Why Do We Develop Lifelong Immunity To Some Diseases?

September 21, 2020

For some diseases, such as measles, we are only infected once and usually have lifelong immunity, but for some, such as the flu, we must be vaccinated year after year. For other diseases, like the flu, we must be vaccinated year after year.

So why do we develop lifelong immunity to some diseases and not others? What does the novel coronavirus have to do with all this?

Whether or not we develop immunity to a disease often depends on our antibodies, which are proteins we produce in response to infection. Antibodies are one of the body’s best known defense systems. They cover invading cells and, in the best case scenario, prevent these invaders from hijacking our cells and replicating. When we clear the infection, antibody levels usually drop, but at least some of the antibodies stay around, ready to increase production again if the same disease strikes again. That’s why an antibody test can tell you if you’ve been infected in the past. It’s also what keeps us from getting sick a second time – usually.

“The body doesn’t really forget,” says Marc Jenkins, an immunologist at the University of Minnesota Medical School. Usually, when we get re-infected with a disease, it’s not because our body has lost its immunity. We get reinfected either because the pathogen mutated and our immune system no longer recognizes it, or because our body tends to mount a much lower immune response, he says.

Take the flu, for example. It’s a virus that can easily change its genes, Jenkins said. Just as our immune system kills one version of the virus, another virus that our immune system doesn’t recognize comes along. Not all viruses mutate so easily. For example, polioviruses can’t easily change their genomes, Jenkins says. That’s why we’ve been so successful in (almost) eradicating it.

Mark Slivka, an immunologist at the Oregon National Primate Research Center, says that the common cold and other viruses that don’t normally pass through our upper respiratory tract re-infect us not necessarily because they mutate quickly, but because our bodies don’t normally produce many antibodies against these pathogens in the first place.” Our bodies don’t worry about the upper respiratory tract,” he said. That’s what we’re seeing with the mild case of COVID-19. The virus sticks to the upper respiratory tract and the body doesn’t see it as a threat. In the 2020 preprint study published in the database MedRxiv (meaning it hasn’t been peer-reviewed), 10 of 175 patients with mild symptoms recovered from COVID-19 and did not develop detectable antibodies.

For diseases that don’t fall into any of these categories – meaning they don’t mutate quickly, and they often prompt a strong immune response – immunity tends to last longer.A 2007 study published in the New England Journal of Medicine found that even half of the antibodies took more than 200 years to disappear after infection with measles or mumps. The same study found similar results for the Epstein-Barr virus, which causes monoclonal antibodies. However, the antibody response doesn’t always last a lifetime. The same study found that it takes about 50 years to lose half the antibodies to chickenpox, and 11 years to lose half the antibodies to tetanus. This means that without booster shots, you could theoretically contract one of these diseases in adulthood.

Scientists are still not sure why our antibody responses to some diseases last longer than others. It’s possible that some of these more common diseases, such as chickenpox and mono, actually re-infect us more often than we realize, but we do crush the infection with antibodies before we notice it, Jenkins says. And in these cases, the immune system is at full capacity over and over again because of reinfection.” That keeps our immune system alert,” he notes. By contrast, “with tetanus, which we may have very little exposure to, we don’t step on [dirty] nails very often.”

Other scientists point out that the human immune system is trained to target pathogens that “look” a certain way, Slifka says. Bacteria and viruses tend to be symmetrical, with repeating patterns of proteins on their surfaces. (Think COVID-19 – it’s a ball with evenly spaced spikes all over it.) One theory is that we mount a larger, more sustained immune response to pathogens with more repetitive appearances. For example, the antibodies we develop against smallpox virus (which is highly repetitive in structure) can last a lifetime. However, tetanus is not repetitive at all. It’s the toxins produced by the tetanus bacteria, not the bacteria themselves, that make us sick. Based on this theory, it’s possible that our bodies aren’t as well trained to target this single, asymmetrical protein, says Slifka.

So will immunity to the new coronavirus – whether from an infection or a vaccine – last as long as our immunity to smallpox, or do we need a new vaccine every year? While it’s true that some people don’t mount large antibody responses, Jenkins remains hopeful about the former. All the evidence from natural infections and vaccine trials suggests that most people are making neutralizing antibodies to prevent the virus from entering our cell varieties, Jenkins says. And unlike the flu, the virus that causes COVID-19, SARS-CoV-2, has not mutated rapidly, Jenkins notes.

“This virus has the characteristics of a virus that we’ve been very successfully vaccinated against,” Jenkins said.