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3 Responses to #TrumpIsNotLikeYou

  1. Eric says:

    I don’t like Trump, but he is not responsible for anyone dying of viral infections. That absurd narrative seems to be the only reason everyone wants the virus to be more than it actually is.

    Sneak preview of my current batch of research – the only people that should be wearing masks (if at all) are the elderly and morbidly obese baby boomers with heart disease, since they are the ones capable of actually spreading it amongst themselves due to a weakened immune system that allows it to reproduce in numbers sufficient to infect others in the first place.

    • I was under the impression that many different types of people were capable of having a heavy viral load; indeed to date the “super spreaders” at least outside retirement homes have not, in the main, been the elderly, have they?

      Most masks, especially cloth ones, protect other people from the wearer more than they protect the wearer. So I’m somewhat uncertain what would be achieved by only having the most vulnerable wear masks (would your rule extend to minorities too?).

      Also, many people exist in multi-generational families, or visit their older relatives and friends, or interact with older co-workers. Even if we can secure sufficient supplies of N99 masks and train the vulnerable to wear them right is it your plan that the vulnerable should wear them at home? 24/7?

      • Eric says:

        An important consideration of PCR tests is that they operate in cycles called the Ct value.

        Specifically, let’s stay you start with a single virus. In theory, the PCR test will bind to the virus and duplicate the unique sequence. We now have 2 strands instead of 1. The next cycle will then double the virus from 2 to 4; the third will double from 4 to 8; the fourth will double from 8 to 16. In essence, it’s an exponential growth rate in the form of 2^N, where N = number of cycles.

        So take for instance the following statement by Harvard researchers in the field of infectious disease examining the concept of viral load and PCR tests: “The Ct value is inversely related to the viral load and every ~3.3 increase in the Ct value reflects a 10-fold reduction in starting material.” When I went to a calculator and typed in the number 2 raised to the power of 3.3, the result became 9.8491553067593 which rounds to 10. What they mean by “reduction in starting material” simply means it would require 1/10th the amount of original sample undergoing 3.3 duplication cycles to produce the same positive result as a sample size that was 10x as numerous without any duplication in the first place.



        So why is viral load relevant? Simply because the body is constantly at war with the environment and the immune system can normally stop the acceleration of a pathogen. The difference between “asymptomatic” and “pre-symptomatic” is merely momentum. A pre-symptomatic person, while technically asymptomatic at the time, will eventually express symptoms after a certain critical mass is reached. In other words, the immune system is being overwhelmed and they become “post-symptomatic.” By contrast, a strictly asymptomatic person has the virus under control.

        And this makes sense, considering I’ve generally known about this concept since childhood that people are contagious right before they express symptoms and the few days afterwards. But this concept involves the momentum of a pathogen increasing in numbers within the person’s body and then decreasing. If there is no momentum building, such as when the person is immune or when the virus is ending, medical science has been quite clear on the issue for a very long time.


        Since I’m not yet prepared to summarize my review of animal studies involved in Koch’s postulates, I will simply state that viral load exposures are typically taken into account. There may be some groups of hamsters that get exposed to a “mild” dose compared to others that get exposed to a “large” dose of a pathogen to create different tiers of study, relative to a control group that gets no dose in the first place.

        The concept is to determine how much of a pathogen is necessary to overwhelm an otherwise healthy immune system. A corollary concept is that sicker individuals are more contagious because their body is producing more substance per breath than a healthy person without symptoms.

        As a brief example of the concept involving influenza, it has been observed in general that: “Specific host factors that may render some individuals more efficient spreaders of influenza virus than others have, for the most part, not been identified. Epidemiological observations as well as clinical data on the duration of viral shedding suggest that children (most likely with no prior exposure to influenza viruses) and immunocompromised individuals are good transmitters. Thus, immune competence and history of exposure to influenza are most likely major factors affecting influenza virus transmission.”


        The key part of the observation is that children are super spreaders because they have never built immunity to influenza. In the case of coronavirus, children are exposed to that family of virus all the time as evidenced by the widespread development of runny noses and subsequent building of a generalized immunity. The other end of the spectrum as it relates to Covid-19, involving “immunocompromised individuals” such as the elderly and comorbid Baby Boomers, makes sense because they are essentially unable to utilize their innate immunity due to poor health.

        The irony of the situation, therefore, is that the group of people most susceptible to this particular pathogen are also the ones responsible for spreading it amongst themselves and should be quarantined from the rest of healthy society, not the other way around.

        And if you don’t want to take my word for it, perhaps you’ll believe the New York Times:


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