Key process discovered in the replication cycle of Hepatitis D
It is defined as a key process in the hepatitis D (VHD) virus replication cycle as discovered by the research team of Patrick Labonté, professor at INRS. This is important news because hepatitis D still affects several million people around the world (an estimated 15 to 20 million) and at the same time it is not yet at its best.
The why is soon said: the virus that causes it can be considered special because it only infects people who already have hepatitis B virus (HBV). It is a combination of infections that naturally causes greater damage to the liver and the body in general. The VHD virus needs the HBV virus to survive in the human body and to spread like a parasite.
An attempt is currently being made to eradicate the hepatitis D virus by targeting an enzyme that controls hepatitis B. However, as Labonté himself explains in the press release, this is not always effective because in most cases VHD virus manages to survive and continues to do damage.
In the new study, published in the Journal of Virology, the Labonté team shows that the VHD virus uses the same cellular protein as the HBV virus to grow. This protein, called ATG5, allows the virus to replicate in the nucleus of the cells it seeks to parasitize. What this protein does precisely is clean up cellular waste by implementing a process called “autophagy”. This is a process that theoretically should destroy the invading viruses but most viruses have learned to use it to their advantage.
ATG5 therefore reveals a protein that is essential for the development and spread of hepatitis D and the researchers in this study were the first to determine the effect of this same protein on the hepatitis D virus.
Now that we know the process in more detail, we could act on autophagy to interrupt the life cycle of the hepatitis D virus, but the situation is not as simple as Labonté himself explains: “If we block autophagy, we prevent a phenomenon that is important for all cells in the body. We do not know what it could do in the long term. It should therefore be inhibited in a specific, temporary and localised way”.