A team of researchers has discovered how a protein called TRBP regulates the immune response to viral infections in mammal cells. This discovery has the potential to aid in the development of antiviral treatments and nucleic acid medications for genetic conditions.
A team of researchers has discovered how a protein called TRBP regulates the immune response to viral infections in mammal cells. This discovery has the potential to aid in the development of antiviral treatments and nucleic acid medications for genetic conditions.
Cells have a natural defense mechanism against viral infections, which involves a process called apoptosis and interferon signaling. Apoptosis is a normal process that leads to the death of a cell, and it can help prevent the reproduction of abnormal cells, including those infected by viruses. Interferons are proteins that animal cells produce in response to viral infections. These proteins play a role in the body’s immune response to eliminate infected cells.
The researchers aimed to investigate how cells protect themselves from viral attacks and stop the virus from multiplying. It was not well understood how cells maintain a balance between apoptosis and interferon response to effectively suppress viral replication during infection.
For this study, a team of researchers from the University of Tokyo focused on TRBP, a specific protein that belongs to a category of proteins known as RNA silencing factors.
RNA is a nucleic acid found in living cells and viruses that regulates protein synthesis and the genetic characteristics of many viruses. RNA creates proteins through a process called transcription.Through the process of translation, genetic sequences are read and converted into instructions for cells to produce proteins. These proteins play a major role in the structure and function of organisms, whether they are plants or animals. RNA silencing, also referred to as RNA interference, is a method utilized by plants and invertebrate animals to defend against viruses by cutting viral RNA to suppress viral replication. This study offers valuable insight into the protein associated with the RNA silencing mechanism, which serves as a strong antiviral mechanism in plants and invertebrates.The scientists examined TRBP, which stands for TAR RNA-binding protein and is involved in RNAi as well as in the antiviral response in mammals through another means,” noted Tomoko Takahashi, a co-author and visiting researcher at the University of Tokyo, as well as an assistant professor at Saitama University in Japan.
While the function of RNA silencing in regulating gene expression is well-known under normal circumstances, it remains unclear how this process operates during a viral infection.
The role of a protein (protein) in RNA silencing during a viral infection has been significant.
This protein interacts with a virus sensor protein early in the infection phases in human cells. Caspases, proteins activated in the later stages of viral infection, are chiefly responsible for triggering cell death.
Kumiko Ui-Tei, another co-author and associate professor from the University of Tokyo (at the time of the study), stated, “RNA silencing and interferon signaling were previously considered as independent pathways, but multiple reports, including ours, have demonstrated crosstalk between them.”
When a virus infects a cell, TRBP undergoes a functional conversion that regulates the interferon response and apoptosis. This results in TRBP increasing the programmed cell death of infected cells while reducing interferon signaling. TRBP induces cell death and stops viral replication, whereas the interferon response pathway only subdues viral replication without eliminating the infected cells.
The main objective is to comprehend the molecular mechanism of the antiviral defense system, which involves the interplay between internal and external RNA pathways.The researchers discovered a new type of defense mechanism against viruses in human cells,” said Takahashi. The goal is to use this knowledge to advance the development of nucleic acid medicines, which work similarly to the body’s natural antiviral response. These medicines show potential for treating patients with viral infections, genetic mutations, and genetic defects. The study was a collaboration with several universities in Japan, including Saitama University, Chiba University, Kyoto University, and Maebashi Institute of Technology.
Journal Reference:
- Shibata, K., Moriizumi, H., Onomoto, K., Kaneko, Y., Miyakawa, T., Zenno, S., Tanokura, M., Yoneyama, M., Takahashi, T., Ui-Tei, K. Caspase-mediated processing of TRBP regulates apoptosis during viral infection. Nucleic Acids Research, 2024; DOI: 10.1093/nar/gkae246