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)

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.

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

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.

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

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.

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 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.

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