Bengaluru: Scientists at the Indian Institute of Science (IISc), Bengaluru, have uncovered how a virus takes control of a host cell’s protein-making machinery to reproduce, a breakthrough that could pave the way for the development of new antiviral therapies.
The findings, published in the peer-reviewed journal eLife, provide fresh insights into how the encephalomyocarditis virus (EMCV) manipulates infected cells, offering researchers a potential target for future treatments against viral diseases.
Virus hijacks the cell’s protein factory
Viruses cannot produce proteins on their own and depend entirely on the cells they infect to multiply.
The IISc team discovered that EMCV uses a specialised section of its genetic material, known as an Internal Ribosomal Entry Site (IRES), to take control of the host cell’s ribosomes—the microscopic structures responsible for producing proteins.
Once inside the cell, the virus blocks the production of normal cellular proteins and redirects the ribosomes to manufacture viral proteins instead, allowing it to replicate rapidly.
Researchers capture the process in unprecedented detail
Using advanced cryo-electron microscopy, the researchers captured the virus while it was assembling a complex with the host cell’s ribosome.
The study revealed that the viral IRES directly binds to the cell’s 40S ribosomal subunit and the initiator transfer RNA (tRNA), a mechanism that researchers say has not previously been observed in other viruses.
To obtain the images, the team isolated the viral protein-making complex from rabbit reticulocyte cell extracts using a specially designed bait protein before successfully determining its structure after several attempts.
Discovery could aid antiviral drug development
Associate Professor Tanweer Hussain from IISc’s Department of Developmental Biology and Genetics, who served as the study’s corresponding author, said little was previously known about how the virus captured and controlled the host ribosome.
Researchers believe the discovery identifies a vulnerable step in the virus’s life cycle that could be targeted by future antiviral drugs.
Since similar IRES-based mechanisms are used by related viruses, including the poliovirus, scientists say treatments designed to block this process could potentially be effective against multiple viral infections.
The study provides one of the clearest molecular views yet of how certain viruses hijack a host cell’s protein-making machinery, laying the foundation for future research into preventing viral replication.