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It’s been a long time since we could watch a film in the cinema or attend a gig with a group of friends. And until there is an effective vaccine in widespread use, some form of social distancing will likely have to remain in place. At least 60 per cent of the population will have to become immune to Covid-19 to stop the virus that’s causing it from spreading in the first place – either through vaccination or by naturally recovering from an infection. But either scenario requires the body’s immune response to last for long enough.
Studies of recovered patients are starting to paint a picture of what our immune system looks like after a coronavirus infection. The good news is that recovered patients do have antibodies to show they were infected. The bad news is their immunity may be short-lived.
Scientists at King’s College London repeatedly tested 96 patients and healthcare workers at Guy’s and St Thomas’ NHS Foundation Trust for antibodies between March and June. According to their preprint study, which yet has to be subjected to peer review, the levels of virus-fighting antibodies peaked at about three weeks after the onset of symptoms but started to dwindle in as little as two to three months – in some people with mild disease, they became completely undetectable. Although 60 per cent of the participants produced a “potent” antibody response to the virus, only 17 per cent retained the same potency at the end of the three-month study period.
So if antibodies disappear after a couple of months, does this mean people could become reinfected in seasonal waves? A waning antibody response to Sars-Cov-2 is not all too surprising as this is also the case with other human coronaviruses. Antibodies to the four strains of seasonal coronaviruses that cause the common cold are lost within a year while people who had severe acute respiratory syndrome (caused by Sars-Cov-1) in 2003 still showed antibodies after three years. Drawing from what we know about other coronaviruses, it’s possible that neither a vaccination nor infection will provide lifelong immunity.
“When the body no longer has a Covid-19 infection, the [B] cells that produced these antibodies don’t need them,” says Raj Thaker, lecturer in immunology at the University of Essex. B cells are specialised white blood cells of the immune system. When they encounter a pathogen – a virus or bacterium – they transform into plasma cells, which start producing antibodies that bind to, for example, the spike protein on the surface of the novel coronavirus and stop it from infecting cells.
Once the antibodies have defeated the invading virus, a small pool of memory B cells are formed. These white blood cells persist for much longer and remain dormant until they encounter the same virus again. The next time, they will produce a much faster and stronger immune reaction. There have been anecdotal reports of patients becoming reinfected with Sars-Cov-2 for a second time, but there is currently no evidence supporting the notion.
Antibody tests can tell us more about past infections and are useful to track the spread of the Covid-19 pandemic. But antibodies are not the only line of defence against viruses. Our immune system has multiple ways of fighting an infection and it turns out another, more enigmatic type of white blood cell might play a more important role in the fight against Covid-19: T cells.
T cells, which also remember past infections, also help stimulate the B cells that make antibodies. Then killer T cells seek out and destroy cells that are infected with the virus by rupturing their cell membranes. This interplay between T cells and B cells is the key to an immune response to any infection. Danny Altmann, professor of immunology at Imperial College London offers an analogy. “If you had a typical field of a battle scene from a movie, you wouldn’t have all tanks. You’d have tanks, infantry and artillery doing different complementary things, always working together.” Antibodies, he adds, have been likened to throwing out missiles to attack an invading virus while T cells ordinarily would be attacking and blowing up any houses where the invading virus takes hold.
Because T cells circulate in the blood for years after an infection, they contribute to the immune system’s long-term memory. A study published on July 15 in the journal Nature showed people who recovered from Sars still have memory T cells 17 years after infection. This revelation raises the hope that T cells protect people who have been infected and recovered from the novel coronavirus but have no detectable antibodies in their blood.
In a separate study published in July, researchers from the University of Melbourne compared the immunity levels of 41 Australians adults who had recovered from mild to moderate Covid-19 with uninfected individuals. They found that people produced varying levels of antibodies that some had higher levels of helper T cells than others. These people could have better immunity, at least in the short term. “One of the key questions that remains is what level of antibody or T cell/B cell response is required to protect people from infection. At this point, we don’t know what level of immune response will be protective in the long term,” says lead author Jennifer Juno, a postdoctoral fellow at the University of Melbourne.
The main problem with studying T cells is that they are much smaller in size than antibodies. While antibodies can be detected in a single drop of blood collected from a finger-prick test, analysing T cells is a much longer and elaborate process. “First we need to understand which parts of the virus are immunogenic. This means they will provoke an immune response in the body and be attacked by the T cells,” says Thaker. “Then we need to develop the technologies to identify these Covid-specific T cells. The question will be how important it is for these technologies to look for both T cells and B cells.” While antibody tests are useful to screen the general public, he adds, further understanding the T cell responses will be particularly important for vaccine development.
One vaccine developed by the University of Oxford has already shown to trigger the production of T cells in addition to antibodies. The hope is that the combination of neutralising antibodies and T cells raised by vaccines will provide stronger and longer lasting immune responses to the virus than contracting and recovering from the disease without vaccination.
After seven months, there are still many unanswered questions about immunity to Covid-19 – and about how vaccines could help the immune system to do its job better and faster. Will vaccines work? Do they offer long-lasting immunity or will we need a booster shot? Getting people around the world vaccinated against the disease could become “one of the biggest things humankind has ever tried to organise,” says Altmann. “That suggests that we need some really good health service monitoring to keep check on people. How often are we going to check them if life on planet Earth is ever going back to normal?” he says.
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