In reply to captain paranoia:
> That led me to thinking about the concept of viral load, and what happens in the body if it is exposed to a viral load below some threshold of infection. What happens to the viral contamination that does enter the body? Is it attacked and destroyed without triggering a full immune response (antibody generation and t-cell memory)? Or does the body learn from that sub-infectious viral load? If that is indeed 'a thing'.
Hmmm. I guess the answer to the last bit is yes, your immune system quite often identifies and eliminates pathogens subclinically, especially if the infection comprises few pathogens or is concentrated locally. You only really become aware of feeling poorly when infections become systemic, with the systemic release of cytokines like IL-1, IL-2 and TNF alpha.
For bacteria, the correlation of load and time to symptoms is easy to picture. If you, for instance, eat something that contains a small inoculation of some potentially pathogenic bacterium (Salmonella, Campylobacter etc) then it's a race between the doubling time of the bugs and the speed with which they are passing though the gut. It's complicated by the potency of any toxins they are releasing and, especially, whether they can attach to the wall of the gut (like the enteropathic E coli strains) and/or penetrate the gut wall and enter the blood stream (like, from memory, typhoid). However, a big inoculum from, for example, a single bad mussel (to cite a vivid personal experience) can produce a very rapid onset of symptoms.
For viruses, it's a bit more complicated. A single virus, once it binds to and enters a suitable host cell, can replicate itself into hundreds of new viruses in one round of replication. So, yes, having a greater initial dose is likely to lead to more serious symptomatic disease more quickly. In the case of an individual who has encountered the virus before, there may be sterilising antibodies (sIgA) present on the surface of mucous membranes or IgM or IgG in the blood. it seems logical that a massive dose of virus is more likely to escape or saturate the population of specific antibodies and then go on to successfully find its preferred receptor and infect a host cell. It's a lot more complicated than that because of the presence of the innate neutrophil and macrophage response, NK cells and Tc cells, and the question of relatively inaccessible immune privileged sites.
For an airborne infections, it's also probable to being exposed to a high concentration of aerosol particles will result in more of them penetrating more deeply into the lungs, and so contacting not just the tracheal and bronchial epithelia (with their wonderfully named mucociliary escalator that traps such particles and transports them back up the respiratory tract for swallowing into the stomach) but the crucial alveolar cells.
So, it's difficult to model exactly, but, in general, a smaller dose definitely helps to produce less serious disease, assuming it's accessible to the immune system, but small doses are normally adequate to provoke a (hopefully proportionate) immune response.
And I know there's a whole literature on how small doses of antigens can lead to tolerance and anergy in some circumstances. As I say, it's complicated.
Post edited at 17:24