Hepatolog: Introduce The Molecular Mechanism Of Hev Entry And Infection Of Host Cells

Feb 14, 2023

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Hepatitis E virus (HEV) is the major cause of acute viral hepatitis, About 70,000 people die from the disease each year; Although hepatitis E is a common disease, But scientists know very little about the life cycle of the virus, recently, Published in a study report entitled "Epidermal growth factor receptor modulates hepatitis e virus entry in human hepatocytes HEP-22-1113" in the international journal Hepatology, Scientists from Bochum University and other institutions have revealed the molecular mechanism by which hepatitis E enters and infects cells.

The researchers said, called epidermal growth factor receptor (EGER) special protein plays a decisive role in the process of viral particles into cells, the discovery or is expected to help to develop human liver new therapy, because there are for EGFR drugs approved to inhibit the activity and effect of the receptor. One reason researchers have done relatively little research on hepatitis E is that about three years ago they developed a powerful cell culture model for research, which researchers can now use to investigate how the virus infects cells.

First author Jil Alexandra Schrader said, we in some cell lines using the drug in the virus into the EGFR protein activity, in these cultures, we observed the infected cells significantly reduced, to verify this, the researchers use co-receptor is overproduced cell cultures, in this case, the infection is more than untreated cells. This may indicate that EGFR protein mechanism is very important for the virus into the cell, in addition, the protein outside the cell and can combine with ligand part is particularly important for the entry of the virus, if its absence, the virus cannot penetrate the cell, researchers need further research to determine whether there are other factors in the process of virus infection cells or whether the receptors itself can introduce the virus.

In the case of HCV, it is well known that even more receptors are involved in the entry of the virus into cells, which may also be the case for HEV studies. The evidence for the involvement of EGF receptors in infection is particularly interesting because there are currently approved drugs that inhibit their activity that are approved in Europe and the US to treat specific cancer types in which the receptor is hyperactive and causes uncontrolled growth of cells. Further studies show whether these agents can be used as a novel therapy against HEE infection.

In conclusion, the results of this paper provide new clues to identify the life cycle of EGFR or as a potential target for future scientists to develop antiviral strategies against HEE infection.

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