This isn’t really accurate because it fails to take into account how infections work. Viruses don’t replicate like bacteria, so they don’t just double every X amount of time. They infect a cell and hijack the cell to produce copies (sometimes millions) of the virus until the cell exhausts itself and dies, bursting open and releasing all those copies of the virus. While this is happening, the body is attempting to fight this. What is particularly relevant are several of the varieties of T-cells, or killer cells. They are attempting to find cells infected with the virus and destroy them before they burst. While some copies of viruses escape cells as they are producing them, the overwhelming majority escape when it dies and bursts.
What this means is that 30 viral particles do not become 300,000 in 14 seconds. Say that all 30 find cells and infect them, and T-cells destroy 50% before they burst. You have 15 cells that burst and release viruses to infect nearby cells. If you start with 300,000 infected cells, and T-cells destroy 50% before they burst, you have 150,000 cells that burst and release viruses to infect nearby cells.
Low initial infections can often be well controlled and managed by the immune system in this way until antibodies are produced. High load infections can often spiral out of control due to so many initial cells being infected, the physical damage of higher numbers of killed cells, either burst or destroyed, and the high numbers outpacing the body’s ability. Of course this is also a simplification, but I think it demonstrates how initial viral load can have a big effect on outcome.
What this means is that 30 viral particles do not become 300,000 in 14 seconds. Say that all 30 find cells and infect them, and T-cells destroy 50% before they burst. You have 15 cells that burst and release viruses to infect nearby cells. If you start with 300,000 infected cells, and T-cells destroy 50% before they burst, you have 150,000 cells that burst and release viruses to infect nearby cells.
Low initial infections can often be well controlled and managed by the immune system in this way until antibodies are produced. High load infections can often spiral out of control due to so many initial cells being infected, the physical damage of higher numbers of killed cells, either burst or destroyed, and the high numbers outpacing the body’s ability. Of course this is also a simplification, but I think it demonstrates how initial viral load can have a big effect on outcome.