IFNA1 and coinfection: We find that: (1) our model captures the ring–like and patchy plaque morphologies observed experimentally; (2) IFN production peaks at an intermediate DIP ratio, reflecting a trade–off between early immune activation and sufficient co–infection; and (3) even a small fraction of long–range spread of virus and DIPs escape containment despite longer IFN ranges; this causes stronger antiviral responses but earlier peaks in lysis at similar levels of cell loss.