Your risk of contracting COVID-19 might depend on which bacteria call your nose home, according to groundbreaking research that provides new insights into why some people are more susceptible to the virus than others.
Scientists from George Washington University have discovered that certain bacteria living in the nose can affect levels of key proteins that SARS-CoV-2 needs to enter human cells, potentially explaining one of the pandemic’s most persistent mysteries – why infection rates vary so dramatically between individuals with similar exposure risks.
“We’ve known that the virus SARS-CoV-2 enters the body through the respiratory tract, with the nose being a key entry point. What’s new—and surprising—is that bacteria in our noses can influence the levels of proteins that the virus uses to infect cells,” said Cindy Liu, associate professor of environmental and occupational health at the GW Milken Institute School of Public Health.
The study, published April 9 in the journal EBioMedicine, analyzed nasal swab samples from more than 450 people, including some who later tested positive for COVID-19. Researchers focused on two proteins – ACE2 and TMPRSS2 – which serve as doorways for the virus to enter nasal cells.
People with high expression of these proteins were three times more likely to test positive for COVID-19, while those with moderate levels faced double the risk. More troubling, the study found expression levels often spiked just days before individuals tested positive, potentially signaling increased vulnerability to infection.
When researchers examined what influenced these protein levels, they turned to the nasal microbiome – the community of bacteria naturally residing in the nose. They identified three bacterial villains and one potential hero.
“Some bacteria in your nose may be setting the stage — or even holding the door open — for viruses like SARS-CoV-2 to get in,” explained Daniel Park, a senior research scientist at GW and the study’s first author.
Three bacteria in particular – Staphylococcus aureus, Haemophilus influenzae, and Moraxella catarrhalis/nonliquefaciens – were linked to higher expression of the viral entry proteins and increased COVID-19 risk. The research showed that approximately 20% of participants carried enough S. aureus to nearly double their risk of having elevated levels of these key proteins.
However, another common nasal bacterium, Dolosigranulum pigrum, was associated with lower levels of the entry proteins and might offer some protection against the virus.
The study revealed interesting sex-based differences as well. Women generally had higher levels of these viral entry proteins, consistent with previous studies showing higher COVID-19 infection rates among women. However, men with elevated levels faced a greater risk of infection, suggesting these proteins may present a more significant vulnerability for males.
These findings open intriguing possibilities for COVID-19 prevention. Monitoring these protein levels could potentially identify high-risk individuals before they become infected. More significantly, modifying the nasal microbiome could become a novel prevention strategy.
“We’re only beginning to understand the complex relationship between the nasal microbiome and our health,” Liu said. “This study suggests that the bacteria in our nose—and how they interact with the cells and immune system in our nasal cavity—could play an important role in determining our risk for respiratory infections like COVID-19.”
The research team is now exploring whether interventions targeting the nasal microbiome, such as specialized nasal sprays or live biotherapeutics, could reduce infection risk – potentially creating new tools to prevent respiratory viral infections in future pandemics.
As variants continue to emerge and COVID-19 transitions to an endemic disease, understanding these biological risk factors becomes increasingly important. This research suggests that while masks, vaccines, and social distancing remain crucial protective measures, the microscopic ecosystem inside our noses may be another critical battleground in our ongoing struggle with coronavirus.
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