How hepatitis A virus (HAV) manages to enter liver cells called hepatocytes and initiate infection had remained a mystery for fifty years until now. University of North Carolina School of Medicine researchers designed experiments using gene-editing tools to discover how molecules called gangliosides serve as de facto gatekeepers to allow the virus entry into liver cells.
The research, published in Nature Microbiology, has revealed gangliosides as a key player in HAV and has led to several other questions, such as how exactly viral RNA transitions between different compartments in human liver cells to replicate and cause disease.
“Discovering that gangliosides are essential receptors for HAV infection adds an interesting plot twist to the hepatitis A story,” said senior author Stanley Lemon, MD, professor of medicine and microbiology at the UNC School of Medicine and member of the UNC Institute for Global Health and Infectious Diseases. “Gangliosides are structurally similar across mammalian species, unlike proteins, which helps explain cross-species transmission of ancient hepatoviruses. Understanding what helps a virus jump from one animal species to another is incredibly important, as evidenced so plainly by the current Covid-19 pandemic.”
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