Scientists discovered that a virus called hepatitis E, which can spread from pigs to humans, may interfere with how your body uses vitamin B2 (also called riboflavin). Using laboratory cells, researchers found that a specific viral protein changes how cells handle this important vitamin. Vitamin B2 helps your body break down fats and produce energy. When this process gets disrupted, it could affect how your liver works and how the virus spreads. This study is one of the first to show this connection, suggesting that vitamin B2 deficiency might play a role in hepatitis E infections.

The Quick Take

  • What they studied: How a specific protein from hepatitis E virus affects the way liver cells process and use vitamin B2
  • Who participated: Laboratory-grown human liver cells (HepG2 cells) that were modified to contain a viral protein from swine hepatitis E virus genotype IV
  • Key finding: Researchers identified 4 circular RNA molecules involved in vitamin B2 metabolism that change when the viral protein is present, along with 26 different molecular networks that connect these changes
  • What it means for you: This research suggests that hepatitis E virus may work by disrupting how your body uses vitamin B2, which could explain some of the liver problems seen in infected people. However, this is early laboratory research and doesn’t yet mean you should change your vitamin B2 intake—more human studies are needed first

The Research Details

This was a laboratory study using human liver cells grown in dishes. Scientists used a special technique called adenovirus to insert a viral protein (called ORF3) from swine hepatitis E virus into these liver cells. They then extracted all the RNA (genetic instructions) from the cells and analyzed it using high-tech sequencing machines to see which genes were turned on or off. The researchers used a computer analysis method called KEGG to organize their findings and identify patterns related to vitamin B2 metabolism.

The study focused on circular RNAs, which are special molecules that act like sponges to soak up other regulatory molecules called microRNAs. By mapping out how these circular RNAs and microRNAs interact, the scientists created a network map showing how the viral protein disrupts normal vitamin B2 processing in liver cells.

This type of research is important because it helps scientists understand the basic mechanisms of how viruses cause disease at the molecular level, before testing treatments in animals or humans.

Understanding exactly how viruses damage cells is crucial for developing treatments. By identifying that hepatitis E virus interferes with vitamin B2 metabolism, researchers have found a potential new target for therapy. If vitamin B2 deficiency is part of how this virus causes liver damage, then maintaining adequate vitamin B2 levels might help protect people or improve their recovery.

This is a well-designed laboratory study that uses modern molecular techniques. The researchers used high-throughput sequencing, which is a reliable method for identifying genetic changes. However, this study was conducted only in laboratory cells, not in living organisms or people. The findings are preliminary and represent the first step in understanding this mechanism. The study doesn’t specify how many independent experiments were performed or whether results were repeated multiple times, which would strengthen confidence in the findings.

What the Results Show

The main discovery was that when the viral ORF3 protein was present in liver cells, it changed how 4 specific circular RNA molecules functioned. These circular RNAs are normally involved in controlling vitamin B2 metabolism. The researchers also mapped out 26 different molecular networks showing how these circular RNAs interact with microRNAs to affect genes involved in vitamin B2 processing.

This is significant because it shows, for the first time, a direct connection between this particular virus and disruption of vitamin B2 metabolism. The viral protein appears to work by changing how cells regulate these circular RNAs, which then affects the entire vitamin B2 processing system.

The findings suggest that when vitamin B2 metabolism is disrupted, it can lead to problems with fat metabolism in the body. Since the liver is responsible for processing fats, this disruption could explain why hepatitis E causes liver damage.

The research revealed that the viral protein’s effects on vitamin B2 metabolism are connected to broader problems with how the body processes and stores fats. This is important because fat accumulation in the liver is a known problem in hepatitis E infections. The study also identified specific molecular pathways that could be targeted with future treatments.

This is one of the first studies to investigate how hepatitis E virus affects vitamin B2 metabolism. Previous research showed that the ORF3 protein is important for virus assembly and release, but this study adds a new dimension by showing it also disrupts metabolic processes. The findings align with observations that hepatitis E causes liver damage, but they provide a new explanation for why this happens.

This study was conducted entirely in laboratory cells, not in living animals or humans, so the findings may not translate directly to real infections. The sample size and number of experimental repetitions are not specified, which makes it harder to assess how reliable the results are. The study identifies associations between the viral protein and changes in RNA molecules, but doesn’t prove that these changes directly cause the virus to spread or cause disease. Additionally, the research doesn’t test whether correcting vitamin B2 levels would actually help prevent or treat hepatitis E infection.

The Bottom Line

Based on this preliminary research, there is no current recommendation to change vitamin B2 intake for hepatitis E prevention or treatment. However, this research suggests that maintaining adequate vitamin B2 levels may be important for liver health, especially for people at risk of hepatitis E. Anyone concerned about hepatitis E should focus on proven prevention methods like food safety and hygiene. If infected with hepatitis E, consult a healthcare provider rather than self-treating with supplements.

This research is most relevant to people living in areas where swine hepatitis E is common, healthcare providers treating hepatitis E patients, and researchers studying viral hepatitis. It’s also important for public health officials considering prevention strategies. The general public should be aware of this research as background information, but it doesn’t yet change everyday health recommendations.

This is very early-stage research. It typically takes 5-10 years or more for laboratory discoveries to lead to treatments that can be tested in humans. Before any practical applications emerge, researchers will need to confirm these findings in animal studies and eventually human clinical trials.

Want to Apply This Research?

  • Users at risk for hepatitis E could track their vitamin B2 intake (measured in milligrams per day) and any symptoms of liver problems, noting dates and amounts of B2-rich foods consumed (eggs, almonds, mushrooms, salmon)
  • For users concerned about hepatitis E risk, the app could suggest tracking consumption of vitamin B2-rich foods and maintaining a food safety log to prevent infection through contaminated food or water
  • Long-term tracking could include weekly vitamin B2 intake logs, monthly liver health markers if available through medical testing, and symptom tracking for anyone with confirmed hepatitis E infection

This research is preliminary laboratory work and does not yet provide clinical guidance for preventing or treating hepatitis E in humans. The findings are based on studies in laboratory cells, not living organisms or people. Do not change your vitamin B2 intake or medical treatment based on this research without consulting a healthcare provider. If you suspect hepatitis E infection or have liver disease, seek immediate medical attention. This summary is for educational purposes only and should not be considered medical advice.