Understanding how immunity to COVID-19 is generated in individuals who have experienced either mild or no symptoms (asymptomatic) is important in allowing us to know whether they are susceptible to reinfection. UK Coronavirus Immunology Consortium (UK-CIC) Theme Lead Professor Mala Maini and Postdoctoral Research Fellow, Dr Leo Swadling, both from University College London have collaborated with researchers from across London to better understand the different components of the immune response to COVID-19 at four months after infection and how this relates to protective immunity. The study has been published today in the journal, Science Immunology.
The immune system is extremely complex and there are many different potential routes whereby it can generate immunity to a disease after an infection. For this study, Dr Leo Swadling, a research fellow in Professor Maini’s group funded by UK-CIC, worked with researchers from Imperial College London, Queen Mary University of London, Barts and the London School of Medicine and Dentistry, Public Health England, Barts Health NHS Trust and Royal Free London NHS Foundation Trust to analyse immune responses in a group of 136 London healthcare workers, 76 of whom had a mild or asymptomatic COVID-19 infection and a matched group of uninfected controls. These healthcare workers were part of a larger cohort followed from the start of UK lockdown in March 2020. Each week, every healthcare worker took a PCR test, had their blood analysed and kept a symptom diary to allow the researchers to record any COVID-19 infection and the subsequent antibody and T cell responses generated.
Out of the 76 healthcare workers tested at 16-18 weeks post mild or asymptomatic COVID-19 infection, 89% of them had neutralising antibodies present in their blood, with high levels likely to correlate with functional protection present in 66%. This is important because this is the type of antibody that stops the virus entering cells, thereby potentially protecting against reinfection. The majority of individuals also had a variety of T cells in their blood that could recognise different parts of the SARS-CoV-2 virus. T cells can help to direct effective antibody responses as well as providing a direct added layer of protection by removing any cells that the virus has managed to infect.
When the researchers delved deeper into the results, they found a complex pattern of immune responses between individuals – about half of people had mismatched antibody and T cell responses. This suggests that these two arms of protective immunity can act in a complementary manner, with some individuals showing T cell immunity but no evidence of antibodies, and vice versa.
“This study is one of the most complete accounts of immunity to COVID-19 generated in individuals who experienced mild or asymptomatic infection,” said UK-CIC Theme Lead, Professor Mala Maini. “Our results show that the immune response following COVID-19 is complex with varying contributions from the complementary actions of antibody and T cell responses in different individuals. This highlights the importance of making sure that we study both of these aspects of immune protection when trying to understand immunity to COVID-19."
The study also shows some hints of differences in immune response depending upon severity of infection with T cell responses higher in mild versus asymptomatic cases but neutralising antibodies just as likely to be detectable in individuals whose infection had been completely asymptomatic.
“Our understanding of how immunity to COVID-19 is generated following infection is increasing all the time,” said Dr Leo Swadling. “However, it is a complex situation and we must maintain a cautious approach. Whether you think you have previously had COVID-19 or not, it’s still very important for us all to follow the Government guidelines on social distancing to make sure that we minimise the spread of COVID-19 within our communities.”
Read the full article: Reynolds et al. Discordant neutralizing antibody and T cell responses in asymptomatic and mild SARS-CoV-2 infection. Science Immunology doi: 10.1126/sciimmunol.abf3698