Researchers Discover How Norovirus Infections Begin


By studying norovirus infections in mice, researchers have discovered how the virus targets rare intestinal cells to cause intense illness.

Norovirus is the biggest cause of acute gastroenteritis worldwide, and there is no antiviral drug or vaccine for the virus. In a new study, however, researchers have made a discovery on how norovirus infections begin in mice, a key finding which may help in the fight against the deadly virus.

Each year in the United States, norovirus causes as many as 21 million cases of acute gastroenteritis, leading to up to 1.9 million outpatient visits, 400,000 emergency room visits, 71,000 hospitalizations, and 800 deaths. The highly contagious virus causes inflammation of the stomach or intestines, leading to nausea, stomach pain, diarrhea, and vomiting. Norovirus spreads through contaminated food, water, or surfaces, and through infected individuals. According to the Centers for Disease Control and Prevention (CDC), food can become contaminated with norovirus during growing, shipping, handling, and preparing; in fact, the virus causes about half of all outbreaks of food-related illness.

While most norovirus symptoms pass within 1 to 3 days, some cases can cause severe dehydration and complications, and in some individuals, the virus can persist in the intestines for months and cause prolonged inflammatory bowel disorders. Young children and older adults are at higher risk of becoming seriously ill from norovirus, and as such, most norovirus deaths tend to occur in these age groups. There is little known about how norovirus infections begin, but a recent study led by researchers from the Washington University School of Medicine has revealed more about how the virus infects the intestines.

In the study, published in the journal Science, the researchers studied norovirus in mice, as human norovirus is difficult to grow in a lab. They found that the virus targets tuft cells, a rare type of epithelial cell that protrudes into the intestines which trigger an immune response to parasitic and worm infections. In addition, the researchers observed tuft cells multiply up to 5 to 10 times in response to intestinal parasites, which, in turn, intensifies a norovirus infection and allows the virus to replicate and persist. The finding also explains why norovirus is deadlier in parts of the world where intestinal worms and parasites are more common.

“We were most surprised that the virus infects such a rare cell type and that even with so few cells infected, the infections can be intense and easily transmitted,” said the study’s first author Craig B. Wilen, MD, PhD, in a recent statement. “In a single mouse, for example, maybe 100 cells will be infected, which is very few compared with other viruses such as the flu.”

The researchers also found that in “healthy carriers” of norovirus, the virus can essentially hide inside tuft cells and evade the immune system, while continuing to shed through the carrier’s feces. The study team treated the mice with a broad-spectrum antibiotic to decrease the number of tuft cells, giving the norovirus fewer targets, but in humans, the authors warned that such treatment would kill off important gut flora.

The study authors posit that their findings offer new insights into how norovirus works in the gut. “This raises important questions about whether human norovirus infects tuft cells and whether people who have chronic norovirus infections and continue to shed the virus long after infection do so because the virus remains hidden in tuft cells,” said Dr. Wilen. “If that’s the case, targeting tuft cells may be an important strategy to eradicate the virus.”

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