A longitudinal study by the researchers from King’s College London — first reported by The Guardian on Sunday — has suggested that immunity to Covid-19 might be lost in months. The suggestion is based on a steep drop in patients’ antibody levels three months after the infection. A look at the findings, implications and limitations of the new study, and the broader question of how the body develops immunity against an infection:
What are the findings of the study?
The researchers analysed the immune response of 90 recovered Covid-19 patients and healthcare workers. In their study, which is not yet peer-reviewed, they found that antibodies that specifically help in neutralising the coronavirus SARS-CoV-2 decreased 2-23-fold during an 18-65 day follow-up period. This is similar to the decrease in antibodies seen in seasonal coronaviruses associated with the common cold.
They suggested that immunity developed by the formation of antibodies against SARS-CoV-2 lasts only a few months, and recovered Covid-19 patients are likely to remain susceptible and could get re-infected.
The analysis found “a potent” level of antibodies produced in 60% of participants during the peak of their infection; and that only 16.7% retained that level of potency 65 days later. While the level of antibodies was at a higher level in patients with severe symptoms, the researchers said it is not clear why antibody response correlates with disease severity. The researchers noted that asymptomatic individuals also generate antibodies against the virus.
What are the implications and the limitations of these findings?
The researchers said the study has important implications when considering widespread serological testing, antibody protection against re-infection with SARS-CoV-2, and the durability of vaccine protection.
In a separate statement issued by King’s College London, Dr Katie Doores from the School of Immunology & Microbial Sciences, who led the study, said “further research is needed to determine the level of antibodies required for protection from infection.” “We also need to know more about the titre of antibody that is required to prevent re-infection in humans,” she said.
Does a drop in antibodies result in losing immunity against the virus?
Not necessarily. Antibodies are like fingerprints that give us evidence that a pathogen (the coronavirus in this case) has caused an infection and that the immune system has responded. The antibodies usually remain in the blood for a period of time and quickly activate the immune system when the body is exposed to the pathogen again. Some antibodies not only recognise when the pathogen returns, but also protect the body for a lifetime from re-infection, as in the case of measles. However, in the case of seasonal flu, the antibodies give protection for a very small period.
In the case of the novel coronavirus, it is not yet clear how long the antibodies provide a recovered person protection. “Further studies are needed to determine the longevity of the antibody response and what level of antibodies is required to protect against re-infection,” the researchers said in a statement. Until then, the presence of antibodies only gives us the evidence that a person was exposed to the virus.
The researchers flagged the fact that antibodies are just one of the ways in which the body can fight a virus such as SARS-CoV-2.
So, what is the other way?
The researchers make an observation: “… the role T-cell responses generated through either infection or vaccination play in controlling disease cannot be discounted in these studies”.
T cells are a key component of the immune response against a virus. A human body has two mechanisms of immunity response within the adaptive immune system. First is the humeral immune, which is also called antibody-mediated immunity and has been discussed above. However, when a virus enters a cell and can no longer be detected by antibody-mediated immunity, a cell-mediated immune response can take over to kill the virus.
Cellular immunity occurs inside the infected cell, and are mediated by cells called T lymphocytes. These are the T cells, which recognise the infected cell. Before that, these cells have to be activated by interacting with an antigen (virus)-presenting cell. Once the T cells are activated, they clone themselves generating numerous T cells, and destroy the infected cells.
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During the process of activation, some of the T cells remain inactive as memory cells. These produce more T cells if the infection returns. Therefore, memory plays a crucial role in providing cell-mediated immunity. There are also helper T cells, which function indirectly by communicating to other immune cells about potential pathogens.
What is the evidence so far on cell-mediated immune response to infection with SARS-CoV-2?
AIIMS Director Dr Randeep Guleria said data emerging on immune response shows that cell-mediated immunity is also activated in some cases and is giving protection through T cells in the blood.
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In a study published in the journal Cell, researchers from Germany found that T cell clusters emerge over the course of disease in recovering patients. It said T cells reactive to SARS-CoV-2 have been identified in “individuals exposed to other common cold coronaviruses”, therefore suggesting that T-cell response detected in healthy individuals is likely to be activated from the memory T cells derived from this earlier exposure.
In a commentary published in Nature on July 7, researchers from the US said T-cell reactivity against SARS-CoV-2 was observed in unexposed people. “However, the source and clinical relevance of the reactivity remains unknown. It is speculated that this reflects T cell memory to circulating ‘common cold’ coronaviruses. It will be important to define the specificities of these T cells and assess their association with Covid-19 disease severity and vaccine responses.”
In another article, published in the journal Immunity, researchers from the US reviewed the immunology of Covid-19 and posed two questions relating to T-cell response: first, what is the contribution of T cells to initial virus control and tissue damage in the context of Covid-19; and second, how do memory T cells established thereafter contribute to protective immunity upon reinfection. The researchers wrote: “While the induction of robust T cell immunity is likely essential for efficient virus control, dysregulated T cell responses may cause immunopathology and contribute to disease severity in Covid-19.”
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