Venom immunotherapy (VIT) retrains the immune system with gradually increasing venom doses. Over weeks of injections it builds IgG4 "blocking" antibodies that intercept venom proteins in the bloodstream before they can trigger the IgE-coated mast cells that cause anaphylaxis.
Reaction risk after t weeks of VIT:
Risk(t) = R0 × [ 1 − Emax × (1 − e^(−t/τ)) ]
R0 ≈ 0.60 baseline untreated systemic-reaction risk (prior reactor)
Emax ≈ 0.95 maximum protection (sourced range ≈ 90–98%)
τ ≈ 55 wk time constant — protection starts appearing after
build-up (~3-6 mo) and approaches full effect during
the 3-5 yr maintenance phase
Blocking antibody level: IgG4(t) = 100% × (1 − e^(−t/τ))
- Weeks of VIT — drives both curves above; the dots orbiting the mast cell are blocking antibodies, and their density is the interception probability.
- Simulate a field sting — fires a venom particle at the mast cell; watch whether blocking antibodies intercept it or it triggers degranulation.
- Beta blocker / ACE inhibitor — these can blunt epinephrine's effect in a real emergency; here they slow and cap the simulated recovery.
- Epinephrine — becomes available once a systemic reaction is triggered; injected promptly, it reverses the airway/blood-pressure crisis.
Even with full protection, biphasic anaphylaxis — symptoms returning hours after they first ease — is why continued observation matters after any epinephrine use.