Vito

Worth noting the other defences that are easy to overlook, because they are behavioural rather than anatomical.

Seeking shade in the middle of the day, covering up, and simply disliking the feeling of burning are all real protections, and every human society in a sunny climate developed clothing and shade practices. Discomfort is itself an adaptation — it is the signal that stops you before the damage gets worse.

Modern life removes a lot of that. Sunburn on a beach holiday takes hours to hurt, by which time it has happened.

The disease point deserves emphasis because it is the usual way these populations eventually run into trouble.

A genetically uniform population is uniform in its immune variation too. A pathogen that gets past one individual's defences tends to get past all of them, so outbreaks in such populations can be far more severe than in diverse ones.

So the answer to "why has it not collapsed" may well be "because nothing has tested it yet".

Two practical points for the matching you are doing.

Testing company matters. Different companies use different chips and different thresholds for reporting a match, and they have different customer pools. A relative who does not appear on one platform may appear on another, and uploading raw data to a third-party comparison site widens the pool considerably.

Small matches are unreliable in both directions. At the very low end, some reported matches are false — short segments that look shared by chance rather than by descent. So a tiny match with a distant cousin is weak evidence and no match is weak counter-evidence. Neither should move your confidence in a documented line very much.

Which means for anything beyond about third cousins, the paper trail is the stronger evidence and the DNA is the supporting hint, not the other way round.

There are two further constraints worth adding.

Viruses are picky about which cells they can enter. Infection requires a specific receptor on the cell surface, and often other factors inside. A respiratory virus can infect certain cells in the airway lining and simply cannot enter most other cell types. So the infection is confined to a subset of cells even within the tissue it reaches — the "nearby cells" in your model are frequently not susceptible at all.

Not every infected cell bursts. Some release particles gradually while surviving, some are killed by the immune system before producing much, and many produce defective particles that infect nothing. The yield per cell in practice is far below the theoretical maximum.

So the exponential you are imagining is damped at every step.

Your model is a reasonable first approximation and it is missing the two things that dominate the outcome.

The immune response is fast and local. Infected cells detect they are infected and immediately signal it — releasing molecules that put neighbouring cells into an antiviral state before the virus reaches them. So the expanding front you imagine runs into tissue that has already been warned and is much harder to infect. That response begins within hours, long before any antibodies exist.

The tissue is renewing constantly. The surfaces most infections attack — airway lining, gut lining — replace themselves rapidly as a matter of routine. Cells are dying and being replaced there continuously with or without a virus. Losing a scattering of them is absorbed by a process already running at high speed.

Between those two, the infection is contained and the damage is repaired concurrently rather than accumulating.