At first glance, results from REACT-2, the huge Imperial College London study tracking immune response to Covid-19, make for grim reading. In many people, antibodies – those marvellous Y-shaped proteins in the body that lock on and do battle with nasty viruses – seem to decline rapidly. In a quarter of people, in just a few weeks, they seem to disappear entirely. But while these findings, at this scale, are extremely important, they are not all doom and gloom. Because: The test has limitations The study used a rapid home blood test to detect antibodies which is extremely useful but is less sensitive than lab tests. These rapid tests only detect high levels of antibodies, so it is certainly possible that some of those whose antibodies appear to have “disappeared” may actually still have very low levels in the blood. And that is critical, because: We still don’t know what concentration of antibodies confers immunity It may be that low levels suffice, or that previous exposure allows the body to speedily ramp up antibody production in case of a new threat from the virus. Immune “memory” remains important. Therefore, someone “testing negative” for antibodies may still be protected from reinfection. Healthcare workers in the study seemed to show no decline in antibody levels, which may be because they are constantly exposed to the virus, and so “top up” levels when necessary. It is also important to remember that naturally high antibody levels (as opposed to those induced by a vaccine) are not always a good thing. They may represent consistent exposure to disease, or the fact that a patient is not healing. Which is another way of saying… We have long known antibody levels can decline quickly The fact that antibodies levels can tail off within weeks of infection has long been known. And that’s a good sign, a sign that you are getting better. People with high antibody levels tend to have had severe Covid-19; you may never have had very high levels in the first place if you had a mild bout. We know, for example, that ethnic minorities have suffered disproportionately from the disease, and the Imperial study shows that non-white patients retained high levels of antibodies. Those who had been asymptomatic showed a bigger decline than those who had been through the mill. The real news is about the old. If we knew that antibodies tended to decline, we only suspected that they did so at different rates depending on age. Now we have evidence for that strong suspicion. The truth is that, as yet, no one knows for sure the precise relationship between antibody concentration and immunity. It is striking, that 10 months into the pandemic, despite 43 million confirmed and many more unconfirmed cases, validated examples of reinfection remain vanishingly rare. By September, six had been recorded. Even if antibodies decline after a few weeks, such figures would suggest they confer some protection for longer than that. How much longer? It’s complicated. Seven coronaviruses affect humans. Two – SARS and MERS – were responsible for pandemics of their own. One survivor of the 2003 SARS pandemic had antibodies in his blood that in 2020, 17 years later, killed the new coronavirus that causes Covid-19. It’s also true, however, that with the four other coronaviruses that just cause us colds, antibodies generated by natural infection can be short-lived and we can suffer again as soon as six months later. Does this mean we’re doomed? Not necessarily. Antibodies are not our only immune response. There is still great debate among researchers about the immune role played by T-cells, white blood cells that target invaders, in tackling this new coronavirus. It is likely that both antibodies and T-cells are important, and that any vaccine should attempt to induce a durable response involving both. In trials, for example, the world-leading Oxford vaccine being developed stimulates T-cell and antibody response. Of course, the fact we repeatedly suffer from those four other coronaviruses suggests that natural T-cell response is unlikely to confer long-lasting immunity. So is a vaccine pointless? Absolutely not. Vaccines prompt our bodies to work in ways they wouldn’t do normally – that’s the point. They are designed to stimulate production of a high concentration of defenders over a long time. The immune stimulators used to achieve this differ by vaccine and by disease, which is why some immunisations require one shot, and others several, with boosters following the initial injection. A potential Covid vaccine may require repeat injections. What about herd immunity? As lead researcher, Prof Helen Ward, noted, declining antibody levels suggest “we are a long, long way from anything resembling a population level protection against transmission”. The very prospect of declining natural immunity is devastating to those who want to “let the virus rip”. What if we did, thousands died, and yet a few months later there was no benefit, in terms of immunity? Where does this leave us? This study is a reminder of what has been true about coping pre-vaccine from the beginning: to control transmission without draconian lockdowns, tests must be combined with effective contact tracing. As for the prospects for an effective vaccine, they remain positive. We cannot be sure about durability, but even if it does not confer eternal immunity, a vaccine could still provide long enough immunity essentially to eliminate transmission, with breakout infections being rare, and, hopefully, as is often the case, less severe. A German study on one vaccine candidate showed the antibodies it induced lasted longer than those in patients recovering naturally, though a booster is essential. Just because vaccines are not perfect does not make them useless: smallpox vaccine, for example, protects completely for decades, but protects from severe illness for life. And in pre-vaccine America, hundreds of thousands got mumps, which can lead to severe complications, each year. Last year, 70 cases were reported.