Welcome to Impact Factor, your weekly dose of commentary on a new study in medicine. I’m Dr. F. Perry Wilson, Yale School of Medicine.
It was only three years ago that we called the pathogen we now refer to as coronavirus “nCOV-19.” It was, in many ways, more descriptive than what we have today. The little “n” meant “new” and it was that little “n” that caused us all the problems.[1]
In reality, coronaviruses were not new to us. Little studied, perhaps, but with four strains roaming the planet all the time, giving rise to the common cold, they were viruses that our body understood.
But the coronavirus discovered in 2019 was nuevo, not only for the world, but for our own immune system. He was different enough from his circulating relatives that immune memory cells recognized him. Instead of acting like a cold, he acted like nothing we had ever seen before, at least in our lifetime. The story of the pandemic is largely a story about the immune system, a story of how our immunity grew.
The difference between early 2020 and now, when coronavirus infections remain common but not as deadly, can be measured in terms of immune education. Some of our immune systems were educated by infection, others by vaccination, and many by both.
When the first vaccines appeared in December 2020, the opportunity to educate our immune systems was still enormous. Although, at the time, an estimated 20 million had been infected in the United States and 350,000 had died, there was a large population that remained immunologically unexposed. I was one of them.
If 2020 to early 2021 was the era of immunological education, the post-vaccine period was the era of the variant. From one COVID strain to two, to five, to countless, our immune memory ─trained on a specific version of the virus or its spike protein─ became imperfect again. It’s not a matter of lack of prior exposure; These variants were not “new,” like COVID-19, but they were different. And different enough to cause infection.
Following the example of another virus that loves to dress up in different outfits, the gripewe find ourselves in the era of boosters, a world in which annual doses of a vaccine, ideally adapted to the variants circulating when it is administered, are the recommendation, if not the norm.
But questions remain about the vaccination programme, especially about who must receive it; The doubts fall mainly on two populations: 1) people who have already been infected and 2) children, because their risk of bad outcomes is much lower.
At the beginning of February, we finally had some data that may clarify the matter. The study in question, published in JAMA, tries to analyze the capacity of the bivalent vaccine ─which was the second to be released, in September 2022─ to protect the child population from COVID-19.[1]
To begin with, it was not a randomized trial. The studies that established the feasibility of the messenger ribonucleic acid (mRNA) vaccine platform if they were, were carried out before the vaccine was authorized. But trials of the bivalent vaccine were mainly limited to testing the immune response, not protection against the disease.[2]
However, with some good observation methods and some statistics, we can try to find out if bivalent vaccines worked in the child population.
The study combines three prospective cohort studies. The details are in the document, but what you need to know is that the special component of these studies was that the child population was tested for COVID-19 weekly, whether or not they had symptoms. This is essential because asymptomatic infections can transmit COVID-19.
Let’s look at the variables of interest. First and foremost, the bivalent vaccine. Some of these children received the bivalent vaccine, others did not. Other key variables are previous vaccination with the monovalent vaccine. Some had been vaccinated before with the monovalent vaccine, others had not. And, of course, the previous infection. Some had been infected before (based on nasal swabs or blood tests).
Let’s focus first on the primary exposure of interest: receiving the bivalent vaccine. Again, this was not randomized; The child population that received the bivalent vaccine was different from that which did not receive it. They generally lived in smaller households, were less likely to have had a prior SARS-CoV-2 infection, more likely to be white, and significantly more likely to have at least one chronic illness.
To my understanding, this constellation of factors describes a slightly higher risk group; It makes sense that they would be more likely to receive the second vaccine.
Taking these factors into account, what were the SARS-CoV-2 infection rates? After almost a year of follow-up, around 15% of the child population who had not received the bivalent vaccine became infected, compared to 5% of those who were vaccinated. Symptomatic infections accounted for approximately half of all infections in both groups.
After adjustment for factors that differed between the groups, this difference translated into a vaccine efficacy of around 50% for this population. That is our first data. Yes, the bivalent vaccine worked. Not amazingly, of course, but it worked.
What happened to the child population that had had a previous SARS-CoV-2 infection? Somewhat surprisingly, the vaccine was just as effective, even though their immune systems had been exposed to COVID before. Of the unvaccinated children, 10% became infected, despite having been previously infected. Only 2.5% of those who received the bivalent vaccine became infected, indicating some synergy between previous infection and vaccination.
These data indicate that the bivalent vaccine reduced the risk of SARS-CoV-2 infection in the childhood population. All this is good, but what is missing is the severity of the infections. It does not appear that any of the 426 infections documented in this study resulted in hospitalization or death, fortunately. And no data are presented on the incidence of pediatric multisystem inflammatory syndrome, although given its rarity, I would be surprised if any of them had it.
Where are we at? Well, it seems like the narrative that “vaccines don’t work” or “vaccines don’t work if you’ve already been infected” is probably not true. If they work. This study and others carried out in adults demonstrate this. If they work to reduce infections, as shown here, they will also work to reduce deaths. What happens is that, fortunately, deaths are so rare in children that the number of vaccinations necessary to prevent one death is very high. In this scenario, the decision to vaccinate revolves around the risks associated with vaccination. So far, those risks appear minimal.[3]
Perhaps adopting an annual, flu-like vaccination schedule isn’t simply the result of old habits that refuse to die. Maybe it’s not a bad idea.
El Dr. F. Perry Wilson, M. S. C. E., (@fperrywilson) is an associate professor of medicine and director of the Yale Clinical and Translational Research Accelerator. His science communication work can be found on the Huffington Post, on NPR, and here on Medscape. His new book, How Medicine Works and When It Doesn’tIt is now available.
This content was originally published in the English edition of Medscape.
2024-02-16 18:31:08
#Bivalent #vaccines #protect #children #COVID19
