An antibody nasal spray has shown promise for protecting against flu in preliminary human trials, after first being validated in mice and monkeys. It may be useful for combatting future flu pandemics because it seems to neutralise any kind of influenza virus, including ones that spill over from non-human animals.

The main tool we have for stopping the spread of flu is the annual vaccine, which stimulates our immune system to make antibodies against recently circulating strains of influenza virus. However, because influenza strains are constantly morphing, vaccines are only moderately effective.

To address this, pharmaceutical company Johnson & Johnson developed a special antibody called CR9114 that can neutralise any of these strains. It does this by recognising and binding to a part of the virus that always stays the same, regardless of how other parts of it are changing.

When CR9114 was initially injected into animals’ bloodstreams, it failed to provide robust protection against flu. This was because only a small proportion reached the nose, the main point of entry for influenza viruses. In 2022, the firm Leyden Labs licensed CR9114 and developed a formulation that could be sprayed up the nose instead.

Since then, the company has shown that spraying CR9114 up the noses of mice and macaques stops them from getting sick when they are exposed to various strains of influenza A and B, including one collected from a scientist’s throat during a bad flu season in 1933.

Preliminary tests were also conducted in 143 people aged 18 to 55. Researchers found that administering the spray twice a day maintained steady levels of the antibody inside participants’ noses and didn’t cause any major side-effects. Samples of their nasal mucus collected afterwards also neutralised a range of influenza strains, including a bird flu strain that crossed into people in China in 2013.

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The next step will be to directly expose people who have used the spray to a range of influenza viruses to confirm that it actually stops them from getting sick.

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The spray may not be 100 per cent effective because the virus can enter the body via routes other than the nose, like the mouth, says at the University of Melbourne, Australia. “But nonetheless, blocking nasal entry would still intercept the virus at a major access point for infection.”

It will probably also be less convenient than the flu vaccine because it requires twice-daily administration rather than a single jab, says Wakim. “However, it could be a game changer for specific high-risk groups, such as immunocompromised individuals, frontline healthcare workers, or during a pandemic situation where rapid, short-term population protection is needed while vaccines are being developed or rolled out.”

Respiratory viruses may activate the growth of dormant cancer cells that have spread to the lungs from elsewhere in the body. Infections like flu seem to spark an inflammatory response that helps the immune system fight off the microbial invader, but has negative consequences for cancer progression.

Cancer deaths often occur when tumour cells migrate from their original location in the body. It is difficult to detect when this occurs, as these cells can lie dormant – not dividing – for years or even decades at their new site before they form tumours.

What triggers these cells to eventually proliferate is unclear, but prior studies suggest that when cancer cells reach the lungs, may play a role. “But no one had really done the studies to really establish cause and effect,” says at the University of Colorado.

To fill this gap, DeGregori and his colleagues used mice that were genetically engineered to grow tumours in their mammary glands. At around 2 months old, each mouse had mammary gland tumours and fewer than 10 dormant cancer cells in their lungs.

The team then infected half of the mice with the H1N1 strain of the influenza virus, also known as swine flu, making them sick for about two weeks. Nine days post-infection, the number of cancer cells in their lungs had increased 100-fold, but hardly changed in the uninfected mice.

When the researchers repeated the experiment but with the SARS-CoV-2 virus, which causes covid-19, they saw about a 10-fold increase in the number of cancer cells in the lungs of the mice, but still no changes in the uninfected mice.

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The researchers hypothesised that such expansions occurred because viral infections increase levels of an inflammatory molecule called IL-6, which helps the immune system destroy viruses, but can also promote tumour growth.

To validate this idea, they repeated the experiment in mice that were genetically engineered to lack IL-6, and found they had substantially fewer cancer cells in their lungs compared with mice with typical IL-6 levels.

Another experiment revealed that IL-6 seems to reawaken dormant cancer cells that had already migrated to the lungs, rather than increasing the spread of these cells from the breast.

But IL-6 levels subside once infections have been cleared. At this stage, the team found that cancer cells in the mice’s lungs stopped proliferating, but had gained properties – such as changes in gene expression – that have been linked to tumours spreading, says DeGregori.

The findings could have implications for people with undetectable levels of cancerous cells in their lungs when they are thought to be in remission, says at the National Institute of Health in Rome, Italy.

To explore if the findings really might apply to people, the researchers analysed health records from 36,800 women in the US who were diagnosed before the covid-19 pandemic with breast cancer that wasn’t thought to have spread.

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The women with a positive test during the first three years of the outbreak were much more likely to have a diagnosis of secondary lung cancer over this period than those whose swabs came back negative or who weren’t tested at all. But some of the women may have had asymptomatic infections, and so not have sought a test, while others may not have had access to one, which would reduce the validity of this result, says DeGregori.

Further studies in people are needed to verify the research and explore how various respiratory viruses and cancer types interact, says Zeuner. “Individual factors are [also] likely to profoundly affect the link between respiratory infections and cancer relapse,” she says.

While the team only looked at swine flu and SARS-CoV-2, DeGregori expects a range of viruses to act in the same way, as many induce increased levels of IL-6. He also thinks the results support yet another reason to get vaccinated. “If I were a cancer survivor, I would make sure I was vaccinated against the common respiratory viruses like flu, covid, so on,” says DeGregori.