A molecular saboteur: how SFTSV avoids a tick’s immune system
Published: 27 May 2026
Researchers at the Centre for Virus Research (CVR) have discovered how SFTSV evades tick immune defences using a viral protein called NSs, which suppresses the tick’s antiviral RNAi response. The findings reveal a potential new target for preventing transmission from ticks to humans.
Severe Fever with Thrombocytopenia Syndrome virus (SFTSV) is a dangerous, emerging tick-borne virus that causes high mortality rates in humans.
Recent research led by the Centre for Virus Research has uncovered a critical discovery showing that the virus has evolved a way to counteract this defence using one of its own proteins, called NSs.
The natural host for SFTSV is ticks. Like many invertebrates, ticks do not rely on the same immune responses as humans, and instead mount a sophisticated immune response called RNA interference (RNAi), which acts as a cellular search and destroy system to shred viral genetic material.
When a virus infects a tick cell, the RNAi system finds the invading viral genetic code and cuts up the virus’s genetic material into small fragments called small interfering RNAs (siRNAs) using an enzyme called Dicer, which acts like a pair of molecular scissors. siRNA fragments are then used to recognise and destroy any other virus particles. This response should normally limit or even eliminate the infection, however SFTSV has evolved a clever counter-strategy.
A specific viral protein, NSs, is essential for the virus to survive and replicate within ticks. The NSs protein acts as a molecular saboteur, selectively binding and 'hiding' the tick’s siRNAs. By attaching to these fragments, NSs effectively removes them from circulation, preventing them from being used to guide the destruction of viral genetic code.
In other words, the virus disarms the tick’s defence tools before they can be deployed. Just three days after infection, researchers could find barely any active virus-hunting siRNAs, and the tick’s immune system was totally suppressed, meaning the NSs saboteur was fast and stealthy.
The researchers show that NSs operates even though it is present at very low levels in tick cell - so low that it is extremely difficult to detect. Despite this, it is still highly effective, suggesting that it binds very tightly to siRNA targets.
This efficiency allows the virus to suppress the immune response effectively without needing large amounts of NSs. However, over time, the tick’s RNAi system begins to overcome this suppression, indicating an ongoing 'arms race' between the virus and the tick’s defences.
This study reveals that the virus uses host-specific immune evasion strategies, employing different 'tools' to thrive in ticks versus humans, and shows that viruses are absolute masters of adaptation.
By identifying exactly how the NSs protein disarms the tick's immune system, scientists have found a new target for interventions. If they can find ways to block this protein or disrupt its interaction with RNA, it may be possible to disrupt the virus’s life cycle in its vector, blocking the virus at its source, and stopping transmission from ticks to humans before an infection even begins.
First published: 27 May 2026
<< News