In a new study, researchers found that some healthy people possess immune cells capable of recognizing the novel COVID-19 virus.
The reason for this might be found in prior infections with ‘common cold’ coronaviruses.
Whether or not this cross-reactivity has a protective effect on the clinical course in individuals infected with SARS-CoV-2 will now be addressed by the ‘Charité Corona Cross’ study.
The research was conducted by a team at Universitätsmedizin Berlin and the Max Planck Institute for Molecular Genetics.
Why is it that some people develop severe symptoms following infection with the novel coronavirus, while others hardly notice the infection?
The answer to this question is multilayered and is the subject of intensive research.
One potentially crucial factor identified by the team: prior exposure to harmless ‘common cold’ coronaviruses.
This insight is based on research involving T-helper cells, a type of specialized white blood cell which is essential to the regulation of our immune response.
The researchers found that one in three people with no prior exposure to SARS-CoV-2 nonetheless has T-helper cells capable of recognizing the virus.
The likely reason for this is that SARS-CoV-2 shares certain structural similarities with coronaviruses which are responsible for the common cold.
In the study, the researchers isolated immune cells from the blood of 18 COVID-19 patients receiving treatment at Charité and confirmed PCR positive for SARS-CoV-2.
They also isolated immune cells from the blood of 68 healthy people who had never been exposed to the novel coronavirus.
The researchers then stimulated these immune cells using small, synthetic fragments of SARS-CoV-2 ‘spike proteins’, the characteristic, crown-like protrusions on the outer surface of coronaviruses that enable the virus to enter human cells.
The researchers subsequently tested whether the T-helper cells would be activated by contact with these protein fragments.
They found that this was the case in 15 out of 18 patients with COVID-19 (85%).
The team says the immune system in these patients was in the process of fighting this novel virus, and therefore showed the same reaction in vitro.
The fact that not all patients with COVID-19 showed this T-helper cell response to viral fragments is probably due to fact that T cells cannot be activated outside the human body during an acute or particularly severe phase of an illness.
The team was, however, surprised to find memory T-helper cells capable of recognizing fragments of SARS-CoV-2 in the blood of healthy individuals.
They were found in a total of 24 out of 68 healthy individuals tested (35%).
In fact, the researchers noticed that the immune cells of COVID-19 patients reacted to different fragments of the viral envelope than the immune cells of healthy individuals.
While the T-helper cells of patients recognized the spike protein in its full length, the T-helper cells isolated from healthy individuals were primarily activated by sections of the spike protein which showed similarity to corresponding sections found in the spike proteins of harmless ‘common cold’ coronaviruses.
This suggests that the T-helper cells of healthy individuals react to SARS-CoV-2 because of previous exposure to the endemic ‘common cold’ coronaviruses”.
Notably, the researchers were able to show that the T-helper cells isolated from healthy participants who reacted to SARS-CoV-2 were also activated by various ‘common cold’ coronaviruses—displaying what is known as ‘cross-reactivity’.
What effects this cross-reactivity might have on a previously healthy person infected with SARS-CoV-2 was not addressed in the current study.
It is possible that cross-reactive T-helper cells have a protective effect, for instance by helping the immune system speed up its production of antibodies against the novel virus.
In this case, a recent bout of the common cold would probably result in less severe COVID-19 symptoms.
However, it is also possible that cross-reactive immunity could lead to a misdirected immune response and potentially negative effects on the clinical course of COVID-19. We know this can occur with dengue fever, for instance.
One author of the study is Dr. Claudia Giesecke-Thiel, the head of the Flow Cytometry Facility at the MPIMG.
The study is published in Nature.
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