Jennifer Ogle Dan's numbers are meaningless

Jennifer Ogle Dan's numbers are meaningless. He's taking epidemiological estimates of flu cases (there is no widespread testing for flu virus) and comparing it to "confirmed cases" of COVID, which generally means one positive test, although that number is fuzzy too, because people get tested multiple times. If I get tested 10 times, 3 positives and 7 negatives, that counts as 3 cases.

In other words, "Confirmed Cases" is not a useful metric for comparing one disease to another, because we have never head widespread testing for any other virus. It depends completely on testing rates. Even if we started testing 100% of the population every week now, so we didn't miss any minor cases, we would not detect those who have already recovered.

If Serology (antibody) tests could be developed that work reliably, you might get a more meaningful number. But of course we now know that many people who are exposed to the disease defeat the virus without developing anitbodies.

The epidemiological estimates for COVID-19 in the USA are generally around 50 million... although now that we know about T-cell immunity... people who have been exposed and never reproduce the virus nor develop measurable antibody, it is likely that the number who have been exposed to an infectious quantity of SARS2 in the USA is probably more like 100 million, which would be the right number to compare again 60 million flu cases.

So with COVID, you get 180K deaths out of 100M exposures, or 0.18% IFR. The general number for influenza is about 0.1%, although it is better in some years and worse in others.
Chuck Strouß III Ok. I totally understood you until you got to the part about the number people being exposed to COVID, but not getting it being compared to the number of flu cases. Wouldn't you have to compare the number of people exposed to flu and not actual flu cases?
Jennifer Ogle It might make sense to look at the number of people who actually hosted the virus, ie: became infected. The thing is that these people who beat the virus with T-cell immunity arguably DID become infected, their bodies just beat it so fast that they did not end up having antibody immunity.

It all does get rather nebulous, how to define when an infection occurs. For example, we all carry various bacteria in our noses and throats that could cause an infection if they found their way into our bloodstreams, yet we do not consider that having an infection. It is possible also that some of the people who had a positive PCR nasal swab for SARS2 were in that same boat... viruses being present that had not moved into the cells to start multiplying.

When a pathogen DOES find a portal of entry into the cells, so that our active immune system can start working on it (our skin, mucus, and biome -- bacteria on our skin, and our stomach acid make up our passive immune system), does it have a chance to really set up shop and start multiplying? Or is it basically just fighting for survival?

It is also common for a small number of pathogens to find a portal of entry, but we cannot detect it, because our immune response is too minor to generate a fever.

My late wife was actually exposed to HIV one time, and took part in a University study which showed her immune system defeating the HIV over the course of a few days. So did she have HIV, or not? She had HIV in her blood, but her immune system was "killing" it faster than it could reproduce.

So these people who defeat SARS2 with their T-cell immunity generally fall into that category, I suspect... A sufficient quantity of the pathogen enters their cells to prompt them to mount an immune response, but the response is not serious enough to cause any symptoms.


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