Viral Mechanisms Provide New Hepatitis C Drug Target


Drugs that target the signal-peptide peptidase enzyme may halt HCV development.

A new drug target for the development of hepatitis C virus (HCV) drugs were identified, along with the mechanisms behind the virus in a recent study.

It is known that the cleavage of the HCV core protein by the signal-peptide peptidase (SPP) enzyme in infected host cells plays a key role in the formation of viral particles, as well as the development of pathological liver conditions. Until now, the details of this mechanism remained unclear.

New research by scientists at Osaka University revealed that when SPP is inhibited, HCV particle production becomes reduced, causing pathological liver conditions to improve. A chemical compound that inhibits the SPP was found in the y-secretase inhibitor, which is currently in the developmental process for the treatment of Alzheimer’s disease.

Furthermore, researchers found that immature core proteins that aren’t cleaved by SPP are recognized by the enzyme TRC8, and then quickly become degraded. If the degradation process becomes suppressed, cellular damage is strongly induced by endoplasmic reticulum stress (ER stress), and the process can therefore be considered as a quality control mechanism for new proteins.

In the study, researchers administered the SPP inhibitor to a mouse model. The results of the study showed that HCV particle production significantly dropped, resulting in the improvement of pathological liver conditions, such as fatty liver and insulin resistance.

The findings suggest that SPP inhibitors can be developed as a new HCV drug. Since the observed protein quality control mechanism by SPP/TRC8 is believed to be related to other diseases, it may be useful for the development of drugs for an array of diseases.

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