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Pfizer has an RSV vaccine. What took so long?

Pfizer has an RSV vaccine.  What took so long?

Pfizer has an RSV vaccine. What took so long?

In addition to COVID and the flu, we’re dealing with another serious respiratory bug, respiratory syncytial virus (RSV). A disturbing difference with RSV: Babies and children younger than 2 are severely affected. Infection with the virus can cause inflammation of the lungs and airways, and in the worst cases it causes pneumonia.

RSV is not new – it has been circulating seasonally for decades. USA sees more than 58,000 of hospitalizations every year due to the disease, which also affects children globally. But this year, RSV is particularly bad in the US, with positive cases starting to average around 7,000 per week. The number of hospitalizations in October 2022 is double as they were in October 2021. Recently, a 6-year-old boy in Michigan died of an RSV infection.

Earlier this month, Pfizer released data from the third phase of the trial RSV vaccine in a press release. The research included 7,400 pregnant women and infants (pregnant women can synthesize antibodies and passively transfer them to the fetus via the placenta). The gunshot was determined to be nearby 82 percent effective in the prevention of severe infections of the respiratory tract in babies in the first three months of life. Pfizer plans to submit the trial results to the Food and Drug Administration by the end of this year.

An RSV vaccine would be welcome news for parents. But then again, RSV has been around for a while. What took so long?

The fact that children are the target population for the vaccine is a major challenge, says Julia Hurwitz, an infectious disease researcher at St. John’s Children’s Research Hospital. Jude in Memphis. She is working on the development of an intranasal RSV vaccine for infants, which is currently in phase I trials, and will also target parainfluenza virus infection in children. Hurwitz explains that her team is moving very cautiously in testing the vaccine in humans – starting first with adults, then older children, and then younger children. “Adults can say, hey, I’m willing to try,” she explains. “I’m willing to basically be the guinea pig and make sure this thing runs safely.” That’s what happened with the COVID-19 vaccine: a bunch of adults agreed to try it first, and then after those trials were successful, kids tested it. But for any RSV vaccine, researchers will at some point need newborns as test subjects, Hurwitz explains. And when they test on babies, the researchers just want to move very, very slowly.

All this is complicated by the catastrophic RSV vaccine tragedy that occurred in 1966. vaccine with inactivated virus was injected into children in Washington, DC, in 1966. later, 80 percent of the vaccinated children who were then infected with the virus were hospitalized. Two died. Vaccinated children passed worse against the virus compared to children who were not vaccinated, Hurwitz explains.

Most scientists attribute this failure to formalin, the chemical used by scientists to inactivate the RSV virus in the vaccine. This is thought to have changed the structure of the virus used in the vaccine, and in turn the vaccine itself launched producing only weak antibodies, which eventually restored the children’s immune systems to their ability to fight the real virus.

In 2008, infectious disease pediatrician Fernando P. Pollack proposed another possibility in a study conducted on laboratory animals: A type of white blood cell called an antibody-making B cell may not have had the necessary level of immune affinity to bind to the vaccine. Therefore, the antibodies failed to bind to the inactivated virus in the RSV vaccine and failed to neutralize it, leaving the body unable to neutralize, ie. to fight the actual virus. Failed neutralization not only allowed RSV to replicate indefinitely in infected children, Polack’s theory suggests; it also paved the way for deposition RSV-antibody complexes in the lungs. This led to an exacerbated immune response, including inflammation, and caused increased respiratory illness in vaccinated children. Moreover, the vaccine was also ineffective, according to Pollack’s study, because it did not stimulate a set of receptors, found on the body’s immune and non-immune cells, that were responsible for recognizing invaders.

Because of this tragedy in 1966, “the RSV vaccine world was extremely cautious because we don’t want to repeat that mistake,” Hurwitz says. As Hurwitz works on his RSV vaccine, the most important rule he follows is not to change the structure of RSV. “Show the immune system exactly what RSV looks like so that the appropriate B cell binds to the vaccine,” she says.

That’s easier to do now than it was in the 60s—Hurwitz points out that we’ve come a long way in vaccine design. We are now adept at using genetic material to develop vaccines, as was done with mRNA vaccines for COVID-19. This allows vaccine makers to essentially give the immune system a small piece of the virus to fight against – it looks just like the real thing, but it’s not the whole virus. Pfizer’s RSV vaccine uses one of the virus’ proteins that helps the virus fuse with cells.

Based on the results released by Pfizer, Hurwitz is hopeful and optimistic about the new vaccine’s effectiveness. “I hate to see the years go by with these kids getting sick,” she says. “We don’t want to wait for anything longer.”





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