The Reason COVID Prevents Vaccines From Being More Effective


This novel barrier could also help explain in part why so-called breakthrough infections are so common and why loss of smell is much more commonly associated with these infections than pulmonary symptoms.

Duke researchers discovered a previously unknown barrier that separates the bloodstream from the olfactory cells in the upper airways of mice, most likely protecting the brain.

However, this barrier also serves to block some of the larger components of the body’s immune system, which can reduce the effectiveness of vaccines.

According to lead author Ashley Moseman, assistant professor of immunology at Duke School of Medicine, the olfactory cells lining the nose are useful for having a protective barrier because they provide a direct route to the brain’s olfactory bulb, thereby making them extensions of the olfactory bulb make brain.

The new barrier, dubbed BOB (Blood Olfactory Barrier) by his team, may block antibodies reaching the mucus on the nasal surface, the first barrier a virus encounters.

The team wanted to learn more about how the immune system protects the upper respiratory tract. They did this by giving mice a virus called vesicular stomatitis virus, or VSV, which is known to get into the central nervous system. Once inhaled, VSV easily infects olfactory cells and multiplies rapidly, making its way to the olfactory bulb of the brain in just a day. Although it can cause paralysis and death, it is generally cleared by a T cell response.

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“VSV is excellent at infecting olfactory sensory neurons, and when it can do that, it goes to the brain,” says Moseman. “Even if antibodies are circulating, the blood-odor barrier prevents those antibodies from reaching the airway surface, and VSV gets to the brain.”

They were interested in learning more about how one disease can protect against another. They discovered that while the BOB blocked protection from circulating antibodies, it allowed antibody-secreting plasma cells to enter the olfactory tissue and produce neutralizing antibodies there.

The results were published today in the journal Immunity.

Although researchers were not specifically interested in this topic due to COVID, it is well documented that the SARS-CoV-2 virus infects olfactory cells and renders many affected people smellless. They now believe this novel barrier may help explain in part why so-called breakthrough infections are so common and why loss of smell is much more commonly associated with these infections than pulmonary symptoms.

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“The reason that COVID infections typically remain in the upper respiratory tract and are less likely to reach the lungs of vaccinated individuals may involve this gap in immune protection,” adds Moseman.

“You could have a situation where you have perfectly good (amounts of) antibodies circulating from a COVID vaccine, but those antibodies are blocked from reaching the olfactory cells,” Moseman adds. “You would be protected from severe lung disease, which is great, but you could still have these repeating events happening in the olfactory epithelium because the systemic antibody isn’t getting there. This is obviously uncomfortable for the individual and can help further spread the community.”

According to Moseman, the discovery also brings his team closer to explaining why many vaccines fail to induce antibody-secreting B cells in tissues, while infections can.

“Vaccines create antibody-secreting cells that produce antibodies and give you a good antibody titer in the blood, but these cells don’t necessarily invade and protect those tissues,” he adds. “Circulating antibodies don’t get to the olfactory surface, where they can protect against viral infection.”

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More effective vaccines could result from knowing how the immune system differentiates between an infection and a vaccine, Moseman said.

More effective vaccines could result from knowing how the immune system differentiates between an infection and a vaccine, Moseman said.

To find the BOB in other animals and humans, researchers must first have a deeper understanding of the components that make up the BOB.

According to Moseman, it could be technically very difficult to study this small area in humans.

“Once you understand what constitutes it, what factors maintain it, and all of that stuff in the mouse, then it’s going to be a little bit easier to take that knowledge and look for it in human tissue.”

“We think it’s entirely plausible that this is the case in humans. We just couldn’t test it directly,” adds Moseman. “There are many questions.”

Source: 10.1016/j.immuni.2022.08.017

Photo credit: Ashley Moseman Lab, Duke University

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