Not really. So many things with this virus seem to be highly variable. Simple explanations of observed phenomena seem to be especially elusive.
I recently read about how some percentage of COVID patients never really express the virus through their nasal passages. So all the while their lungs are filling with clots and their O2 saturation drops like a stone, they consistently test negative on any kind of swab-based test. For these patients, doctors will diagnose COVID via a chest X-ray, with a fluid sample taken from the lungs for confirmation if feasible (e.g. patient has been intubated).
So the way it seems to break down is you can very roughly categorize three types of COVID-19 patients:
1) Virus concentration in the nasal passages, little to no virus in the bronchi and lungs -- these patients will be spared the worst of COVID, typically having cold-like symptoms if they are symptomatic at all. However, due to the location of the virus, these patients likely emit virus-laden aerosols at a greater concentration than their symptoms would suggest. These patients will typically test positive via swab within the accuracy limits of a given swab test.
2) Virus concentration in both the nasal passages and in the bronchi and lungs -- these patients will run the gamut from asymptomatics to those requiring intensive care. These patients will also (usually) emit plenty of aerosols, but they'll be "seen coming" -- their illness is more likely to be apparent than those in group 1. These patients will also typically test positive via swab within the accuracy limits of a given swab test.
3) Virus concentration in the bronchi and lungs, little to no virus in the nasal passages -- these patients can also range as widely as group 2. However, these patients will also consistently test negative via swab, which can delay accurate diagnosis. Patients in this groups can "wave off" severe symptoms for a time as they can point to repeated negative COVID tests.
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All of that would seem to play into the general chaotic nature of COVID's transmission. But I don't think all the dots are connected just yet.
I’m guessing where the virus lands, which reflects how it was transmitted, and where you are in the course of infection, determines viral concentration in various areas and symptoms.
I think most people inhale it, especially larger droplets, and the bulk of the virions start their job close to the entry points of the naso- and oropharynx. If your immune system contains it, it doesn’t travel anywhere else. For many people who don’t, it spreads to the deeper airways, usually via aspirated secretions. It’s also possible it disseminates via the bloodstream, though I think that is less likely. Anyway, once it gets deeper in the respiratory tract more severe symptoms develop, which are compounded in a subset of patients by the cytokine storm.
A second group is infected by smaller aerosols, which can avoid the physical barriers of the upper respiratory tract (hair, cilia) more readily and be inhaled deeper in the airways/lungs from the get-go. These guys get sick more quickly.
Still others ingest the virus from contaminated hands or fomites, which inoculate the mouth first. These people have a preponderance of gastrointestinal symptoms early. It spreads to the lungs via aspiration or blood borne dissemination as above. This is the subset who may never carry virus in the nasopharynx and consequently test negative.
As far are superspreading, the article gives us some clues. Probably a number of factors need to align for a superspreader event to occur: wrong host in the wrong place, partaking in the wrong activities for a relatively long time. Stuff like singing with a bunch of people over several hours, working in close quarters all day in a poorly ventilated meat-packing plant, or communal living situation like prisons and long term care facilities.
We don’t know a lot about host factors which contribute to superspreading, but I suspect they may have subtle immunologic defects which allow the virus to proliferate to higher levels in their upper airways. When they cough, sneeze, sing or talk loudly/yell, larger viral quantities are spewed into their surroundings, especially via aerosols, than typical transmissions. If I had to venture a guess, I’d bet they have a mild IgA immunoglobulin deficiency. IgA are mucosal antibodies, which are among our first line of defense against respiratory and gastrointestinal infections. While nobody has preformed SARS-CoV-2 antibodies, many do have IgA antibodies targeting other coronaviruses and viral respiratory infections. It’s been suggested these cross-react enough with SARS-CoV-2 to attenuate its severity. Although other deficiencies of nonspecific, innate immune function may also be in play, IgA deficiency is relatively common in the general population.
Almost none of the above is experimentally validated, so take it with a grain of salt.
