Viral protease 3C
Viral cleavage of antiviral signaling↓
Also searched as Viral cleavage of antiviral signaling.
The cell has a sensor that detects viral genetic material and raises the alarm. This enzyme cuts the sensor first. That is why the infection can establish itself before the body knows it is there.
In depth
A viral enzyme that cuts the cell’s antiviral alarm before it can sound.
What drives it
Coxsackievirus B3 increases it.
The virus brings its own scissors. A coxsackievirus makes one long protein and must cut it into pieces — and the two blades it uses for that also cut the host. 'In CVB3 infections, viral proteases 2A and 3C can impair cellular functions by cleaving an array of host proteins' (pmc10178405 · PMID 37175422 — Role of Coxsackievirus b3-Induced Immune Responses in the Transition from Myocarditis to Dilated Cardiomyopathy and Heart Failure). These are the steps the field names as the actual druggable targets — blocking the virus at attachment, entry, uncoating, RNA or protein synthesis rather than fighting the inflammation afterwards. PMID 37175422
What it drives
It reduces Antiviral sensor relay.
It blinds the alarm before the alarm can ring. '3C protease cleaves mitochondrial antiviral-signaling protein (mavs) and trif, which are important for downstream antiviral responses such as the activation of NF-κB, 2′-5′ OAS, PKR, and Mx, and caspase-dependent apoptosis' (pmc10178405 · PMID 37175422 — Role of Coxsackievirus b3-Induced Immune Responses in the Transition from Myocarditis to Dilated Cardiomyopathy and Heart Failure). And 2A does the same from another angle: it 'disrupts NF-κB activation by cleaving NFAT5 and SQSTM1'. ⇒ the cell has a sensor that would raise the antiviral defense. the virus cuts the sensor first. PMID 37175422
It reduces The Handbrake the Virus Releases.
And this is the cruellest trick in the whole MAP: the virus releases the brake on the cell's self-destruct. 'both 2A and 3C are required for cleavage of CARD8, which normally functions to inhibit activation of CASP1 and pyroptosis' (pmc10178405 · PMID 37175422 — Role of Coxsackievirus b3-Induced Immune Responses in the Transition from Myocarditis to Dilated Cardiomyopathy and Heart Failure). ⇒ CARD8 is a handbrake. Cutting it lets the inflammatory cell-death machinery run. the bursting cell death is not an accident of the infection — the virus actively unlocks it. PMID 37175422
It increases Cell turnover.
It blinds the alarm before the alarm can ring. '3C protease cleaves mitochondrial antiviral-signaling protein (mavs) and trif, which are important for downstream antiviral responses such as the activation of NF-κB, 2′-5′ OAS, PKR, and Mx, and caspase-dependent apoptosis' (pmc10178405 · PMID 37175422 — Role of Coxsackievirus b3-Induced Immune Responses in the Transition from Myocarditis to Dilated Cardiomyopathy and Heart Failure). And 2A does the same from another angle: it 'disrupts NF-κB activation by cleaving NFAT5 and SQSTM1'. ⇒ the cell has a sensor that would raise the antiviral defense. the virus cuts the sensor first. PMID 37175422
Blends that modulate it
Each blend page names this pathway and carries the study behind its claim.
See it on the map
Open the causal map to follow this pathway upstream and downstream, arrow by arrow, each with its study.