Canada Covid Positivity Metric July 30

The map shows that in Canada 8929 deaths have been attributed to Covid19, meaning people who died having tested positive for SARS CV2 virus.  This number accumulated over a period of 182 days starting January 31. The daily death rate reached a peak of 177 on May 6, 2020, and is down to 7 as of yesterday.  More details on this below, but first the summary picture. (Note: 2019 is the latest demographic report)

Canada Pop Ann Deaths Daily Deaths Risk per
Person
2019 37589262 330786 906 0.8800%
Covid 2020 37589262 8929 49 0.0238%

Over the epidemic months, the average Covid daily death rate amounted to 5% of the All Causes death rate. During this time a Canadian had an average risk of 1 in 5000 of dying with SARS CV2 versus a 1 in 114 chance of dying regardless of that infection. As shown in a previous post, the risk varied greatly with age, much lower for younger, healthier people.

The Key Covid Metric

With easing of lockdowns and increased testing in many places, epidemiologists are focusing on a key metric to inform public policies: Positivity. The positivity metric is the rate (%) of people who test positive out all people sampled. The significance is that (by definition) a presumed case is a person who tests positive once. If a second test comes back positive it is a confirmed case. The metric is not perfect for two reasons.

The first problem is false positives from the testing procedure itself or from errors in the data processing and reporting. For this we have to hope that quality assurance protocols are being followed and mistakes corrected along the way.

The larger issue appeared in Florida recently when officials discovered that numerous batches of samples were reported 100% positive and other batches 100% negative. While the latter result is expected sometimes, all people testing positive seems unlikely. Behind this is the reality that in many situations (eg hospital ICU) a single patient will be tested many times with many positive results in the course of monitoring that individual’s clearing of the virus. Obviously a batch of samples from that ICU might legitimately be 100% positive.

But it is also true that 10 or 20 positive tests from one patient should not be reported as 10 or 20 new cases. In some jurisdictions, officials say they go to the effort to link test results to the individuals tested, and can distinguish between number of cases and number of positives. In other places, cases and positives may be the same number. Thus confirmed cases could be only 1/2 of the total positives, or less.

How is Canada Doing?

Because of some irregularities in national data reporting, this update is based on Ontario and Quebec statistics combined.  Together the two provinces account for 72% of national testing, 85% of cases and 95% of deaths after testing positive for Covid19.  Like many places, the Canadian contagion is not a pandemic, but rather a few hot spots within a largely untouched geography,  This post is reporting the two central provinces as representing the Canadian epidemic.  Quebec data is here: https://www.inspq.qc.ca/covid-19/donnees.  Ontario data is here: https://covid-19.ontario.ca/data.

The line shows the Positivity metric for Canada starting at nearly 10% for new cases April 22, 2020.  That is, for the 7 day period ending April 22, there were a daily average of 13225 tests and 1283 new cases reported. Since then the rate of new cases has dropped down, now holding steady at ~1% for the last month. Yesterday, the daily average number of tests was 35,747 with 274 new cases. So despite 2.7 times the testing, the positivity rate is not climbing.

Another view of the data (all Canadian provinces) is shown below.

Note that increased testing has led to a slight bump in new cases, but the positivity rate is little changed.  Meanwhile, the death rate has continued to decline from a high of 177 on May 6 down to 7 deaths presently.

Meanwhile the national messaging focuses on rising cumulative case totals, ignoring evidence the contagion is winding down.

Canada Mask2

My bad. That is the Health Minister of PEI solemnly announcing in July their first Covid case in two months.

Background at previous post Canada Succeeds on Key Covid Metric

SARS Cross-Immunity from T-cells

The functions of helper T cells in increasing immune activity (A) and killer T cells in killing virus-infected cells (B).

The breaking news is in an accelerated preview article at Nature SARS-CoV-2-reactive T cells in healthy donors and patients with COVID-19. Excerpts in italics with my bolds.

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused the rapidly unfolding coronavirus disease 2019 (COVID-19) pandemic1,2 . Clinical manifestations of COVID-19 vary, ranging from asymptomatic infection to respiratory failure. The mechanisms determining such variable outcomes remain unresolved. Here, we investigated SARS-CoV-2 spike glycoprotein (S)-reactive CD4+  T cells in peripheral blood of patients with COVID-19 and SARS-CoV-2-unexposed healthy donors (HD). We detected SARS-CoV-2 S-reactive CD4+ T cells in 83% of patients with COVID-19 but also in 35% of HD. S-reactive CD4+ T cells in HD reacted primarily to C-terminal S epitopes, which show a higher homology to spike glycoproteins of human endemic coronaviruses, compared to N-terminal epitopes. S-reactive T cell lines generated from SARS-CoV-2-naive HD responded similarly to C-terminal S of human endemic coronaviruses 229E and OC43 and SARS-CoV-2, demonstrating the presence of S-cross-reactive T cells, probably generated during past encounters with endemic coronaviruses. The role of pre-existing SARS-CoV-2 cross-reactive T cells for clinical outcomes remains to be determined in larger cohorts. However, the presence of S-cross-reactive T cells in a sizable fraction of the general population may affect the dynamics of the current pandemic, and has important implications for the design and analysis of upcoming COVID-19 vaccine trials.

Discussion

Our study demonstrates the presence of S-reactive CD4+ T cells in COVID-19 patients, and in a considerable proportion of SARS-CoV-2  unexposed HD. In light of the recent emergence of SARS-CoV-2, our data raise the intriguing possibility that such pre-existing S-reactive T cells represent cross-reactive clones, probably acquired in previous infections with endemic HCoVs. HCoVs account for approximately 20% of “common cold” upper respiratory tract infections, are ubiquitous, but display a winter seasonality30–32. Based on epidemiological data, it may be extrapolated that adults contract an HCoV infection on average every two to three years. Protective antibodies may wane mid-term but cellular immunity could remain13,33. Although the overall amino acid sequence homology of S is relatively low compared to spike glycoproteins of HCoVs, there is an overlap of MHC-II epitopes especially in the C-terminal domain of the here used peptide pools (Fig. 1a, Extended Data Fig. 1). This may explain the preferential reactivity of CD4+ T cells to the C-terminal domain in one third of HD.

The biological role of pre-existing S-cross-reactive CD4+ T cells in 35% of HD remains unclear for now. However, assuming that these cells have a protective role in SARS-CoV-2 infection, they may contribute to understanding the divergent manifestations of COVID-19, and the striking resilience of children and young adults to symptomatic SARS-CoV-2 infection.  Especially children in day care centers but also young adults have more frequent social contacts than elderly, and thus may have a higher HCoV prevalence. This hypothesis requires further investigation in future longitudinal studies assessing the presence of pre-existing SARS-CoV-2-cross-reactive CD4+ T cells and their impact on the susceptibility to SARS-CoV-2 infection and age-related clinical outcomes of COVID-19.

SARS-CoV neutralizing antibodies are associated with convalescence, and they have been detected 12 months after disease9 . However, the durability of neutralizing antibody responses against SARS-CoV-2 remains unknown. Although antibodies against HCoV can wane within months after infection, HCoV re-infection is accompanied by low-level and short-lived virus shedding with only mild symptoms of short duration pointing towards humoral-independent residual immunity10. Cellular immunity has not yet been studied in this context. In mouse models, however, CD4+ as well as CD8+ T cell responses directed against structural proteins such as spike or nucleocapsid protein of SARS-CoV critically contributed to viral clearance15,34,35. Understanding the extent to which and how SARS-CoV-2-specific humoral or cellular immunity mediates durable protection against reinfection is of critical importance in the coming months.

Our study reveals pre-existing cellular SARS-CoV-2-cross-reactivity in a substantial proportion of SARS-CoV-2 seronegative HD. This finding might have significant epidemiological implications regarding herd immunity thresholds and projections for the COVID-19 pandemic. Our results provide a decisive rationale to initiate worldwide prospective studies to assess the contribution of pre-existing, potentially region-dependent SARS-CoV-2-cross-reactive immunity to the diverse clinical outcomes of SARS-CoV-2 infections. Together with currently introduced novel serological tests, the data generated by such studies may critically inform evidence-based risk evaluation, patient monitoring, adaptation of containment methods, and last but not least, vaccine development.

Don’t Fence Me In!

Implications of This Research are explained in a previous post Herd Immunity Already?

Professor Sunetra Gupta provides a wise, wholistic perspective on the pandemic in her interview published at Reason We may already have herd immunity.  Excerpts in italics with my bolds. H/T Paul Yowell.

I particularly appreciate her sense of the complexity of multiple factors and values, and humility in the challenge of getting the balance right.  This contrasts with so many narrow and overly confident technical pronouncements we read and hear in the media.

Are we already immune to coronavirus? Professor Sunetra Gupta, a theoretical epidemiologist at Oxford University, discusses her recent study on the herd immunity threshold, as well as her views on the social costs of lockdown, the inaccuracy of epidemiological models, and the curtailment of academic debate.

A study produced by a team at Oxford University indicated that some parts of the United Kingdom may already have reached herd immunity from coronavirus. A significant fraction of the population, according to the study published last week, may have “innate resistance or cross-protection from exposure to seasonal coronaviruses”, making the proportion vulnerable to coronavirus infection much smaller than previously thought.

The Oxford team is led by Sunetra Gupta, a professor of theoretical epidemiology. In recent months, she has argued that the cost of lockdown will be too high for the poorest in society and questioned the language and quality of debate on the pandemic’s impact.

Reaction interviewed Professor Gupta about these matters and more, with questions from Maggie Pagano, Alastair Benn and Mutaz Ahmed.

Cross-immunity Matters

Yes, exactly. The principle of protection from exposure to related viruses, and indeed any kind of pathogen, is one that we’ve known for a very long time. The very first vaccine we had, which is smallpox, was based on the idea that cowpox protects against smallpox. This idea was already there well in advance of us knowing that smallpox was a virus – and indeed in advance of germ theory having been properly established. So we knew about this cross protection even before we knew that diseases were caused by germs. It’s a very old idea.

In my own studies, beginning with malaria and then later thinking about flu, the role of cross-immunity in protecting against disease seemed to be something that very much needed to be factored into our thinking. Most of the people who die from malaria are children, and they die upon their first exposure, because they have no immunity at that stage. That was one of the first things that struck me when I was working on malaria.

And then later when I was working on flu, it seemed to me a very good way of explaining why the 1918 flu had killed so many people, but why that didn’t seem to be repeating itself, was that it was likely that people hadn’t been exposed to flu. Many people would have not had the flu at all. So then that built up this population of naive immunity in people under the age of thirty who were very badly affected when the pandemic came through.

Having those ideas in mind, when the Covid-19 virus started to spread, I was pretty certain it wouldn’t have a huge, devastating impact in terms of mortality, because we had all these other coronaviruses circulating.

What I didn’t anticipate was that some of our responses to previous exposure to seasonal coronaviruses might actually protect us from infection. It’s one thing to get infected and not ill, but what the new studies are showing is that people are actually fighting off infection. So at an even more basic level, the pre-existing antibodies or T-cell responses against coronaviruses seem to protect against infection, not just the outcome of infection.

Low Seroprevalence May be a Good Thing

What we know is that the seropositivity rates in many parts of the world are much lower than we’d expect them to be if we assume that the epidemic has passed through and that people are resistant. If you take a very simple scenario where everyone is susceptible, you’d expect 60-70% of them to have some marker of exposure. And that is not what’s been observed.

One of the things that’s been done in reporting the seroprevalence, which is not correct, is that they’ve been homogenised. When people say only 5-6% of the UK population has been exposed, that’s not correct. I think very few people would agree that exposure rates in London are less than 20%.

The picture that we’re getting is heterogeneous. But even in hotspots, apart from a few reports, they’re still quite low. So why is that?

One reason might be that lockdown stopped the spread of infection, so it was halted at a stage when, say, 20% of people were immune and the rest of the people were still susceptible to infection. Well, under those circumstances, the easing of lockdown should result in fairly rapid growth of cases. And that’s not something we’re seeing.

So we’ve got those two bits of information. The third bit, the missing piece of the puzzle, is this idea that some people are fully resistant to infection, because they just have really good defences. That could just be part of our innate immunological makeup. It’s also becoming clear that some of the people that have beaten it off have had responses to other coronaviruses which could have played a role.

The other bit of the puzzle is that some people do get infected and they make antibody responses, but those responses die very quickly. So if you’re trying to measure exposure, you won’t get the full picture. Some of the measures of seroprevalence might be underestimates.

We’ve got four pieces of the puzzle, then. If we put them all together, which is what the paper that we published on Friday does, it gives you a theoretical framework that you can use to look at how these bits connect up together.

You can see two things. You can see why the seroprevalence level might be low, and you can also infer that the level of herd immunity needed to stop the thing from exploding again is actually much lower than the figures that are currently being thrown around quite incautiously might suggest.

The fifth piece of this jigsaw could be that there is some seasonality. I suspect that in the winter it will probably come back, but hopefully only to the regions where it was kept from going by lockdown, and where the seroprevalence levels are genuinely extremely low.

We can be cautiously hopeful that in areas where the seroprevalence levels have achieved a certain value that’s compatible with there being a proportion who are resistant, that it might not come back with such vehemence.

Quality of Life Matters

What’s disappointed me about the way this has been approached is it has been approached along a single axis, which, if you like, is a scientific one. Even within that context, you could argue that it’s too one-dimensional, so we’re not thinking about what’s happening with other infectious diseases or how many people are going to die of cancer.

That’s the axis of disease, but then there’s the socioeconomic axis, which has been ignored. But there’s a third, aesthetic access, which is about how we want to live our lives. We are closing ourselves off not just to the disease, but to other aspects of being human.

I think the trade-off is very extreme. Obviously the most extreme manifestation of that trade-off is the 23 million people who will be pushed below the poverty line as a result of this sledgehammer approach. The costs to the arts is I think also incredibly profound – the theatres and all other forms of performing art. But also the inherent art of living, which I think is being compromised.

Acts of kindness are being eschewed. Someone was telling me yesterday that their mother said to them “please don’t come home, you’re going to kill us”.

Carrying On with Living is Social Responsibility

Because actually, the only way we can reduce the risk to the vulnerable people in the population is, for those of us who are able to acquire herd immunity, to do that.

Even if there is a little bit of a risk. I’m 55 years old, there’s some slight risk out there. But I would be willing to take that, just as I do with the flu. There’s a risk I might die of flu, but I’m willing to take that risk, because I know that if I don’t then flu will appear as it did before, it will enter the population of immunologically naive individuals, and then there will be a high risk of infection which will have a disproportionate effect on the vulnerable sector of the population.

Maybe the way to counter it now is to say, actually, not only is it a good thing for young people to go out there and become immune, but that is almost their duty. It’s a way of living with this virus. It’s how we live with other viruses. Flu is clearly a very dangerous virus, but the reason we don’t see more deaths from flu every year is because, through herd immunity, the levels of infection are kept to as low a level as we can get.

The truth is that herd immunity is a way of preventing vulnerable people from dying. It is achieved at the expense of some people dying, and we can stop that by preventing the vulnerable class in the process. In an ideal situation, you would protect the vulnerable as best you can, let people go about their business, allow herd immunity to build up, make sure the economy doesn’t crash, make sure the arts are preserved, and make sure qualities of kindness and tolerance remain in place.

We live, it seems, in this state of terror. Yes, international travel facilitates the entrance of contagion, but what it also does is it brings immunity.

Good Thing It’s Not Our First Coronavirus

If coronavirus had arrived in a setting where we had no coronavirus exposure before, we might be much worse off. It also seems that in addition to protection against severe disease as a result of exposure to related coronaviruses, some fraction of us seem to be resistant to infection.

That’s just fantastic news, actually. Hopefully that will be consolidated at a scientific, laboratory level. We ourselves are looking at how antibodies to seasonal coronaviruses can impact on protection against infection and disease.

Maybe we will be able to build up a picture that will reassure the public that actually we are much better off having been exposed to related coronaviruses. We are in a better place to fight off this infection than we actually thought.

The paper is The impact of host resistance on cumulative mortality and the threshold of herd immunity for SARS-CoV-2

Abstract
It is widely believed that the herd immunity threshold (HIT) required to prevent a resurgence of SARS-CoV-2 is in excess of 50% for any epidemiological setting. Here, we demonstrate that HIT may be greatly reduced if a fraction of the population is unable to transmit the virus due to innate resistance or cross-protection from exposure to seasonal coronaviruses. The drop in HIT is proportional to the fraction of the population resistant only when that fraction is effectively segregated from the general population; however, when mixing is random, the drop in HIT is more precipitous. Significant reductions in expected mortality can also be observed in settings where a fraction of the population is resistant to infection. These results help to explain the large degree of regional variation observed in seroprevalence and cumulative deaths and suggest that sufficient herd-immunity may already be in place to substantially mitigate a potential second wave.

 

 

HCQ Works. She Knows and Won’t Shut Up

https://www.bitchute.com/embed/ukmtlokiGHRr/

H/T Palmer Foundation (here) for transcript synopsis, printed in italics with my bolds.

A Nigerian-born and trained physician, Dr Stella Immanuel, is trending on social media after delivering an impassioned COVID-19 speech in the U.S.

That was until U.S. President Trump retweeted it. Now the video is being removed from all over the internet. Facebook has gone so far as to completely remove her account.

Speaking at a news conference in Washington, Immanuel claimed that antimalarial drug, hydroxychloroquine, zinc, and antibacterial drug, Zithromax, were effective cures for the virus.

She said she had successfully treated no fewer than 350 patients with hydroxychloroquine, zinc, and Zithromax.

The following are excerpts of Immanuel’s speech:

“Hello, I’m Dr Stella Emmanuel. I’m a primary care physician in Houston, Texas.

“I went to medical school in West Africa, Nigeria, where I took care of malaria patients, treated them with hydroxychloroquine and stuff like that.

“So I’m used to these medications. I’m here because I have personally treated over 350 patients with COVID-19. Patients that have diabetes, patients that have high blood pressure, patients that have asthma, old people … I think my oldest patients are 92 … 87-year-olds.

“And the result has been the same. I put them on hydroxychloroquine, I put them on zinc, I put them on Zithromax, and they’re all well. For the past few months, after taking care of over 350 patients, we’ve not lost one. Not a diabetic, not a somebody with high blood pressure, not somebody who asthma, not an old person.

“We’ve not lost one patient. And on top of that, I’ve put myself, my staff, and many doctors that I know on hydroxychloroquine for prevention because by the very mechanism of action, it works early and as a prophylaxis.

“The study that made me start using hydroxychloroquine was a study that they did under the NIH in 2005 that says it works.

“I know you’re going to tell me that you treated 20 people, 40 people, and it didn’t work. I’m a true testimony. So I came here to Washington DC to tell America nobody needs to get sick.

“This virus has a cure. It is called hydroxychloroquine, zinc, and Zithromax. I know you people want to talk about a mask. Hello? You don’t need a mask. There is a cure.

“I tell all of you doctors that are sitting down and watching Americans die. You’re like the good Nazi … the good one, the good Germans that watched Jews get killed and you did not speak up.

“If they come after me, they threaten me. They’ve threatened to … I mean, I’ve gotten all kinds of threats. Or they’re going to report me to the bots.

“I say, you know what? I don’t care. I’m not going to let Americans die. And if this is the hill where I get nailed on, I will get nailed on it. I don’t care.

“And today I’m here to say it, that America, there is a cure for COVID-19. All this foolishness does not need to happen. There is a cure for COVID-19.

My Comment:

Dr. Immanuel is not alone, and was speaking along with a group of frontline doctors who have had similar experience as Covid caregivers.  There are those already dismissive of HCQ treatments, unless and until there is incontrovertible double blind large scale trials.  In fact the bad press exaggerating HCQ risk factors makes recruiting trial volunteers nearly impossible, and maybe that was the intention. Of course also being an evangelical preacher is an easy target for cancellation, despite her being an outspoken black woman.

One negative reaction came from Nigeria, Dr Stella’s COVID-19 treatment claim unproven, mere speculation, medical directors insist.

Abuja, July 28, 2020 The Guild of Medical Directors (GMD) has reacted to video claims by Dr Stella Immanuel, a General Practitioner (GP) in the U.S. that she has treated over 350 patients of COVID-19 with combination of Hydrochloroquine (HCQ), Zinc and Zithromax, saying it is her own personal, unsubstantiated claim.

In a statement seen by Naija247news from the President of GMD, Prof. Olufemi Babalola in Abuja on Tuesday, the doctors said “there is no scientific evidence to prove the claim.”

The guild president noted that while some studies suggested that it was effective, others felt otherwise.

He added that “it is true that Senegal, where HCQ is routinely used, has one of the lowest COVID-19 case fatality rates in the world at 0.64 per cent compared to 3.4 per cent in the U.S.

“As we speak, a study is underway at Lagos University Teaching Hospital (LUTH) on its efficacy and safety. Subsequently, a meta-analysis of all these studies should be undertaken to pool all the results and come up with analysis which will guide clinicians.

“So, until then, all anecdotal claims such as the one from Dr Stella Immanuel must be taken with a pinch of salt.”

[Meta analyses have been published and are ongoing.  See HCQ Proven First Responder to SARS CV2]

[Others in Nigeria are not so dismissive: NEWSCOVID-19: Nigeria takes delivery of 7-tons of hydroxychloroquine from India]

The observation about Senegal also shows why the HCQ treatment is worth pursuing.

Consider this chart produced in early June.

Now that is only suggestive, not proven association because inter-country comparisons have many complicating factors, and case fatalities change over time and with greater data collected. Still, it indicated that places that use HCQ routinely appeared to have lower lethality compared, for example, to Europe which mostly followed WHO’s position discouraging HCQ.  Other national experiences are compelling:

Algeria – Started using Chloroquine in late March. Results came very soon

According to one infectious disease specialist, “near-total effectiveness.”

Morocco – Also started treating in late March

Again, almost immediate results

Fun fact: more people have died of COVID in the Moroccan diaspora than in Morocco! Think about that for a second…

Conclusion:

Yes, they will go after Dr. Immanuel and cancel her if possible.  But this is much bigger than her.

For more charts and discussion of HCQ and Covid19 see My Hydroxychloroquine Deep Dive

 

 

 

 

 

Florida Covid Facts Missing in the Media

Issues and Insights editorial board exposes the media disinformation in an article Florida Is A Case Study In Media-Induced COVID-19 Panic.  Excerpts in italics with my bolds.

What do all these news accounts have in common?

“Florida Sets Yet Another Coronavirus Record: 173 Deaths In A Day.”

“A record 173 Floridians died from the virus Thursday, an average of more than one every eight minutes.”

“The 134 new confirmed deaths is the second-largest increase on record, coming five days after the largest one-day jump of 156 last week.”

“COVID-19 has ravaged Florida, with more than 237,000 people testing positive and 2,013 dying from the virus in July alone.”

So what characteristic do all of the reports share? They are all false.

It is not true that 173 people died from COVID-19 “in a day” in Florida. Nor did 134, or 156 on previous days.

It is also untrue than 2,013 had died in July when that story was published.

All of these scary headlines are based on the number of deaths reported by the state on any given day. This is not the same as the number of deaths that occurred on those days.

The difference might seem trivial. But it’s crucial because the press is using the timing of Florida’s death reports to whip up a frenzy about COVID-19 running riot in the state.

Take a look at the chart below. The blue bars are the number of deaths reported in four days last week. Notice the sharp uphill climb? That’s the story the press has been telling.

But those deaths didn’t occur on those days. In fact, the vast majority of them occurred days, or even weeks, before. The actual date of these deaths is indicated by the orange bars.

In fact, as of Sunday, the biggest one-day death toll so far in the state happened back on July 16, when 114 are known to have died. And when the press was claiming that 2,013 had died in July, the actual number of known deaths was 1,847.

As we noted in this space last week, this distortion is being repeated by the media in state after state that has seen a recent spike in coronavirus cases. While deaths attributed to coronavirus have increased, the “surge” is a fiction because many of those deaths happened earlier.

This is only one of the problems with the death counts being shouted from the media rooftops.

Here again, Florida serves as a model of how to sow fear.

First there’s the missing context.

Another way to look at it is that the death rate in Florida at the moment is 273 per million residents. In New York, it’s 1,680 and in New Jersey it’s 1,785.

In other words, the current situation in Florida is nothing at all like what happened in the northeast in the spring. Yet that critical information never gets conveyed by the press.

Another bit of missing context is where these deaths are occurring.

Of the more than 5,000 coronavirus deaths in Florida, 45% of them involved residents and staff at long-term care facilities.

That’s not to say these deaths are less important. But it does provide a needed backdrop for everyone else in the state. Their risk is tiny by comparison.

This finding also shows that what’s needed most is to protect at-risk populations, something that the generalized lockdowns failed to do. Pretending that coronavirus “doesn’t discriminate” is a dangerous fiction.

Then there’s the fact that Florida’s death count is almost certainly inflated because the state is counting people who died with the virus, not just those who died because of it.

A report by CBS-12 in West Palm Beach, for example, found that the state has counted as coronavirus deaths:

    • A 60-year-old man who died from a gunshot wound to the head.
    • A 90-year-old man who fell and died from complications of a hip fracture.
    • A 77-year-old woman who died of Parkinson’s disease.

Out of 581 deaths attributed to coronavirus in that county, “The I-Team found eight cases in which a person was counted as a COVID death, but did not have COVID listed as a contributing cause of death.”

What’s more, only 169 deaths were listed as due to coronavirus without any other contributing factors.

(As a side note, why is a local TV news team digging into the numbers, while the national media are content to repeat whatever the government tells them?)

As we’ve said before, this sort of overcounting is going on nationwide, largely because the CDC has told states to report deaths this way.

The question that deserves to be answered is why the mainstream press seems so willing and eager to whip up fear, rather than provide all the relevant facts, in context, so the public can make its own informed decisions about how to respond to this disease.

 

 

Siberian Arctic Ice Melt July 2020

The image above shows melting of Arctic sea ice extent over the last 20 days, July 5 to 25, 2020.  At the bottom right, the shallow Hudson Bay goes to water rapidly, losing 500k km2 of ice.  Even so, at 172k km2 that region is nearly average.  The remarkable 2020 event is the effect of high Siberian temperatures causing extensive melting of the nearby shelf seas, seen on the left vertical. Already on July 5, Laptev was mostly water, and now has only 5% ice. Neighboring seas East Siberian and Kara also melted rapidly. The other feature is Baffin Bay, center right, losing 300k km2 to retain only 7% of its maximum ice extent.

The graph below shows the ice extent retreating during July compared to some other years and the 13 year average (2007 to 2019 inclusive).

Note that the  MASIE NH ice extent 13 year average loses about 2.6M km2 during July, down to 7M km2. MASIE 2020 started nearly 500k km2 lower and lost ice at a higher rate, now 1.1M km2 below average.  Both MASIE and SII show this year below other recent years, reaching the present ice extent 7 days ahead of 2019 and 14 days ahead of average.

The table shows where the ice is distributed compared to average.  Bering and Okhotsk are open water at this point no longer shown in these updates. The deficit of 1.1M km2 represents 15% of the total, or an ice extent melting 14 days ahead of average.

Region 2020207 Day 207 Average 2020-Ave. 2007207 2020-2007
 (0) Northern_Hemisphere 6350401 7453623  -1103222  7011118 -660717 
 (1) Beaufort_Sea 892059 794821  97238  748948 143111 
 (2) Chukchi_Sea 542328 559045  -16717  440010 102318 
 (3) East_Siberian_Sea 460336 853373  -393037  647006 -186670 
 (4) Laptev_Sea 50561 485152  -434591  389317 -338756 
 (5) Kara_Sea 122978 215126  -92147  265137 -142159 
 (6) Barents_Sea 33044 37953  -4910  38346 -5302 
 (7) Greenland_Sea 342772 335165  7607  353806 -11034 
 (8) Baffin_Bay_Gulf_of_St._Lawrence 115572 198402  -82831  231942 -116371 
 (9) Canadian_Archipelago 570728 614794  -44067  595262 -24534 
 (10) Hudson_Bay 172014 203861  -31847  114225 57789 
 (11) Central_Arctic 3047196 3154007  -106811  3185794 -138598 

Note that all of the deficit to average is accounted for by the Russian shelf seas of East Siberian, Laptev and Kara, along with Baffin Bay

Illustration by Eleanor Lutz shows Earth’s seasonal climate changes. If played in full screen, the four corners present views from top, bottom and sides. It is a visual representation of scientific datasets measuring Arctic ice extents.

Best Climate Model: Mild Warming Forecasted

Links are provided at the end to previous posts describing climate models 4 and 5 from the Institute of Numerical Mathematics in Moscow, Russia.  Now we have forecasts for the 21st Century published for INM-CM5 at Izvestiya, Atmospheric and Oceanic Physics volume 56, pages218–228(July 7, 2020). The article is Simulation of Possible Future Climate Changes in the 21st Century in the INM-CM5 Climate Model by E. M. Volodin & A. S. Gritsun.  Excerpts are in italics with my bolds, along with a contextual comment.

Abstract

Climate changes in 2015–2100 have been simulated with the use of the INM-CM5 climate model following four scenarios: SSP1-2.6, SSP2-4.5, and SSP5-8.5 (single model runs) and SSP3-7.0 (an ensemble of five model runs). Changes in the global mean temperature and spatial distribution of temperature and precipitation are analyzed. The global warming predicted by the INM-CM5 model in the scenarios considered is smaller than that in other CMIP6 models. It is shown that the temperature in the hottest summer month can rise more quickly than the seasonal mean temperature in Russia. An analysis of a change in Arctic sea ice shows no complete Arctic summer ice melting in the 21st century under any model scenario. Changes in the meridional stream function in atmosphere and ocean are studied.

Overview

The climate is understood as the totality of statistical characteristics of the instantaneous states of the atmosphere, ocean, and other climate system components averaged over a long time period.

Therefore, we restrict ourselves to an analysis of some of the most important climate parameters, such as average temperature and precipitation. A more detailed analysis of individual aspects of climate change, such as changes in extreme weather and climate situations, will be the subject of another work. This study is not aimed at a full comparison with the results of other climate models, where calculations follow the same scenarios, since the results of other models have not yet been published in peer reviewed journals by the time of this writing.

The INM-CM5 climate model [1, 2] is used for the numerical experiments. It differs from the previous version, INMCM4, which was also used for experiments on reproducing climate change in the 21st century [3], in the following:

  • an aerosol block has been added to the model, which allows inputting anthropogenic emissions of aerosols and their precursors;
  • the concentrations and optical properties of aerosols are calculated, but not specified, like in the previous version;
  • the parametrizations of cloud formation and condensation are changed in the atmospheric block;
  • the upper boundary in the atmospheric block is raised from 30 to 60 km;
  • the horizontal resolution in the ocean block is doubled along each coordinate; and,
  • the software related to adaptation to massively parallel computers is improved, which allows the effective use a larger number of compute cores.

The model resolution in the atmospheric and aerosol blocks is 2° × 1.5° in longitude and latitude and 73 levels and, in the ocean, 0.5° × 0.25° and 40 levels. The calculations were performed at supercomputers of the Joint Supercomputer Center, Russian Academy of Sciences, and Moscow State University, with the use of 360 to 720 cores. The model calculated 6–10 years per 24 h in the above configuration.

Four scenarios were used to model the future climate: SSP1-2.6, SSP2-4.5, SSP3-7.0, and SSP5-5.8. The scenarios are described in [4]. The figure after the abbreviation SSP (Shared Socioeconomic Pathway) is the number of the mankind development path (see the values in [4]). The number after the dash means the radiation forcing (W m–2) in 2100 compared to the preindustrial level. Thus, the SSP1-2.6 scenario is the most moderate and assumes rapid actions which sharply limit and then almost completely stop anthropogenic emissions. Within this scenario, greenhouse gas concentrations are maximal in the middle of the 21st century and then slightly decrease by the end of the century. The SSP5-8.5 scenario is the warmest and implies the fastest climate change. The scenarios are recommended for use in the project on comparing CMIP6 (Coupled Model Intercomparison Project, Phase 6, [5]) climate models.  Each scenario includes the time series of:

  • carbon dioxide, methane, nitrous oxide, and ozone concentrations;
  • emissions of anthropogenic aerosols and their precursors;
  • the concentration of volcanic sulfate aerosol; and
  • the solar constant. 

One model experiment was carried out for each of the above scenarios. It began at the beginning of 2015 and ended at the end of 2100. The initial state was taken from the so-called historical experiment with the same model, where climate changes were simulated for 1850–2014, and all impacts on the climate system were set according to observations. The results of the ensemble of historical experiments with the model under consideration are given in [6, 7]. For the SSP3-7.0 scenario, five model runs was performed differing in the initial data taken from different historical experiments. The ensemble of numerical experiments is required to increase the statistical confidence of conclusions about climate changes.

[My Contextual Comment inserted Prior to Consideration of Results]

Firstly, the INM-CM5 historical experiment can be read in detail by following a linked post below, but this graphic summarizes the model hindcasting of past temperatures (GMT) compared to HadCrutv4.

Figure 1. The 5-year mean GMST (K) anomaly with respect to 1850–1899 for HadCRUTv4 (thick solid black); model mean (thick solid red). Dashed thin lines represent data from individual model runs: 1 – purple, 2 – dark blue, 3 – blue, 4 – green, 5 – yellow, 6 – orange, 7 – magenta. In this and the next figures numbers on the time axis indicate the first year of the 5-year mean.

Secondly, the scenarios are important to understand since they stipulate data inputs the model must accept as conditions for producing forecasts according to a particular scenario (set of assumptions).  The document with complete details referenced as [4] is The Scenario Model Intercomparison Project (ScenarioMIP) for CMIP6.

All the details are written there but one diagram suggests the implications for the results described below.

Figure 5. CO2 emissions (a) and concentrations (b), anthropogenic radiative forcing (c), and global mean temperature change (d) for the three long-term extensions. As in Fig. 3, concentration, forcing, and temperature outcomes are calculated with a simple climate model (MAGICC version 6.8.01 BETA; Meinshausen et al., 2011a, b). Outcomes for the CMIP5 versions of the long-term extensions of RCP2.6 and RCP8.5 (Meinshausen et al., 2011c), as calculated with the same model, are shown for comparison.

As shown, the SSP1-26 is virtually the same scenario as the former RCP2.6, while SSP5-85 is virtually the same as RCP8.5, the wildly improbable scenario (impossible according to some analysts).  Note that FF CO2 emissions are assumed to quadruple in the next 80 years, with atmospheric CO2 rising from 400 to 1000 ppm ( +150%).  Bear these suppositions in mind when considering the INMCM5 forecasts below.

Results [Continuing From Volodin and Gritsun]

Fig. 1. Changes in the global average surface temperature (K) with respect to the pre-industrial level in experiments according to the SSP1-2.6 (triangles), SSP2-4.5 (squares), SSP3-7.0 (crosses), and SSP5-8.5 (circles) scenarios.

Let us describe some simulation results of climate change in the 21st century. Figure 1 shows the change in the globally averaged surface air temperature with respect to the data of the corresponding historical experiment for 1850–1899. In the warmest SSP5-8.5 scenario, the temperature rises by more than 4° by the end of the 21st century. In the SSP3-7.0 scenario, different members of the ensemble show warming by 3.4°–3.6°. In the SSP2-4.5 scenario, the temperature increases by about 2.4°. According to the SSP1-2.6 scenario, the maximal warming by ~1.7° occurs in the middle of the 21st century, and the temperature exceeds the preindustrial temperature by 1.4° by the end of the century.

[My comment: Note that the vertical scale starts with +1.0C ( not 1.3) as can be seen in the historical experiment. Thus an anomaly of 1.4C by 2100 is an increase of only 0.4C, while the SSP2-4.5 result adds 1.4C to the present].

The results for other CMIP6 models have not yet been published in peer-reviewed journals. However, according to the preliminary analysis (see, e.g.  https://cmip6workshop19.sciencesconf.org/ data/Session1_PosterSlides.pdf, p.29), the INM-CM5 model shows the lowest temperature increase among the CMIP6 models considered for all the scenarios due to the minimal equilibrium sensitivity to the CO2 concentration doubling, which is ~2.1° for the current model version, like for the previous version, despite new condensation and cloud formation blocks. [For more on CMIP6 comparisons see post Climate Models: Good, Bad and Ugly]

Fig. 2. Differences between the annual average surface air temperatures (K) in 2071–2100 and 1981–2010 for the (a) SSP5-8.5 and (b) SSP1-2.6 scenarios.

The changes in the surface air temperature are similar for all scenarios; therefore, we analyze the difference between temperatures in 2071–2100 and 1981–2010 under the SSP5-8.5 and SSP1-2.6 scenarios (Fig. 2). The warming is maximal in the Arctic; it reaches 10° and 3°, respectively. Other features mainly correspond to CMIP5 data [8], including the INMCM4 model, which participates in the comparison. The warming on the continents of the Northern Hemisphere is about 2 times higher than the mean, and the warming in the Southern Hemisphere is noticeably less than in the Northern Hemisphere. The land surface is getting warmer than the ocean surface in all the scenarios except SSP1-2.6, because the greenhouse effect is expected to weaken in the second half of the 21st century in this scenario, and the higher heat capacity of the ocean prevents it from cooling as quickly as the land.

The changes in precipitation in December–February and June–August for the SSP3-7.0 scenario averaged over five members of the ensemble are shown in Fig. 4. All members of the ensemble show an increase in precipitation in the winter in a significant part of middle and high latitudes. In summer, the border between the increase and decrease in precipitation in Eurasia passes mainly around or to the north of 60°. In southern and central Europe, all members of the ensemble show a decrease in precipitation. Precipitation also increases in the region of the summer Asian monsoon, over the equatorial Pacific, due to a decrease in the upwelling and an increase in ocean surface temperature (OST). The distribution of changes in precipitation mainly corresponds to that given in [6, Fig. 12.22] for all CMIP5 models.

The change in the Arctic sea ice area in September, when the ocean ice cover is minimal over the year, is of interest. Figure 5 shows the sea ice area in September 2015–2019 to be 4–6 million km2 in all experiments, which corresponds to the estimate from observations in [11]. The Arctic sea ice does not completely melt in any of the experiments and under any scenario. However, according to [8, Figs. 12.28 and 12.31], many models participating in CMIP6, where the Arctic ice area is similar to that observed at the beginning of the 21st century, show the complete absence of ice by the end of the 21st century, especially under the RCP8.5 scenario, which is similar to SSP5-8.5.

The reason for these differences is the lower equilibrium sensitivity of the INM-CM5 model.

Note that the scatter of data between experiments under different scenarios in the first half of the 21st century is approximately the same as between different members of the ensemble under the SSP3-7.0 scenario and becomes larger only after 2070. The sea ice area values are sorted in accordance with the radiative forcing of the scenarios only after 2090. This indicates the large contribution of natural climate variability into the Arctic ice area. In the SSP1-2.6 experiment, the Arctic ice area at the end of the 21st century approximately corresponds to its area at the beginning of the experiment.

Climate changes can be also traced in the ocean circulation. Figure 6 shows the change in the 5-year averaged intensity of the Atlantic meridional circulation, defined as the maximum of the meridional streamfunction at 32° N. All experiments show a decrease in the intensity of meridional circulation in the 21st century and natural fluctuations against this decrease. The decrease is about 4.5–5 Sv for the SSP5-8.5 scenario, which is close to values obtained in the CMIP5 models [8, Fig. 12.35] under the RCP8.5 scenario. Under milder scenarios, the weakening of the meridional circulation is less pronounced. The reason for this weakening of the meridional circulation in the Atlantic, as far as we know, is not yet fully understood.

Conclusion

Numerical experiments have been carried out to reproduce climate changes in the 21st century according to four scenarios of the CMIP6 program [4, 5], including an ensemble of five experiments under the SSP3-7.0 scenario. The changes in the global mean surface temperature are analyzed. It is shown that the global warming predicted by the INM-CM5 model is the lowest among the currently published CMIP6 model data. The geographical distribution of changes in the temperature and precipitation is considered. According to the model, the temperature in the warmest summer month will increase faster than the summer average temperature in Russia.

None of the experiments show the complete melting of the Arctic ice cover by the end of the 21st century. Some changes in the ocean dynamics, including the flow velocity and the meridional stream function, are analyzed. The changes in the Hadley and Ferrel circulation in the atmosphere are considered.

Resources:

Climate Models: Good, Bad and Ugly

2018 Update: Best Climate Model INMCM5

Temperatures According to Climate Models

Herd Immunity Already?

Don’t Fence Me In!

Professor Sunetra Gupta provides a wise, wholistic perspective on the pandemic in her interview published at Reason We may already have herd immunity.  Excerpts in italics with my bolds. H/T Paul Yowell.

I particularly appreciate her sense of the complexity of multiple factors and values, and humility in the challenge of getting the balance right.  This contrasts with so many narrow and overly confident technical pronouncements we read and hear in the media.

Are we already immune to coronavirus? Professor Sunetra Gupta, a theoretical epidemiologist at Oxford University, discusses her recent study on the herd immunity threshold, as well as her views on the social costs of lockdown, the inaccuracy of epidemiological models, and the curtailment of academic debate.

A study produced by a team at Oxford University indicated that some parts of the United Kingdom may already have reached herd immunity from coronavirus. A significant fraction of the population, according to the study published last week, may have “innate resistance or cross-protection from exposure to seasonal coronaviruses”, making the proportion vulnerable to coronavirus infection much smaller than previously thought.

The Oxford team is led by Sunetra Gupta, a professor of theoretical epidemiology. In recent months, she has argued that the cost of lockdown will be too high for the poorest in society and questioned the language and quality of debate on the pandemic’s impact.

Reaction interviewed Professor Gupta about these matters and more, with questions from Maggie Pagano, Alastair Benn and Mutaz Ahmed.

Cross-immunity Matters

Yes, exactly. The principle of protection from exposure to related viruses, and indeed any kind of pathogen, is one that we’ve known for a very long time. The very first vaccine we had, which is smallpox, was based on the idea that cowpox protects against smallpox. This idea was already there well in advance of us knowing that smallpox was a virus – and indeed in advance of germ theory having been properly established. So we knew about this cross protection even before we knew that diseases were caused by germs. It’s a very old idea.

In my own studies, beginning with malaria and then later thinking about flu, the role of cross-immunity in protecting against disease seemed to be something that very much needed to be factored into our thinking. Most of the people who die from malaria are children, and they die upon their first exposure, because they have no immunity at that stage. That was one of the first things that struck me when I was working on malaria.

And then later when I was working on flu, it seemed to me a very good way of explaining why the 1918 flu had killed so many people, but why that didn’t seem to be repeating itself, was that it was likely that people hadn’t been exposed to flu. Many people would have not had the flu at all. So then that built up this population of naive immunity in people under the age of thirty who were very badly affected when the pandemic came through.

Having those ideas in mind, when the Covid-19 virus started to spread, I was pretty certain it wouldn’t have a huge, devastating impact in terms of mortality, because we had all these other coronaviruses circulating.

What I didn’t anticipate was that some of our responses to previous exposure to seasonal coronaviruses might actually protect us from infection. It’s one thing to get infected and not ill, but what the new studies are showing is that people are actually fighting off infection. So at an even more basic level, the pre-existing antibodies or T-cell responses against coronaviruses seem to protect against infection, not just the outcome of infection.

Low Seroprevalence May be a Good Thing

What we know is that the seropositivity rates in many parts of the world are much lower than we’d expect them to be if we assume that the epidemic has passed through and that people are resistant. If you take a very simple scenario where everyone is susceptible, you’d expect 60-70% of them to have some marker of exposure. And that is not what’s been observed.

One of the things that’s been done in reporting the seroprevalence, which is not correct, is that they’ve been homogenised. When people say only 5-6% of the UK population has been exposed, that’s not correct. I think very few people would agree that exposure rates in London are less than 20%.

The picture that we’re getting is heterogeneous. But even in hotspots, apart from a few reports, they’re still quite low. So why is that?

One reason might be that lockdown stopped the spread of infection, so it was halted at a stage when, say, 20% of people were immune and the rest of the people were still susceptible to infection. Well, under those circumstances, the easing of lockdown should result in fairly rapid growth of cases. And that’s not something we’re seeing.

So we’ve got those two bits of information. The third bit, the missing piece of the puzzle, is this idea that some people are fully resistant to infection, because they just have really good defences. That could just be part of our innate immunological makeup. It’s also becoming clear that some of the people that have beaten it off have had responses to other coronaviruses which could have played a role.

The other bit of the puzzle is that some people do get infected and they make antibody responses, but those responses die very quickly. So if you’re trying to measure exposure, you won’t get the full picture. Some of the measures of seroprevalence might be underestimates.

We’ve got four pieces of the puzzle, then. If we put them all together, which is what the paper that we published on Friday does, it gives you a theoretical framework that you can use to look at how these bits connect up together.

You can see two things. You can see why the seroprevalence level might be low, and you can also infer that the level of herd immunity needed to stop the thing from exploding again is actually much lower than the figures that are currently being thrown around quite incautiously might suggest.

The fifth piece of this jigsaw could be that there is some seasonality. I suspect that in the winter it will probably come back, but hopefully only to the regions where it was kept from going by lockdown, and where the seroprevalence levels are genuinely extremely low.

We can be cautiously hopeful that in areas where the seroprevalence levels have achieved a certain value that’s compatible with there being a proportion who are resistant, that it might not come back with such vehemence.

Quality of Life Matters

What’s disappointed me about the way this has been approached is it has been approached along a single axis, which, if you like, is a scientific one. Even within that context, you could argue that it’s too one-dimensional, so we’re not thinking about what’s happening with other infectious diseases or how many people are going to die of cancer.

That’s the axis of disease, but then there’s the socioeconomic axis, which has been ignored. But there’s a third, aesthetic access, which is about how we want to live our lives. We are closing ourselves off not just to the disease, but to other aspects of being human.

I think the trade-off is very extreme. Obviously the most extreme manifestation of that trade-off is the 23 million people who will be pushed below the poverty line as a result of this sledgehammer approach. The costs to the arts is I think also incredibly profound – the theatres and all other forms of performing art. But also the inherent art of living, which I think is being compromised.

Acts of kindness are being eschewed. Someone was telling me yesterday that their mother said to them “please don’t come home, you’re going to kill us”.

Carrying On with Living is Social Responsibility

Because actually, the only way we can reduce the risk to the vulnerable people in the population is, for those of us who are able to acquire herd immunity, to do that.

Even if there is a little bit of a risk. I’m 55 years old, there’s some slight risk out there. But I would be willing to take that, just as I do with the flu. There’s a risk I might die of flu, but I’m willing to take that risk, because I know that if I don’t then flu will appear as it did before, it will enter the population of immunologically naive individuals, and then there will be a high risk of infection which will have a disproportionate effect on the vulnerable sector of the population.

Maybe the way to counter it now is to say, actually, not only is it a good thing for young people to go out there and become immune, but that is almost their duty. It’s a way of living with this virus. It’s how we live with other viruses. Flu is clearly a very dangerous virus, but the reason we don’t see more deaths from flu every year is because, through herd immunity, the levels of infection are kept to as low a level as we can get.

The truth is that herd immunity is a way of preventing vulnerable people from dying. It is achieved at the expense of some people dying, and we can stop that by preventing the vulnerable class in the process. In an ideal situation, you would protect the vulnerable as best you can, let people go about their business, allow herd immunity to build up, make sure the economy doesn’t crash, make sure the arts are preserved, and make sure qualities of kindness and tolerance remain in place.

We live, it seems, in this state of terror. Yes, international travel facilitates the entrance of contagion, but what it also does is it brings immunity.

Good Thing It’s Not Our First Coronavirus

If coronavirus had arrived in a setting where we had no coronavirus exposure before, we might be much worse off. It also seems that in addition to protection against severe disease as a result of exposure to related coronaviruses, some fraction of us seem to be resistant to infection.

That’s just fantastic news, actually. Hopefully that will be consolidated at a scientific, laboratory level. We ourselves are looking at how antibodies to seasonal coronaviruses can impact on protection against infection and disease.

Maybe we will be able to build up a picture that will reassure the public that actually we are much better off having been exposed to related coronaviruses. We are in a better place to fight off this infection than we actually thought.

The paper is The impact of host resistance on cumulative mortality and the threshold of herd immunity for SARS-CoV-2

Abstract
It is widely believed that the herd immunity threshold (HIT) required to prevent a resurgence of SARS-CoV-2 is in excess of 50% for any epidemiological setting. Here, we demonstrate that HIT may be greatly reduced if a fraction of the population is unable to transmit the virus due to innate resistance or cross-protection from exposure to seasonal coronaviruses. The drop in HIT is proportional to the fraction of the population resistant only when that fraction is effectively segregated from the general population; however, when mixing is random, the drop in HIT is more precipitous. Significant reductions in expected mortality can also be observed in settings where a fraction of the population is resistant to infection. These results help to explain the large degree of regional variation observed in seroprevalence and cumulative deaths and suggest that sufficient herd-immunity may already be in place to substantially mitigate a potential second wave.

 

 

The Victim Song

In the 1990s bluesman R.L. Burnside performed his song composed entirely of words he heard blaming others to avoid looking in the mirror.

R. L. Burnside 1926-2005

Canada Immunity Testing: Antibodies 8 * Cases

The media announcement is New study offers first glimpse into how widespread COVID-19 antibodies are in Canada’s adult population. Published July 23, 2020.

Initial results indicate fewer than 1 in 100 blood donations have antibodies to the novel coronavirus that causes COVID-19.

The header emphasizes how few blood samples showed antibodies, while the more important finding about reduced lethality of Covid19 requires searching in the fine print.

Context

Today, Canadian Blood Services and Canada’s COVID-19 Immunity Task Force (CITF) are releasing initial results of the first 10,000 blood donor samples assessed for SARS-CoV-2 antibodies. This analysis reveals that over the period May 9 through June 8, 2020, fewer than 1 per cent of the 10,000 samples from blood donors tested positive for antibodies to the novel coronavirus. Antibodies indicate past infection with SARS-CoV-2, and population studies like this one tell us how many people have likely been exposed to the virus.

These results offer a first, high-level glimpse into an ongoing Canadian Blood Services study assessing SARS-CoV-2 antibodies across nine provinces. They will be updated once Canadian Blood Services completes their analysis of the full sample of 37,800 donations made during the months of May and June 2020. In addition, Héma-Québec will have results for Quebec in the near future, which will be important for a complete national picture, given the COVID-19 rates in that province.

“What is clear is that only a small percentage of adult Canadians has been infected by SARS-CoV-2,” Hankins says. “By far, the majority of us remain vulnerable to infection. We need to ramp up testing and tracing capacity across the country to interrupt any chains of transmission quickly to prevent unchecked spread.”

Acknowledging that many more adult Canadians are infected than currently documented, Professor Timothy Evans, CITF Executive Director cautioned against over-interpreting the apparent reduction in risk. “Among adults, the death rate from being infected with SARS-CoV-2 is likely closer to one per cent, as compared to the eight per cent reported to date among those diagnosed with COVID-19. But this is a highly infective virus that could take a huge toll if we allow it to spread, and we are only now learning that many survivors have persistent symptoms.”

This report expands on an earlier result from BC:

As is to  be expected the headline buried the good news Serology study estimates less than 1 per cent of B.C. was infected by first coronavirus wave.  Excerpts in italics with my bolds.

B.C. Centre for Disease Control research also suggests province’s true infection rate is about eight times the rate based on reported cases

The study is the first in Canada to report infection rates based on seroprevalence, which is a measure of the presence in blood samples of antibodies produced to resist the virus. Determining exactly how many people in Canada have been exposed to COVID-19 is a key goal of the immunity task force the federal government set up in April.

Timothy Evans, a member of the task force and director of McGill University’s school of population and global health in Montreal, said the B.C. survey indicates the province’s deft management of the first wave of the pandemic resulted in very low exposure across its population.

“The low prevalence of population immunity suggests that continued vigilance and adherence to best practices to reduce risk of infection will be critical, especially in the context of the second wave of the pandemic,” Dr. Evans said.

He added that the eight-to-one ratio of actual to reported cases is consistent with international studies and that he expected a similar result across Canada. The survey was based on blood samples from more than 1,700 people in two periods, one in mid-March and a second in late May. The data were gathered anonymously from residual blood drawn from individuals at diagnostic clinics in B.C.’s Lower Mainland. The subjects were males and females of varying ages, including children.

Dr. Jha, who is leading a seroprevalence study that aims to sample as many as 10,000 Canadians, also said the individuals in the B.C. study may not be representative of the province’s population. For example, the study may be skewed toward healthy people who were having their blood tested as a precaution, or by those who were already ill.

It also captured the presence of antibodies in blood samples before and after the first wave but not during the peak in April. Another key piece of information the B.C. study does not provide – and was not designed to – is whether the individuals found to have antibodies for COVID-19 are now immune to the coronavirus and, if so, for how long.

My Comment:

Up to now, we have only been able to estimate the lethality of Covid19 by comparing death rates to confirmed cases. In Canada as of July 17, 2020, there were 8839 deaths of people with Covid19 compared to 109669 confirmed cases, or 8.1%.  If the actual # of infections was 8 times higher, that ratio drops to 1% lethality.  Furthermore, the ratio of deaths/cases ranged as high as 14% early June, and is now down to 3%.  Factoring in the hidden infections reduces the current lethality to 0.4%.

Of course this is preliminary reporting while we await results from the nation-wide study.  I do object to the “second wave” narrative parroted in the media to keep the fears alive. Also the public is never presented the big picture about national mortality.

Canada Pop Ann Deaths Daily Deaths Risk per
Person
2019 37589262 330786 906 0.8800%
Covid 2020 37589262 8839 60 0.0235%

Over the epidemic months, the average Covid daily death rate amounted to 7% of the All Causes death rate. During this time a Canadian had an average risk of 1 in 5000 of dying with SARS CV2 versus a 1 in 114 chance of dying regardless of that infection. As shown later below the risk varied greatly with age, much lower for younger, healthier people. Presently daily Covid deaths are hovering around 10, or 1% of deaths from all causes.

See Canada Succeeds on Key Covid Metric

Four Steps to Take Down a Free Society

Update at end:  July 23, 2020 China Takes the Lead

The process is under way most obviously in the USA, but also in Europe, Australia and elsewhere. Scott McKay helpfully writes at American Spectator Four Stages of Marxist Takeover: The Accuracy of Yuri Bezmenov. Excerpts in italics with my bolds.

The journalist and Soviet defector long ago pegged the current left-wing moment.

But it’s also important to understand that the revolution taking place in America is not yet a “kinetic” one. That may come soon, or it may not. The battle taking place presently is a war of information — or disinformation, as the case may be.

And the revolution is a Marxist revolution. You should make no mistake about that. The groups fomenting it, the intellectuals promoting it, and the money financing it are all quite open about who they are.

This playbook was written long ago. If you think that Bernie Sanders or Kshama Sawant or Alicia Garza are smart enough to dream up a plan for taking down the greatest society the world has ever known, you are out of touch with reality. The only way they could have been as effective as they have so far is to follow somebody else’s plan. Which they are doing.

There is a video interview from a long time ago that you should see if you haven’t already seen it. It’s one of those things that many of our readers may have seen years ago and then forgot about — but all of a sudden it’s incredibly relevant again. The interview dates back to 1984, and it was conducted by the author, filmmaker, and John Birch Society gadfly G. Edward Griffin with a Soviet defector and former KGB operative named Yuri Bezmenov. (Below is a synopsis video)

Forget about Griffin’s background. He was something of an Alex Jones of his time, and he’s still around in his dotage, obsessing about things that cost him his relevance. It’s Bezmenov who matters. The Russian was involved at relatively high levels as a propagandist par excellence before leaving the USSR for Canada, and he laid out in excruciating detail the process by which a free society might be brought to collapse.

Khrushchev and the Soviets weren’t just bragging. What he was talking about was an entire system of Marxist indoctrination and takeover they had perfected and executed in country after country during the 20th century. Eastern Europe. North Korea. North Vietnam, then all of Vietnam. Cuba. Nicaragua. Later, Venezuela. Various African countries, including South Africa, the communist bloom of which has only recently come to pass. Some of those countries went communist because the Soviets rolled the tanks in; most went communist because the pre-communist society collapsed for various reasons. All went communist after they had been infiltrated with Marxist revolutionaries.

The point being that there was a template in place for how to penetrate a society with Marxist ideals and implode it so that the revolutionaries would control the ruins.

Bezmenov, whose father was a high-ranking Soviet military official and who was trained to be an elite KGB overseas operative, was taught the template and put to work in India attempting to infiltrate that country and bring it into the Warsaw Pact. He also worked at the Soviet RIA Novosti news organization, editing and planting propaganda materials into foreign media. The man knew exactly what he was talking about when he outlined how a Marxist revolution might bring America down without firing a shot, just as Khrushchev had predicted.

Bezmenov warned us in 1984 that a free society collapses in four stages, and the first is demoralization.

What he meant by demoralization is a process by which students in schools controlled by disciples of leftist thought would be indoctrinated into a set of values and beliefs foreign to those of the American tradition. Bezmenov said, in 1984, mind you, that this would happen when the 1960s and 1970s student radicals began to control the educational institutions, and their project would be to throw out traditional Judeo-Christian morality, classical education, and American patriotism. Is there any doubt this has happened?

Our young people are the least patriotic in our nation’s history, and the most ignorant of the cultural, intellectual, and ideological patrimony of which they are heirs.

It’s even worse than that, because the cultural Marxist project not just in our schools but in our media and entertainment institutions has poisoned those against the country. Remember when the NFL was an escape from politics? Remember when the movies Hollywood made extolled American values and made viewers feel good about their country?  When was the last time you saw anything from American education or corporate media that made you feel good about your country?

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What’s the second step? Destabilization.

Bezmenov describes that as a rapid decline in the structure of a society — its economy, its military, its international relations. We’ve discussed in this space the unquestionable impetus on the part of Democrats to keep the economy as hamstrung as possible with COVID-19 shutdowns, and those continue despite a precipitous decline in death rates as testing ramps up across the country. It’s clear the virus is no longer a significant threat to the health of Americans who don’t already have serious medical issues, and yet COVID hysteria is increasing, rather than decreasing. Just Wednesday the Ivy League shut down all its sporting events planned for the fall semester, an absurd decision that is nonetheless likely to be copied by other universities dominated by leftist political activists (the Big Ten, ACC, and SEC are all in various stages of planning conference-only schedules this fall, which makes no sense whatsoever).

The virus is the perfect platform by which to impose the economic destabilization the Left has wanted all along.

No, that isn’t a conspiracy theory. They’re telling you it’s what they’re after. Do you believe Ilhan Omar was off-script when she suggested dismantling America’s economy as a system of oppression earlier this week? Ilhan Omar, who paid a political consultant $900,000 in fees last year, money that came from somewhere, isn’t smart enough to say these things without having the script written for her. She’s being trotted out to introduce them because she’s already radioactive and a lightning rod for criticism, and also because she’s (1) black, (2) Muslim, and (3) an immigrant, and even an illegal one. To criticize her statements as cracked bears the signature not of incisive reasoning but rather racism. So when other Democrats join her call you are no longer allowed to object.

That’s destabilization. They’re fully engaged in it, whether you believe they’ve been successful or not. But ask Mark McCloskey, for example, whether or not he thinks it’s outlandish to suggest the American order has been destabilized. McCloskey told Tucker Carlson that after the police told him they couldn’t protect him after the incident where he and his wife used guns to protect their property from a mob of Black Lives Matter trespassers, he called around to private security firms for help and was given advice to get out of his house and let the mob do what they would. Does that sound like a stable society to you?

The third stage is crisis, the catalyzing event that builds on the first two stages to bring on the change the revolutionaries are looking for.

Looking for a crisis? Take your pick. We barely even remember the fact that we just had only the third presidential impeachment in American history half a year ago, a constitutional crisis that was wholly and completely manufactured directly out of thin air. We progressed immediately from that to COVID-19, which was unquestionably a manufactured crisis — not that the virus itself isn’t deadly to a certain portion of the population, but if you think the panic and destruction it’s caused doesn’t smack of manufacture then it’s clear you’ve been demoralized.

And then the George Floyd riots and the paroxysms of violence and virtue-signaling those have brought on, complete with the current campaign to bowdlerize American history and culture in an increasingly indiscriminate fashion. That’s a crisis, everybody, and it’s a completely manufactured one. The speed of the cultural collapse that followed Floyd’s death — when the legal system moved very swiftly against the police officers responsible for it — makes it undeniable this was planned and only needed a catalyst.

What’s the fourth stage? Normalization. As in, a “new normal.”

The statues and monuments are gone, the ball games are out, or at least you aren’t allowed in the stadium to watch them (and you’ve got to watch them on TV interspersed with commercial spots and in-game messaging pushing whatever memes and narratives the ESPNs and NBCs of the world and their Madison Avenue partners wish to implant in your mind), the schools have purged American history and culture, the Universal Basic Income checks have replaced your job, which you can’t do because the small business where you used to work has gone under thanks to the virus.

And Biden is president. For a little while, until it’s clear he’s incapacitated per the 25th Amendment, and then somebody else that you didn’t vote for is in charge of the country.

Out goes Kerensky. In comes … who knows what?

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Let’s hope your confidence none of this can happen is well-placed. Let’s hope Bezmenov was a crank like people think G. Edward Griffin is.

But just to be sure, let’s make damned sure Biden and the Democrats take an historic beating in November. We don’t want to find out what’s behind the curtain in Biden’s basement. Too many nasty things are already peeking out at us from there.

Update July 23, 2020: China Takes the Lead

Of course the leading proponent of this geopolitical strategy is China, and they are effectively applying it to the USA. Brian Kennedy writes in his book:

China’s goal is demoralizing the United States to the point where America believes that further resistance is futile.” They can’t succeed without the help of America’s elite.

From Robert Curry’s review: The Chinese are confident that America has grown corrupt, and that its political, financial, and cultural elites are in near-complete sympathy with the globalist project of an interdependent world, with the P.R.C. [the People’s Republic of China] at its head.

I have a story from my own life that illustrates Kennedy’s point. Recalling what it was like before the pandemic panic took total control of American life will help to set the stage. Back then, the media, the celebrities, and the politicians had not yet mastered the talking points of the COVID-19 narrative. During one of those early days, a local radio news personality announced with great excitement that she had secured an interview with a prominent epidemiologist from the most prestigious university in our region. After thanking the professor profusely for granting the interview, the reporter asked the obvious question, the one that was on my mind at that time: “What is the difference between this flu and the Spanish flu of 1918?”

The professor was greatly offended by the question. She admonished the reporter never to use the term “Spanish” with regard to the flu of 1918 and never to use the word “Chinese” with regard to the flu of 2020. The professor simply would not answer the question and, for that matter, she would not address any other question having to do with epidemiology. She confined herself to scolding and reeducating the reporter, making it clear to the reporter and her listeners what was and what was not politically correct to say about the virus.

It was an astonishing performance. The professor did not speak as an epidemiologist; instead, she spoke as a globalist. When she said, in effect, “Don’t you ever call this flu that came from China ‘Chinese,’” she was acting as a spokesperson for the ideology of globalism.

See also: Patriotism Vs. Multiculturalism