According to scientists having endured a common cold could protect people from getting severe COVID-19.

A study suggests the immune system’s reaction to different coronaviruses could be very similar to its reaction to the one behind the pandemic. 

As a result, lasting immunity from those viruses — known to cause colds — may help the body fight off COVID-19 if someone catches it, meaning they get less seriously ill.

The German research also focuses on a less-discussed type of immunity, instead of antibodies which have been at the forefront of a lot of studies.

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T-cell immunity appears to be more common among infected patients and scientists say it may potentially last even longer. 

Eight out of 10 people who have never even had the disease have some degree of protection because of colds they have had in the past, the study claimed.

And even COVID-19 patients with very mild symptoms developed a strong T-cell immune response, whereas they do not appear to have strong antibody responses.

It is still not clear whether people can catch the coronavirus twice, and this type of immunity might not prevent that, but it could lessen their symptoms if they do.

Researchers at University Hospital Tübingen in Germany studied the blood of 365 people, 180 of whom had had COVID-19 and 185 who hadn’t.

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When the researchers exposed people’s blood to SARS-CoV-2, the virus that causes COVID-19, people who had had the illness already produced the strongest immune response.

But surprisingly, there was also an immune reaction in 81 per cent of the people (150) who had never had COVID-19.

This, the scientists said, was because they had already been infected with one or more of the common cold coronaviruses known to infect humans – named OC43, 229E, NL63 and HKU1 – and their immune systems cross-reacted as a result.

The researchers wrote: ‘Similarity to common cold human coronaviruses provided a functional basis for… immunity in SARS-CoV-2 infection’.

The reaction the researchers were studying is caused by T cells, which are a type of white blood cell that produce long-lasting protection from serious infection.

But they are slower acting than antibodies and may not stop a virus before it takes hold.

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One scientist who was not involved with the research, Professor Francois Balloux – an infectious disease expert working at University College London – explained how they work in a Twitter thread today.

He said: ‘T-cell response is a late immune response and does not generally make the host refractory [resistant] to infection…

‘Though, T-cell immunity is essential for controlling an infection and reducing symptoms. SARS-CoV-2 seems to elicit robust T-cell response even in asymptomatic/mild patients.’

The Tübingen study’s findings raise hope that people may develop natural immunity to COVID-19, which is something antibody studies were not looking hopeful for. 

Antibodies are developed much faster by the body – some within days of infection – and fight off the illness before being stored in the immune system in case it comes back.

The presence of strong antibodies may mean that people do not become ill with a virus a second time because the immune system is so fast to destroy it.

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But many COVID-19 patients – especially those who only had mild symptoms or none at all – did not appear to be developing detectable levels of antibodies, causing concern among scientists.

The Tübingen researchers wrote in their study: ‘At present, determination of immunity to SARS-CoV-2 relies on the detection of SARS-CoV-2 antibody responses.

‘However, despite the high sensitivity reported for several assays [tests] there is still a substantial percentage of patients with negative or borderline antibody responses and thus unclear immunity status after SARS-CoV-2 infection.’

They said that their study found T-cell immune responses even in patients who tested negative for antibodies, meaning they did have some level of protection.


The team said T-cell immunity to COVID-19 deserved more scientific study and that they are now preparing to start human trials of vaccines they hope could develop it.

The study was published on the website Research Square – not in a medical journal – and had not been scrutinised by independent scientists before publication.