Editor's Note: Erin Bromage is an associate professor of biology at the University of Massachusetts Dartmouth. Her research focuses on the evolution of the immune system and how animals defend themselves against infection. Follow him on Twitter @ErinBromage. The opinions expressed are yours. You can read more opinion pieces at CNNe.com/opinion
(CNN) - My son was so excited the day he made enough money to buy his own BB gun. When I brought him home, he immediately went to the shooting range we had built and started shooting. The first pellet came out on the left. The second came out to the right. We never found where the third shot hit.
"The gun is broken," he said, walking away frustrated that each shot landed differently. After giving him a few minutes to put his thoughts in order, we discussed what happened. I told him that the weapon is new and that we still don't know how it behaves. We shouldn't be surprised that there are some issues to solve, but the more we shoot, the better we'll understand how it works. A day later, and with great patience, each shot clustered tightly into the target.
Something similar happens as studies of the body's immune responses to covid-19 emerge. We are still in the stage of spotting a new weapon; the shots are going through the target and people are frustrated by the lack of agreement within the scientific community. Countless questions continue to be asked:
Do the covid-19 antibodies protect us from reinfection? Are they persistent long after recovery or do they decrease rapidly? And what does this mean for the development of a vaccine?
These questions resonated in early April when the first antibody data began to emerge. After reading a previous article on antibody testing, I wrote a note for my undergraduate class on an online forum titled, "This is terrible news, tell me why."
The document clearly showed that people who had recovered from an infection produced antibodies against the virus, but that was not my concern. It was concerning that the antibodies peaked, but then rapidly decreased in concentration, so much so that if the reduction continued linearly within the next 120 to 150 days there would be no protective antibodies left.
This suggested that patients who had recovered from covid-19 could be reinfected and become ill again. Antibody-induced immunity that lasts from six months to a year is what we often see with human coronaviruses that cause the common cold. If this initial study were to be fully trusted, this would really be terrible news.
Another article describing the rapid decline in antibody levels was published in June and followed up with a second report in July showing a similar result. The last article showed that, on average, the patient's antibody levels tended to decrease by half about 36 days after the onset of symptoms, while for a small portion of the sample their antibody levels decreased more slowly.
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Science seemed to be confirming my initial fear that the immunity of the antibodies was not sufficient to protect coronavirus victims recovered from reinfection.
But then science progressed further. A series of posts in recent weeks about antibody responses to vaccines and a fancy serological study (an antibody test in your blood) shifted the focus to our knowledge.
The Oxford and Moderna vaccines generated a robust antibody response, as high or higher than that generated by mild or moderate infection with the live SARS-CoV-2 virus. These vaccines are like a school for your immune system, they teach your body how to respond to a virus without causing disease. This was good news!
If the antibody level starts higher, it will likely persist for longer than previously reported. The limitation is that we still need time to determine how long the antibodies will persist, and whether they will be shown to prevent infection with the virus in the real world.
The serological study, preliminary published by a research team at Mount Sinai Hospital in New York City, clearly showed that after mild to moderate covid-19 infection, antibody levels decreased from their peak, then maintained a stable level for at least three months.
It also demonstrated that this immune response was capable of neutralizing the virus, providing the recovered patient with a strong sign of what might be some level of immune protection. This study differed from the first antibody tests in that the number of patients evaluated was much higher: it included almost 20,000 patient blood samples (more than 9 times the sample size of the largest previous studies) and the methods were designed to specifically measure the concentration of antibodies against the spike protein of the virus that allows it to enter our cells. Although not yet peer-reviewed, the study's comprehensive methods make it the best example of coronavirus serology research.
Not that the early studies were wrong, they simply hadn't considered how their data related to the battle for immunity. In battle you aim to overwhelm your opponent with number strength and superior weaponry. This is also true for the antibody response of the immune system.
When a virus invades your body and an antibody response is required for protection, it not only produces enough antibodies to match your viral opponent, but it significantly outstrips the target to overwhelm the virus and remove it from its system.
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When the viral threat is removed, many of the antibody-secreting cells recruited into the fight can die to free up space and resources for your body to respond to new threats, and with that cell death the antibody they are producing also begins to drop.
This antiviral antibody response would be seen as a rapid increase in antibody levels, and then a rapid decrease in antibodies in the months after infection. This rapid drop in antibodies was what the early studies captured.
But what those early studies failed to resolve was that some of those antibody-secreting cells can live in the bone marrow, possibly persisting for years, secreting virus-neutralizing antibodies. So, after the rapid drop in antibody levels after infection, the antibody levels would stabilize and persist as long as those long-lived antibody-secreting cells remained in the bone marrow. That type of response is well known with many viral infections and, most importantly, it has been documented to occur in people who survive MERS infection.
High concentrations of antibodies are not absolutely necessary to fight future infections. We only require enough antibodies to provide assistance to the innate immune system to prevent further exposure to the virus from establishing an infection.
Given the promising results of antibody stimulation from developing covid-19 vaccines, my confidence continues to grow that a vaccine is in sight that provides at least modest protection against symptoms in severe cases.
However, we must keep in mind that each new antibody study may bring different results, resulting in the need to readjust our understanding, and we must consider what this could mean for asymptomatic victims of covid-19. Remember: tough, long fights help train our immune systems for future threats.
Therefore, being infected and avoiding developing symptoms of infection may not produce the protective antibodies that you may need in the future to prevent future exposure. We are also likely to find differences in antibody responses between children and adults, or between men and women.
Meanwhile, conflicting results are common in science, especially early in the study of a new topic. We should not be too quick to draw conclusions, especially in studies with few samples or with headline grabbing titles. Each new study published helps refine our understanding, and we should keep in mind that we are all looking for quality results, but negative results, or those that do not fit the current narrative, help scientists refine the focus of our understanding.
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