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Coronamonomania Thrives in Darkness, Part 99

By August 4, 2021Commentary

Francis Collins, the head of the the National Institutes of Health also reveals himself to be a mask nut, saying very explicitly that parents should mask in their home around unvaccinated children, and then, just like the Surgeon General, later tried to deny that that was what he said.

Going to put up an Active Cases post, maybe a YOY one.  Interesting that we are seeing a slight swell in cases in Minnesota, little earlier than last year, when it was around the middle of August.  Testing relatively comparable.  The weather has been different this year, I believe warmer, so maybe that plays a role.  And we have been having very bad smoke from Canadian fires, really bad over several weeks, and it appears that particulates may in some way help the virus travel and irritates upper respiratory, and lower, tracts, which may create a better opportunity for the virus to get a foothold.  And of course, the general level of contacts this year is much higher.

Five deaths reported today, three from February.  What is going on, lately a very large percent of deaths are from quite a ways back?  Very misleading picture gets painted.  Here is DD’s summary of how hard it is to figure out what day data relates to, what reporting lags look like and how hard it is to line up events on the same day:

“Actually, with their (DOH’s) new reporting policy of not processing data on weekends, tests are per 4 am the prior business day, and cases are per 4 am 2 business days ago.  So, todays reported tests are through 4 am last Friday, and today’s reported cases are through 4 am last Thursday. When I report active cases now I am using these dates. Since the data is for 4 am it effectively is really for the prior day, but I am ignoring this because it is complicated enough.  I am crediting the reported No Longer Needing Isolation number to the prior business day.  Hospital admissions data lag 2 business days, so today’s data is through last Thursday.  Until the last few days they listed data tables for both death by date, and death by reported date, on the Situation Update page. Now however they no longer publish the date of reported death data table. Last Monday, 7/26, the data table went through 7/26, and the weekend dates were zeroes. I am keeping the same system for date of reported death, meaning the day it hits the Situation Update page is when I am recording the reported deaths, which includes LTC and other places of residence.  Hospital beds in use are listed up to the prior business day. Today’s data goes through last Friday.

In other words, nothing really matches and I’m not really sure what day anything is valid for.”

Another excellent article from Dr. Ionnidis on the issue of attributing deaths to CV-19.  An excellent discussion of the problems and possible solutions.  He suggests that US deaths are likely over-estimated, but are under-estimated in other countries.  Somewhat mathematically complex, but his observations are just outstandingly useful.  (Ionnidis Article)

Asymptomatic transmission is a big problem, right.  We don’t really know that.  Here is systematic review of the literature by the eminent Centre For Evidence-Based Medicine at Oxford University.  Bottom line; a few studies may show the existence of transmission from asymptomatic or pre-symptomatic persons.  In general the quality of the research is not great and there is great variability in findings.  (Medrxiv Paper)

Another study which emphasizes the importance of knowing viral load for tracking an epidemic.    (Science Study)   (Science Comment)    The authors point out that knowing the viral load in a population is a better indicator of epidemic status than are raw case counts.  This is similar to the notion that what matters is how many people are active cases–capable of infecting others.  Trends in average viral load will give a good picture of whether cases are likely to be growing or declining.  Knowing viral load is also important for clinical reasons, as it is a clear reflection of disease severity.  Governments don’t share this data intentionally because they know it will show they are treating positives as cases that are almost certainly not infectious, but that lack of transparency is a serious problem.  In addition to releasing PCR cycle numbers, governments should do random culturing to correlate cycle number and virus viability and release that analysis as well.

Another vaccine safety study comparing rates of clotting disorders between the Pfizer vaccine, the Astra-Zeneca one, infected people and the general population.  (Medrxiv Paper)    Rates among vaccinees were generally similar to background rates in the population, although there was a slightly higher risk of pulmonary embolism among Astra-Zeneca vaccine recipients.  But the risk of pulmonary embolism among those with a CV-19 infection was around 15 times greater than in a vaccine recipient.

At a micro-level, as I have frequently pointed out, where the rubber really hits the road with CV-19 is in the upper respiratory tract.  So a strong immune response to the presence of the virus is important in that region.  And, consistent with past research, it appears that vaccination causes a localized immune response capability in the mucosal passages in the URT.  (Medrxiv Paper).




Join the discussion 9 Comments

  • guest says:

    Paper you might be interested in, published on May 10, 2019 and entitled, “Impact of Obesity on Influenza A Virus Pathogenesis, Immune Response, and Evolution”.

    Abstract: “…As a consequence of the 2009 H1N1 influenza A virus pandemic, obesity was identified for the first time as a risk factor for increased disease severity and mortality in infected individuals. Over-nutrition that results in obesity causes a chronic state of meta-inflammation with systemic implications for immunity. Obese hosts exhibit delayed and blunted antiviral responses to influenza virus infection, and they experience poor recovery from the disease. Furthermore, the efficacy of antivirals and vaccines is reduced in this population and obesity may also play a role in altering the viral life cycle,… Case studies and basic research in human cohorts and animal models have highlighted the prolonged viral shed in the obese host, as well as a microenvironment that permits the emergence of virulent minor variants. This review focuses on influenza A virus pathogenesis in the obese host, and on the impact of obesity on the antiviral response, viral shed, and viral evolution…”

    (They do say in their conclusion that “The extent to which these findings can be extrapolated to other respiratory viruses remains unclear.”)

  • Abhijit Bakshi says:

    Any information on Ivermectin?

    • Kevin Roche says:

      the research appears to support the idea that Ivermectin can lessen disease severity, and it is relatively inexpensive

  • John Oh says:

    Found you through PL. Thanks for doing this.

  • Richard Donnelly says:

    Late arrival to the healthyskeptic blog.
    DD’s charts most helpful; however, nowhere on the site have I found from whence (whom) the charts are sourced. Who or what is DD?

    • Kevin Roche says:

      the Minnesota data comes from the data the state provides on its websites. The US or world data comes from CDC, Worldometers or Johns Hopkins. DD is a person who takes the data and puts it in graphical or other form and does analysis on it. That person prefers to remain anonymous.

  • DaveK says:

    Thanks again, Kevin, for undertaking this useful and enlightening effort. I do not envy the hours and hours that you commit to reading dry, technospeak journal articles. Were it me, I would have pulled out what little hair remains on my head, then considered a play-day with a Yellowstone Grizzly before getting back to the reading.

    Anyway, I have a question not directly related to this post, but germane to the Covid topic in general. It was prompted by a question asked at another site, and while I take everything on that site with a moderate dose of salt, I thought it was actually a good query:

    Just how do we know know the prevalence of the Delta (or for that matter, any other) variant in the current spate of infections? As I understand it the PCR test for Covid, as it currently exists, does not directly identify which variant is causing the test to show “positive”. While it is possible to do additional cycling, while looking for other indicator DNA/RNA fragments, that additional cycling using modified test parameters would be rather expensive, so would not be routinely performed. Also, I don’t know of any other way of identifying the variants (symptoms would be rather similar). I suppose that specialized testing could be done a subset of the “positive” Covid cases, but that is still likely to be a lot of expensive testing that many organizations would be reluctant to perform.

    So, any insight as to how these numbers are created, and how valid they are would be helpful. I’m not to the point of not believing the official numbers, but it seems to me that it would be terribly easy to fudge them rather a lot to support an official narrative.

  • Al Chemy says:

    Some interesting observations about the current U.S. COVID-19 vaccination strategy.

    Is Israel the canary in the coal mine?

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