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Cold viruses seem to typically have incubation periods of 3 days, but from a mechanical point of view, I wonder how this is possible?

For example, if we read this viral assay protocol document: https://www.virapur.com/protocols/Virus%20Plaque%20Assay%20Protocol.pdf we can see that when a viral plaque is grown, then the plaque becomes visible in "5-7 days". So, since viruses have reproductive cycle of 6 hours, then that would be about 24 generations. Presumably each generation can only infect cells immediately adjacent to the infected cells since viruses cannot move on their own. So, the virus spreads in rings emanating outwards from the initial innoculation site.

If the visible plaque is 4mm in diameter, then we presume each generation is growing by 4mm/24 = 0.17mm which in itself is kind of suprising because a cell is only about 0.005mm in diameter, so the virions would seem to be simultaneously spreading by 0.17/0.005 = 34 layers of cells per generation. It is hard to see how they could do that without moving in some way. Maybe diffusion of some kind is occurring?

In any case, from geometrical standpoint I don't understand how a viral plaque in the wild could spread fast enough in only 3 days given what we see in the lab.

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  • $\begingroup$ Viruses could easily be carried by the circulatory system, even if they actively infect only certain kinds of cells. $\endgroup$ – jamesqf Apr 9 at 16:50
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A viral plaque assay is an artificial system which limits the physical dispersion of newly released virions. It is designed to count the number of infectious virions (plaque forming units) in a given sample, not to measure the rate of reproduction or spread. Since each plaque begins with a single infected cell, the number of new cells infected with each cell burst is going to be limited by the physical proximity of cells to the infected cell, not by the number of infectious virions released.

In a living system, a single cell burst from a viral infection can release anywhere from a few hundred to up to several tens of thousands of new virions which will then be carried in all manner of different bodily fluids to infect new cells, dramatically increasing the potential number of new cells infected after each replication cycle, compared to a plaque assay.

Another consideration is that some of the symptoms of the common cold are generally similar to those common in the prodrome phase of most viral infections, so it is probably difficult to distinguish its true incubation period from the onset of any acute viral infection.

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