An oncolytic virus selectively replicates inside tumor cells (many solid tumors have defective antiviral interferon signaling) while sparing healthy tissue. Spread across the tumor is a stochastic branching process on the cell lattice:
P(infect neighbor) = 1 - e^(-β·dt) for each susceptible contact
Cell bursts at t = t_infect + T_lytic, releasing k new virions
Antigen pool A(t): dA/dt = r_release · (bursts/s) - decay·A
T-cell recruitment: dN_T/dt = k_prime · A(t) (up to a carrying capacity)
Lysis is immunogenic: dying tumor cells release damage-associated molecular patterns (ATP, HMGB1, calreticulin) alongside tumor-associated antigens. This "in situ vaccination" primes T cells that then kill not only infected cells but also nearby uninfected tumor cells — a bystander/epitope-spreading effect distinct from direct viral lysis.
- Infectivity β — probability per second an infected cell's virions successfully infect an adjacent healthy tumor cell.
- Lytic period — time from infection to cell burst; shorter periods spread the virus faster but give the immune system less time to catch up.
- Immune priming rate — how strongly released antigen recruits new T cells into the spheroid.
- T-cell kill rate — probability per second a T cell adjacent to a tumor cell (infected or bystander) clears it.
- Inject Virus — infects the central cell of the spheroid, starting a fresh wave of spread.
Real-world relevance: this is the mechanism behind approved oncolytic viruses like T-VEC (talimogene laherparepvec, an engineered HSV-1) — direct tumor lysis combined with converting a "cold" (immune-excluded) tumor into a "hot" one that recruits systemic anti-tumor T-cell immunity.