In the early days of COVID, some people wondered whether coating the insides of their nose with Neosporin might protect them from the frightening new virus.
That’s surprising, given that the common ointment contains antibiotics, which target bacteria, not viruses. But the idea may have some merit, although scientists aren’t ready to encourage anyone to start putting Neosporin in their nose. Early-stage work published in April in Proceedings of the National Academy of Sciences USA combines experiments in rodents with results from a preliminary test of the approach in a small number of humans and finds intriguing hints that the antibiotic may be revving up the body’s innate immune system.
That said, the study was designed only to determine whether it’s worth continuing to investigate this possible new use of an easily accessible over-the-counter drug. “This is a research study—it’s not a clinical study, and it’s certainly not intended for people to go out there and start using Neosporin every day,” says Akiko Iwasaki, an immunologist at Yale University and a co-author of the new research. “It’s just an initial pilot study.”
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Iwasaki hadn’t heard about the interest in nasal Neosporin early in the pandemic, but she is working to find new uses for widely available products, and the popular ointment fits that bill. Intriguingly, one of the three antibiotics it contains is neomycin, which is an aminoglycoside compound—a group of chemicals that she and other researchers had, in 2018, determined increased resistance to a range of viruses in mice.
When an aminoglycoside encounters a bacterium and acts as an antibiotic, the compound interferes with the microbe’s ability to make proteins. But that’s not how Neosporin might fight off viruses. Instead neomycin appears to rev up the innate immune system in this case. That system recognizes foreign substances in general, in contrast to the adaptive immune system, which recognizes and attacks specific foreign materials it has encountered before.
Specifically, neomycin appears to trigger the expression of what scientists call interferon-stimulated genes: a set of hundreds of genes—perhaps even one tenth of a human’s genes—that appear to play a role in the innate immune system. During an infection, the body produces a compound called interferon that binds to these genes and dials up the innate immune system. Neomycin appears to accomplish the same result, although the scientists aren’t sure exactly how. “It’s basically tricking the host into thinking there’s a viral infection and inducing these protective genes,” Iwasaki says.
In the new research, she and her colleagues tested neomycin in a handful of different experiments. In one, they treated mice nasally with concentrated neomycin, then gave them the virus that causes COVID (also via a nasal route). Treated mice lost less weight and were less likely to die from the infection. In a separate experiment, the researchers gave already infected mice neomycin, and the effect was similar. The findings suggest that neomycin both protected the mice from infection and helped them fight it off.
While much of the work was conducted on rodents, the researchers did ask a dozen healthy people to apply Neosporin—which contains a much lower dose of neomycin than the experiments in rodents used—in their nose twice a day for one week and compared them with seven people who used Vaseline—a topical ointment with no neomycin in it. The researchers measured the activity, or expression, of five different interferon-stimulated genes (and one immunoregulatory gene affected by interferon-stimulated gene activity) in each person. They found that even several days after Neosporin administration ended, the people who used it showed higher levels of gene expression, suggesting a stronger immune response. The results were intriguing enough that Iwasaki hopes to conduct more tests on the approach—including testing higher doses of neomycin than are present in Neosporin—in the future.
As Iwasaki’s own previous work and research by other scientists suggests, neomycin’s ability to boost interferon-stimulated genes isn’t unique. “There are lots of ways to reach the same end point,” says Stanley Perlman, a viral immunologist at the University of Iowa, who was not involved in the new research. For example, multiple different forms of interferon itself are already in clinical trials for treatment of early-stage COVID. But Perlman notes that a neomycin ointment may be easier to apply than interferon compounds, some of which are administered by injection under the skin; neomycin may also have gentler side effects.
That said, Perlman does see some risks with the new approach. Dermatologists have encouraged people to move away from using Neosporin to treat wounds, as it can often cause allergic reactions. He’s also concerned about whether regular use of an antibiotic could eventually trigger resistance in harmful bacteria that live in the nose.
Even if the substance was pretty benign, “if you used it for long periods of time, I don’t know what it would do,” Perlman says. “[If you] put an antibiotic in the nose for a long period of time, you’ll clear out the bacteria, and with time, I think you’ll get bacteria growing there that you don’t want—that’s certainly a possibility.”
Both he and Iwasaki say that the ideal times to use a technique such as this would be limited. “I think, for me, I would do it for a high-risk exposure,” Perlman says. For example, he said he would use it if there were a pandemic virus circulating that he had no immunity to and he was in a crowded setting such as a train or an airplane. Or it could be an added tool for those at particularly high risk from even more standard exposures, such as immunocompromised people, Iwasaki suggests. Either way, it wouldn’t mark the end of viral infections—it would just be one more tool to reduce their impact.
“We still need people to [get vaccinated] and wear masks,” Iwasaki says. “We’re just thinking of another layer.”