Targeting A Specific Gene May Help Treat Hepatitis B, C And D in Humans

Chronic viral hepatitis is a long-term inflammation of the liver, usually caused by hepatitis B (HBV), C (HCV) or D (HDV) viruses. Although these viruses replicate differently, they all rely on the endoplasmic reticulum-Golgi pathway for replication. In this process, a gene called TM6SF2 plays a key role. It is estimated that 450,000 people in Australia suffer from chronic viral hepatitis, and about 1,000 people die each year.

Recently, in a research report entitled "Inhibition of Cellular Factor TM6SF2 Suppresses Secretion Pathways of Hepatitis B, Hepatitis C, and Hepatitis D Viruses" published in the international journal The Journal of Infectious Diseases, scientists from the University of Sydney, Australia and other institutions found through research that targeting the TM6SF2 gene may help treat these three types of hepatitis.

The TM6SF2 gene has long been known because it is associated with fatty liver disease. This gene is involved in the process of transporting fat from the liver to the blood. So the researchers began to wonder: If the TM6SF2 gene plays a key role in fat transport, does it also play a similar role in transporting viral particles out of the liver?

Figure 1.Knockdown of transmembrane 6 superfamily member 2 (TM6SF2) in virus cell culture models reduced secretion of infectious HCV virions, HDV virions, and HBV subviral particles.

Figure 1. Knockdown of transmembrane 6 superfamily member 2 (TM6SF2) in virus cell culture models reduced secretion of infectious HCV virions, HDV virions, and HBV subviral particles. (Tu T, et al., 2024)

The researchers first conducted a preliminary study on hepatitis B patients. They found that when the function of the TM6SF2 gene was reduced, blood levels of a specific hepatitis B virus protein (HBsAg) also dropped. This discovery sparked the researchers' interest, and they decided to further investigate whether the TM6SF2 gene had a similar effect on hepatitis C and D viruses.

In the laboratory, the researchers knocked down the TM6SF2 gene and found that the amount of hepatitis B, C and D viruses leaving the liver was significantly reduced. This indicates that the TM6SF2 gene does play an important role in the secretion process of these viruses.

Professor Tu, the leader of the research, said that in the next step, they will continue to conduct in-depth research to find new ways to knock down the TM6SF2 gene and develop a safe and effective treatment that can be used in humans. Although there is still a long way to go, this research offers hope for future treatments. Ultimately, a drug that targets all three hepatitis viruses could transform the lives of millions of people with chronic hepatitis around the world.

The results of this study indicate that the TM6SF2 gene in host cells plays a critical role in the secretion of hepatitis B, C, and D viruses. This discovery provides a potential new pan-viral therapeutic factor for the treatment of patients with chronic viral hepatitis. The TM6SF2 gene is like a "traffic policeman" in the liver, controlling the entry and exit of viral particles. By targeting this gene, we may be able to find a new way to effectively inhibit the spread of these viruses, thereby bringing hope to patients.

Reference

Tu T, et al. Inhibition of Cellular Factor TM6SF2 Suppresses Secretion Pathways of Hepatitis B, Hepatitis C, and Hepatitis D Viruses. The Journal of Infectious Diseases, 2024: jiae098.

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