Every winter, norovirus tears through schools, cruise ships and care homes. A tiny dose is enough to make someone sick, and alcohol hand gel does not reliably kill it. Yet in many outbreaks, some people who shared the same food, the same bathroom or even the same bed never get ill. Part of the reason is a single gene, FUT2, and your version of it is probably already in the raw DNA file you have.
A new strain is driving the season
For two decades, most norovirus outbreaks were caused by one genotype, GII.4. That changed fast. In CDC outbreak data, a genotype called GII.17 went from 7.5% of US outbreaks in the 2022-23 season to 34.3% in 2023-24 and 75.4% in 2024-25, while GII.4 fell to about 11% (Barclay and Vinjé, Emerging Infectious Diseases, 2025). Recent seasons have also started early, with wastewater signals rising from October, and the 2026-27 season is beginning now.
How norovirus gets in, and why some people lock it out
Norovirus does not infect gut cells at random. Most strains first attach to sugars called histo-blood group antigens, the same family of sugars that defines your ABO blood group. These sugars are displayed on the lining of your gut, and in your saliva and mucus, only if your FUT2 gene works.
- Secretors have at least one working copy of FUT2 and display these sugars. That is roughly 80% of people of European ancestry.
- Non-secretors have two non-working copies and do not. In Europeans this is almost always the same variant, rs601338, also written W143X or 428G>A.
The landmark experiment came in 2003. Volunteers drank a dose of Norwalk virus, the original norovirus strain. None of the non-secretors became infected, while most secretors did (Lindesmith et al., Nature Medicine, 2003). Two years later, a Swedish study of hospital and nursing home outbreaks caused by GII strains found that non-secretors were almost completely protected from symptomatic illness (Thorven et al., Journal of Virology, 2005). In American children, FUT2 status again separated who got sick from GII.4 strains and who did not (Currier et al., Clinical Infectious Diseases, 2015).
Does the protection hold against GII.17?
This is the question that matters this winter, and the honest answer is: probably for the most part, but not completely.
- Lab data are reassuring. GII.17 virus-like particles bound to saliva from secretors but showed no significant binding to saliva from non-secretors (Estienney et al., Frontiers in Microbiology, 2022). That points to the same lock-and-key logic as GII.4.
- Protection was never total. Some genotypes, such as GI.3 and GII.3, have infected non-secretors, and reviews describe the protection as strong but dependent on the strain (Nordgren and Svensson, Viruses, 2019).
- The virus keeps changing. GII.17 is still evolving, and outbreak data on non-secretors and the newest variants are limited.
| Your FUT2 result | What it means for norovirus |
|---|---|
| Secretor (one or two working copies) | Susceptible to the common strains, including GII.4 and GII.17 |
| Non-secretor (two non-working copies) | Strongly protected against GII.4, probably against GII.17, but not against every genotype |
Being a non-secretor tilts the odds in your favor. It is not a reason to skip hand washing.
The same gene, other trade-offs
Being a non-secretor is not a pure win. Non-secretors are also resistant to the most common rotavirus strains, those of the P[8] type (Imbert-Marcille et al., Journal of Infectious Diseases, 2014). But they tend to carry fewer bifidobacteria in the gut, and large genetic studies link non-secretor status with a higher risk of Crohn's disease (McGovern et al., Human Molecular Genetics, 2010). Their blood vitamin B12 is slightly higher on average, not lower, contrary to what many websites claim (Hazra et al., Nature Genetics, 2008). We cover these effects in what being a non-secretor means for your gut bacteria and vitamin B12.
What actually stops norovirus
- Soap and water for at least 20 seconds, especially after the toilet and before eating. Alcohol gels are not enough on their own.
- Bleach-based cleaners on toilets, taps and door handles after someone has been sick.
- No cooking for others while you are ill and for at least two days after symptoms stop: you keep shedding the virus.
- Fluids with a little salt and sugar if you are ill, and medical advice if you see signs of dehydration, especially in young children and older adults.
Find out if you are a non-secretor, for free
If you have tested with 23andMe, AncestryDNA, MyHeritage or FamilyTreeDNA, your FUT2 result is already in your raw data file. Our free secretor status test reads it in your browser in under a minute, without sending your file anywhere. MyHeritage files do not contain rs601338, so the test reads a marker inherited with it, rs492602. One limit: in people of East Asian ancestry, other FUT2 variants are more common, and the result is less complete.
The Complete report reads FUT2 together with your other gut genes, such as lactase persistence and histamine clearance.
Educational information, not medical advice. Norovirus can be dangerous for babies, older people and anyone who becomes dehydrated: seek medical help if symptoms are severe or last more than a few days.
References
- Barclay L, Vinjé J. Increasing predominance of norovirus GII.17 over GII.4, United States, 2022-2025. Emerg Infect Dis. 2025;31(7).
- Lindesmith L, Moe C, Marionneau S, et al. Human susceptibility and resistance to Norwalk virus infection. Nat Med. 2003;9(5):548-553.
- Thorven M, Grahn A, Hedlund KO, et al. A homozygous nonsense mutation (428G→A) in the human secretor (FUT2) gene provides resistance to symptomatic norovirus (GGII) infections. J Virol. 2005;79(24):15351-15355.
- Currier RL, Payne DC, Staat MA, et al. Innate susceptibility to norovirus infections influenced by FUT2 genotype in a United States pediatric population. Clin Infect Dis. 2015;60(11):1631-1638.
- Estienney M, Tarris G, Abou-Hamad N, et al. Epidemiological impact of GII.17 human noroviruses associated with attachment to enterocytes. Front Microbiol. 2022;13:858245.
- Nordgren J, Svensson L. Genetic susceptibility to human norovirus infection: an update. Viruses. 2019;11(3):226.
- Imbert-Marcille BM, Barbé L, Dupé M, et al. A FUT2 gene common polymorphism determines resistance to rotavirus A of the P[8] genotype. J Infect Dis. 2014;209(8):1227-1230.
- McGovern DPB, Jones MR, Taylor KD, et al. Fucosyltransferase 2 (FUT2) non-secretor status is associated with Crohn's disease. Hum Mol Genet. 2010;19(17):3468-3476.
- Hazra A, Kraft P, Selhub J, et al. Common variants of FUT2 are associated with plasma vitamin B12 levels. Nat Genet. 2008;40(10):1160-1162.
- Centers for Disease Control and Prevention. Preventing norovirus. Guidance for the public.