Why norovirus is so hard to avoid – and what lactoferrin may do about it

It was first described as the "winter vomiting disease" but wasn't formally monitored until 1968, after an outbreak in a school in Ohio. The norovirus has evolved over time into 10 genogroups, with 3 that can affect humans. It typically lasts 2 – 3 days – except in immune-compromised cases – but it can cause chronic diarrhoea in children.

Yes. The problem is there's no vaccine or established medication, because of the difficulty in replicating the virus in a lab. The surge of cases we see is probably because it disappeared for a while and has re-emerged. Norovirus also has a huge socioeconomic impact – something that tends to get underreported.

Vomiting, nausea, diarrhoea, high temperature, headache. If you have it, you should avoid contact with others for 48 hours and not prepare food. Disinfect everything, because it's extraordinarily contagious – which is why it's called the "cruise ship virus."

When I was at the University of Michigan, we found that human norovirus infecting a type of immune cell called a B cell can trigger cell activation. It could affect the immune system and the long-term response – though we don't yet have in-vivo studies on this. What it suggests is that blocking the virus at entry might not be the only way to intervene.

We'd found a model of infection that could support the human norovirus in a lab setting – which had previously been very difficult to do. We had a collaboration with a Japanese company with a long-standing interest in lactoferrin, and they funded our research.

We first tested lactoferrin against the murine surrogate – the mouse version of norovirus – because we already knew lactoferrin was active against that. Then we moved to the human version, using a cellular model of B cells. We pre-treated the cells with lactoferrin, then added the virus.

Two days after infection, viral replication was significantly reduced in the cells that had received lactoferrin. And importantly: the effect was dose-dependent. The more lactoferrin, the greater the reduction in replication.

With SARS, we saw the effect at the entry level: lactoferrin was able to block the virus from binding to cells in the first place. With norovirus, we didn't find an effect at binding, but replication was still reduced. It was primarily affecting what we call the interferon response – the body's signalling system that alerts the immune system to an active infection.

Lactoferrin acts as an immune modulator. It creates a signal cascade that mobilises the body's own defences. That appears to be the key mechanism here.

Yes. There was a clinical trial with bovine lactoferrin for children aged 12 – 18 months who were not breastfed. They still got norovirus – the incidence wasn't reduced – but the severity of symptoms was meaningfully lower in the lactoferrin group.

There was also a Japanese study in 2020, a randomised double-blinded placebo-controlled trial, for staff at nurseries and kindergartens who were repeatedly exposed to norovirus. Both 200mg and 600mg doses significantly reduced the prevalence of symptoms. That's a strong signal from a well-designed study in a real-world setting.