When a Virus Steps on a Mine: Ancient Mechanism of Infected Cell Self-Destruction Discovered
When a virus enters a cell, it disrupts the cell’s normal functions. It was previously believed that the cell's protective response to the virus triggered cellular self-destruction. However, a study involving bioinformatics researchers at HSE University has revealed a different mechanism: the cell does not react to the virus itself but to its own transcripts, which become abnormally long. The study has been published in Nature.
Many viruses act in a similar way: they block the activity of cellular genes and reprogram the cell to produce viral proteins. As a result, the cell stops making its protective molecules and becomes vulnerable. However, as researchers have discovered, this process can sometimes backfire against the viruses themselves.
Biologists and bioinformatics researchers from the USA, the UK, Germany, China, and Russia have investigated how cells are able to recognise a viral attack. The researchers infected cells with herpes and influenza viruses and used RIP sequencing to analyse the cells. This technology makes it possible to isolate RNAs associated with specific proteins within a cell and thereby observe how the activity of cellular genes changes after infection.
The analysis revealed that viral proteins prevent the cell from properly completing transcription—the process of reading information from DNA. As a result, RNA synthesis fails to stop at the right time, producing excessively long molecules instead of the required transcripts. These elongated RNAs contain fragments of 'junk' DNA—ancient viral insertions that have accumulated in our genome over millions of years of evolution. Under normal conditions, these regions remain inactive, but when transcription goes awry, they are read and form structures with a unique shape: left-handed double helices, known as Z-RNA.
An increased number of such molecules is perceived by the cell as a danger signal. Their recognition is carried out by the ZBP1 protein, a sensor of intracellular immunity. As soon as it detects the accumulation of Z-RNA, the cell activates a self-destruction program—apoptosis or necroptosis. As a result, the virus does not have time to exploit the cell’s resources for its own replication.
Maria Poptsova
'It turns out that when a virus tries to suppress the activity of cellular genes and exploit the cell’s resources for its own replication, it triggers the cell’s self-destruction mechanism. It’s as if the virus steps on a mine laid by innate immunity: the cell dies along with the virus, preventing its further spread,' comments Maria Poptsova, Head of the Centre for Biomedical Research and Technology at the HSE Faculty of Computer Science.
The scientists suggest that this protective mechanism may also operate in other viral infections that disrupt the transcription process. Moreover, the researchers were able to reproduce the same effect artificially: the drug JTE-607, currently in clinical trials as an anticancer agent, also induces the formation of Z-RNA. This mechanism could potentially be harnessed in therapy—for instance, to selectively trigger the death of cancer cells or to enhance the immune response.
The study was conducted with support from HSE University's Basic Research Programme within the framework of the Centres of Excellence project.
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