cross-immunity is not a new addition – it has existed in the population from the very beginning. But if it really protects against severe disease progression or even infections, that would be good news.
WELT: In your work you concentrate on the T-cell response. However, these cells hardly play a role in the public discussion about immunity. There is always talk about antibody tests. What is more important for long-term protection – antibodies or immune cells?
Sander: You can’t say that in general. For some infections, antibodies play a more important role for the immune protection, whereas for other T-cells they play a more important role. Antibodies are easier to detect, there are also rapid tests for this. T-cells are more complicated to handle, you need blood samples and special laboratories. The immune system is extremely complex – and sometimes very surprising. For example, textbooks say that measles protects those who have a certain concentration of antibodies in their blood from infection. However, there are also people who are unable to produce measles antibodies due to a rare disease – but who are nevertheless protected. This is probably where T-cells provide protection. Whether we need antibodies, T-cells or even both for protection against the new coronavirus is not clear.
WELT: If one is optimistic and assumes that after an infection a medium-term sustained immune protection is built up and that perhaps even many people are already protected thanks to cross-immunity, could we still achieve herd immunity?
Sander: If most of the sick people would build up a good and lasting immune protection, as is the case with measles, then it could work. If this is not the case, as with rhinitis, then it doesn’t work. We know too little to give a conclusive answer to this.
But it is more important to know that in order to build up herd immunity, we would have to take the risk of many infections and also severe courses. Nobody can want that. The lockdown bought us time, which we should now invest in research into the correct handling of the virus. Establishing natural herd immunity would probably not be the right strategy. Rather, I am banking on a multi-layered approach with herd immunity achieved through vaccination.