As countries start to relax lockdown measures and look for novel ways of safely getting economies back online, some are considering the potential use of “immunity passports”, which would allow greater freedom for people who have already been infected with COVID-19. Apart from the social and ethical implications of such a policy, this raises an important scientific question as to what constitutes COVID-19 immunity and how we can measure it.

For the last few months, much of the focus has been on antibody testing. Antibodies are proteins that can bind to viral particles in the blood or mucous membrane, and either neutralise them so that they are unable to invade the hosts’ cells or mark them for destruction by other cells in the immune system.

Antibodies are produced by B cells, a type of white blood cell, when they encounter a cell or particle that they recognise as foreign, such as a virus. These B cells can continue to produce antibodies even after the infection has been cleared, which means that the immune system can quickly respond if the host is exposed to the same virus again. Detection of antibodies in the blood can indicate that a person has been previously exposed to a specific virus and might be protected against future infection. In the case of some viruses, such as measles, this protection may be lifelong; for others, it may only last a matter of months.

With COVID-19, recent studies suggest that the protection provided by antibodies against the SARS-CoV-2 virus that causes it may decline rapidly following infection. A study in patients who had been hospitalised with COVID-19 found that weeks after infection, 10% of patients did not have detectable levels of antibodies. Another found that within 2-3 months, antibodies could not be detected in 40% of patients who had been infected but had not shown symptoms.

What’s more, even if antibodies can be detected, there is still debate about whether or not antibodies can prevent reinfection and, if so, what levels are required to provide that protection. Infection with a contagious disease doesn’t necessarily lead to complete protection against reinfection. For example, respiratory syncytial virus (RSV), which usually only causes mild, cold-like symptoms but can cause severe viral pneumonia in young children, is so common that most infants have had it by age two. People develop antibodies in response to RSV infection, but these only protect against severe disease over time, not re-infection. Concerns about the validity of the antibody tests currently available serve to further muddy the waters.

Also, antibodies are only one part of the vast, complex immune response that is set in motion when a person becomes infected with a virus like SARS-CoV-2. A recent study looking at another major player in immune response, the T cell, tells a more optimistic story.

Where antibodies respond to the virus before it invades human cells, T cells have the task of detecting and killing cells that have already become infected. When a virus invades specific host cells, proteins associated with the virus are displayed on the cell surface. These act as a signal to T cells that there are viruses hidden within that cell, prompting them to kill the infected cell or to activate other immune cells to help with the response. When T cells encounter a specific antigen that they are able to bind to, they rapidly proliferate to produce an army of identical T cells that are able to respond to the infection. These T cells will remain in the body in higher numbers, even after the infection has been cleared.

A recent study carried out in Sweden found that whilst antibodies could only be detected in about 15% of people, around double that had developed T cell immunity. This suggests that people who are currently testing negative in antibody tests may still have some level of immunity provided by this other part of the immune system.

However, this does not necessarily mean that we are any closer to reaching herd immunity - the proportion of the population that needs to be immune to ensure that transmission of the virus is interrupted, so that cases decline. As T cells only respond to the virus once it has already invaded host cells, there is a possibility that people may still be able to transmit the virus even if they do not themselves develop disease. Further research is needed to determine whether the presence of T cells confers “sterilising immunity,” i.e. complete protection against infection and therefore transmission.

Unfortunately, detecting T cell immunity is also a lot more complex than carrying out tests for antibodies, so it is not likely to become a widespread approach to predicting immunity any time soon. However, it is a reminder that there is still a lot we don’t know about SARS-CoV-2 and about the mark that it leaves on our immune system. Before we place too much stock in the results of an antibody test, we need to remember that the presence or absence of antibodies is far from the full story.

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