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We should probably address a key distinction in research on SARS-CoV-2:
The METHOD used often changes the ANSWER we get.

METHODS:
viral RNA tests
viral antigen tests
infectious particle tests
host antibody tests
host clinical measures or biomarkers
The most sensitive test is a PCR based test for viral RNA. But not all viral RNA is going to be packaged in infectious viral particles.

It's also true that a single viral RNA may not result in successful infection of a patient. We might detect sub-infectious levels.
There is a test that only detects infectious viral particles (TCID50), but it's very low sensitivity and clunky to set up. We mostly use it to check assumptions.

So we have a too sensitive test and an insensitive test, and which one we use determines our answer in some cases.
There are also issues with calculating the spread of the virus:
If we use direct detection of viral antigens in blood, the testing window for accurate results is only a few days, around when the person first gets symptoms.
On the other hand, if we test for antibodies, we'll be detecting anyone who was ever exposed to the virus, even if they were never successfully infected.

Hence, I suspect, the consistently high seroprevalence for SARS-CoV-2 that doesn't seem to reflect clinical reality.
You may have heard of the parable of the blind men and the elephant?

Scientists and clinicians generally understand these distinctions, so we tend to view results based on a single test as "one aspect of the elephant". It tells an incomplete picture & we need a holistic view.
If viral RNA is found somewhere by PCR (park benches, market stalls), and it's confirmed by TCID50, and it results in clinical manifestations of COVID-19 in patients... then we have a pretty complete picture of disease transmission.

No one measure is sufficient.
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