Nikhil Prasad Fact checked by:Thailand Medical News Team Mar 07, 2026 1 hour, 46 minutes ago
Medical News: A new scientific discovery is shedding light on how the deadly avian influenza virus, commonly known as bird flu, manipulates human cells to reproduce faster. Researchers have discovered that the virus hijacks a specific human protein that normally helps cells produce other proteins. By exploiting this protein, the virus is able to dramatically increase its replication during the early stages of infection.
Scientists discover that bird flu uses the human protein RPS27A to boost viral replication inside infected cells
Avian influenza viruses primarily infect birds but have increasingly crossed into mammals, including humans. Some strains such as H5N1 are known for causing severe disease and raising fears of potential pandemics. Understanding how these viruses replicate inside human cells is therefore essential for developing new strategies to stop them.
Scientists Investigate How Bird Flu Takes Over Cells
Researchers from the China Institute of Veterinary Drug Control in Beijing, the College of Animal Science and Technology at Shihezi University in Xinjiang, and the College of Veterinary Medicine at Gansu Agricultural University in Lanzhou conducted a detailed investigation into how bird flu interacts with human cells.
Their study focused on a viral protein known as PA, an important component of the influenza virus replication machinery. This protein forms part of a complex that allows the virus to copy its genetic material and produce viral proteins after entering a host cell.
To understand how PA works inside infected cells, the scientists infected human lung cells with a highly pathogenic H5N1 strain of avian influenza virus. They then analyzed how the infection changed the activity of thousands of human genes and proteins.
The results revealed that bird flu rapidly reshapes the host cell’s internal environment to favor viral growth.
Massive Changes in Human Cells After Infection
The researchers discovered dramatic changes in gene activity shortly after infection. More than ten thousand genes showed altered behavior, with many becoming highly active while others were strongly suppressed.
Genes involved in protein production, immune signaling, and energy metabolism were strongly activated. At the same time, genes involved in cell division, DNA regulation, and normal cellular maintenance processes were suppressed.
These changes suggest that the virus forces the host cell to redirect its resources toward making proteins and generating energy—two processes that help the virus multiply quickly.
To identify which host proteins the virus interacts with, scientists used advanced protein analysis techniques. They discovered more than two hundred human proteins that directly associate with the viral PA protein. Many of these proteins are involved in ribosome activity and RNA metabolism, which are central to protein production inside cells.
Key Human Protein Helps the Virus Replicate
Among the many interacting proteins, one stood out as particularly important. The protein RPS27A, a ribosomal protein involved i
n building cellular proteins, was found to directly interact with the viral PA protein.
Microscopy studies showed that the viral protein and RPS27A appear together inside infected cells, suggesting they work as a functional pair during infection.
The researchers then tested what happens when the levels of RPS27A are changed inside cells. When cells were engineered to produce more RPS27A, the virus replicated much faster during the early phase of infection. However, when the researchers reduced RPS27A levels using gene-silencing techniques, viral replication dropped significantly.
This clearly demonstrated that RPS27A helps the bird flu virus multiply more efficiently.
This
Medical News report notes that viruses often hijack the host’s protein manufacturing machinery, but this study provides strong evidence that RPS27A plays a central role in helping influenza viruses replicate.
A Potential Target for New Antiviral Treatments
The discovery could have important implications for future antiviral therapies. Instead of targeting viral proteins, scientists may be able to develop drugs that block the interaction between viral proteins and key host factors like RPS27A.
Such an approach could make treatments more effective because viruses mutate quickly, while host proteins remain relatively stable targets.
Interestingly, RPS27A has also been linked to replication processes in other viruses, suggesting that it may serve as a common pathway exploited by multiple pathogens.
Conclusion
The findings reveal a critical strategy used by avian influenza viruses to hijack human cellular machinery. By binding to the ribosomal protein RPS27A, the viral PA protein creates conditions that enhance viral protein production and accelerate early viral replication. This discovery significantly improves scientific understanding of how bird flu viruses manipulate host cells and highlights RPS27A as a promising target for future antiviral research. Continued studies will be needed to determine whether disrupting this interaction could lead to effective treatments against influenza and possibly other viral infections.
The study findings were published in the peer reviewed journal: Viruses.
https://www.mdpi.com/1999-4915/18/3/317
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https://www.thailandmedical.news/articles/h5n1-avian-flu
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