On this page, i will take images from the galleries and put them in posts here – and provide my analysis of their contents.
- Virology & Mythology: Vol. 2
Should we open schools or not? Is COVID-19 losing momentum through mutation?
(3) To School, or not to School?
Remember when we shut down schools to stop the spread of Smallpox? Mono? Chicken Pox? H1N1? Polio? The Opioid
Crisis? Me neither. Every year, older teachers are at risk of influenza-triggered pneumonia, and the NEA never managed to discover that connection. That is an actual double standard, and I hope that school districts will do more to protect at-risk teachers in the future; however, a majority of teachers and 99.8% of students are safer than during flu season.
Perhaps I have too much faith in America, but I believe we are capable of protecting vulnerable people while putting kids back in school. The physical stress of a parent who is stuck and unable to earn their normal income (surrounded by kids on an eternal summer
break) probably just makes them more susceptible to infection by weakening their immune system. The hard truth is that COVID-19 will probably be here for at least six more months, but our economy won’t be if parents can’t work. The hardest-hit jobs have been lower-wage positions that can’t be performed remotely, and all size businesses have either gone bankrupt or started investigating ways to increase automation. I refuse to believe that high-risk populations are safer in a closed economy – subsidize all 55+ workers/employers that can’t work from home, and have Amazon provide Prime and Fresh services for free until the pandemic ends.
If we don’t put our kids back in school, it becomes less likely that they will grow up having enough common sense to think of simple answers, like that. I’m not sure what that says about Congress.
(4) Is the Virus getting Weaker?
No. I’ve only made it through about 250 of the 31,000+ COVID-19 articles that the NIH has gathered and provided free to the public, but several recent studies show almost no mutation, relative to typical virus outbreaks. I will be laying out the latest research in a separate article, because the origin and evolution of COVID-19 is becoming clearer (and has disturbing implications). To preview, the stability of the genome indicates a direct bat-human transition with severe infection prior to the start of the pandemic. Viruses evolve much faster when their environment requires it for survival, but COVID-19 has been so effective and transmissible that not much tweaking has been necessary. The last CFR update:
Along with new developments in looking for origins, there’s actually evidence that survivor’s antibodies are losing their effectiveness within months; if true, that would nullify the possibility of herd immunity and greatly reduce the impact of most vaccines. The primary reasons that case fatality rates (CFR) have been declining across the globe are the increasing quantities of tests and a faster rate of exponential growth among countries in the southern hemisphere – i.e. the part of the globe currently in winter. One small silver lining is that the US trend is exploding because of simple math – the three most populous states took months to begin peaking, and all three (Texas, California, Florida) have maintained fatality rates much lower than the East Coast states in April.
Russia has the lowest CFR of any large country in the world; must be nice to fabricate statistics. If I were a member of the media, I’d stop holding up Russia or Europe or China as examples just to make President Trump look bad; if the US CFR was as high as most of the big European countries, we’d have 420,000 dead instead of 140,000. It’s a lucky break for the vocal opposition, then, because by the time Denmark/UK/France/Italy/Spain/etc. get overwhelmed by 14% CFRs again our election will already be over.
CH Rixey
(C) rixanalytics.com 2020
- Virology & Mythology: Vol I
A series to support the spread of facts; today’s topics – (A) Does a Mask really matter? (B) Is it worse for minorities?
The amount of confusion regarding pandemic urban legends has made it easier for opinion to magically transform into fact, and it has become a popular past-time to vilify political opponents by condemning COVID responses by any means necessary. In order to combat this alarming trend, I will periodically provide my own opinion (lol) and randomly sprinkle in scientific research to support my conclusions. It’s true that one could just act like they are an expert without any encouragement from the internet, but if I was that lazy I’d just go work for the media.
(A) Masks are dumb – or smart. They are a sign of sheeple – or intelligence. They are useless – or vital.
I heard each of those opinions on the news today. It would be impressive enough to have experienced news-anchor disagreement at the beginning of the pandemic, but nearly 7 months after the Huanan Market their use remains controversial. The real answer is they DO work, and also that they DONT.
The truth is that face coverings are not an all-or-nothing solution; their effectiveness is in the middle of the spectrum, not polarized at opposite ends. Viruses are small enough to pass through most of the cloth varieties being worn, but when everybody is wearing one far fewer nasties are floating in the air. We can detect flatulence because some of the offender’s poo particles / gasses escape through clothing, but no one advocates universal full nudity since it’s useless to fight the ‘system.’ Prior to the development of gas masks, soldiers in World War I had to pee on a rag to protect against Chlorine gas; I doubt it was that much fun, and it doesn’t work against pathogens, but the key takeaway is that something is better than nothing.*
*Actually, the key takeaway is that we have made masks less effective by bypassing them – many of you have seen mask-wearers leave a public restroom without washing their hands. The COVID virus is an equal-opportunity-orifice exiter, which has helped fuel its transmission rate despite our near universal mask adoption. Hand sanitizer, masks and social distancing can’t protect us from our own stupidity.
(B) The ‘Madrid Malaise’ and Minorities
I came face-to-face with this question in March, when I analyzed demographics with case rates (by state) for the first time. Many researchers, then and now, have drawn conclusions about how COVID-19 impacts groups in unbalanced ways, but my low expectations in modern political discourse nudged my fevered brain into some number-crunching of my own (given that ‘Wuhan Virus’ is offensive, perhaps I should call it ‘Madrid Malaise,’ in recognition of my likely infection source).
The header image for this article represents the updated correlation calculations between pairs of COVID/demographic data. I’ve added color for fellow right-brained individuals, but the numbers represent the strength of the relationship between any two figures; as the result gets closer to 1 or -1, their connection to the other statistic gets stronger. For instance, a state’s ‘people per household’ and % of population younger than 18 has a strong positive correlation (.5933), which makes sense because most children live at home and more kids live with their families than adult siblings, grandparents, etc.
It’s vital to note that the correlations I compiled are not national per se; they are the result of two sets of 52 numbers (including Puerto Rico and DC). Immediately, it becomes clear that total infections and deaths go up as a state’s proportion of white residents decreases. However, none of the correlations with ‘white share of population’ even approaches .5 in either direction – this mostly shows that white Americans are more evenly sprinkled and more numerous in general.
The murder of George Floyd drastically increased the attention paid to what had been largely painted over during the pandemic – the huge disparity between pandemic cases in urban areas and prisons, compared to the rest of the country. I must emphasize the horror I felt watching such a callous indifference fuel a murderer’s disregard for the value of human life. It immediately sparked the memory of struggling to breathe that i had experienced two months earlier, and the psychological trauma that can be inflicted when choking and terrified. I had spent a career teaching Marines about chemical and biological weapons, and while stuck in bed in mid-March I compared COVID’s symptoms to Sarin gas or Anthrax – both cause asphyxiation that can be traumatic just to observe, and it breaks my heart to know that medical and financial reasons make it more likely for minority families to experience severe infections.
Despite this, the last three months have led to a reduced share of cases amongst black Americans, as well as a weakening of the mortality correlation. The strong positive correlation between higher levels of education and higher CFR has continued, and greater wealth also leads to higher risk, but the consistency of that pattern shows that affluent residents of urban areas are victims of population density, regardless of skin color. The most vulnerable minorities are foreign-born, Asian or Hispanic, and living in higher-density urban areas. The crisis in New York City was fueled by high volume international traffic, because ‘foreign born’ residents are far more likely to travel during events like Christmas and Chinese New Year. The spread was so fast, in such perfect conditions, that the tipping point for exponential growth fell before the city’s initial lockdown attempts. Based on what I saw in Europe, President Trump’s controversial decision to close down air travel saved the rest of the country from New York City’s fate; the slow response of the European Union doubled or tripled the eventual death toll.
If this analysis seems disjointed, the fault lies with the huge number of implications that can be gleaned from the data. I was very reluctant to point out my results in March, because politically-motivated types would be quick to spin and frame the numbers in order to justify discriminatory policies (immigration changes, racial tension, etc.). In the aftermath of the Floyd protests, I was torn about whether or not to share the interpretation of another portion of my research;
But, I have decided to provide the primary projection in hopes that future unscrupulous leaders will consider alternatives to the protests from 29 May – 2 June. The prevailing narrative was that red states had opened too soon and case numbers would skyrocket as a result, but opportunistic politicians ignored their own advice to allow (and lead) massive demonstrations through many of the nation’ largest cities.
When COVID-19 began exponentially growing again, this time in the south and midwest, the chorus condemning Republican governors was almost unanimous. My second attached image depicts the sudden shift in new cases across many states, and the key dynamic is that the start or re-start of peak growth (depicted by an X) that occurred almost simultaneously nationwide. Texas’ first phase of opening began 4/27, with new cases beginning to explode on 6/13 – an outcome that seems to have validated the dire projections that drove federal actions during the second half of March.
However, the data continues to reject a direct link between early re-opening and our current peak: I sorted the states by their governor’s political party, and then by the re-opening date (colored brown, except for South Dakota which never officially closed). The only red states that opened later than early May were New Hampshire, Vermont, Massachusetts and Arizona (VT & MA are blue states that just happen to have Republican governors), and all of them were open by May 26th, when George Floyd was killed in Minneapolis.
The red line denotes the 26th of May, and the period from May 29th to June 2nd saw more than a million protestors march through the streets in most major US cities. If the sudden spike in confirmed infections was driven largely by re-opening measures. then we could expect the “X” dates of new infection spread to roughly follow the same curve as the emergence from lockdown; instead, most states saw sudden changes that correlated well with the incubation period of COVID-19 (3-14 days) when counting from the start of mass protests. For example, daily new cases in Texas began rising between June 13th-15th, six weeks after re-opening on April 27th, despite remaining flat for more than a month. There have been a few outliers, but infection rates rose exponentially in June regardless of when lockdowns were lifted.
In sum, the correlation table has continued to reflect the same basic characteristics as the pandemic shifted towards the south and west, but Americans below the poverty line are susceptible because they are more likely to to live in densely populated areas and carry high rates of comorbidities. The second chart shows the epidemiological impact of the protests. By encouraging mass protests (in defiance of orders largely written by themselves) mayors and governors in places like Dallas and California ensured that COVID-19 would spread faster and further, especially amongst the most vulnerable demographic groups. The impact of bars and shopping re-opening is dwarfed by the impact of encouraging masses of young people to vent their frustration in the middle of a pandemic.
I’m optimistic that the global response to Floyd’s murder will spark greater efforts to support the elevation and inclusion of minorities. However, by placing the value of virtue-signaling above social distancing measures, politicians have ensured that future iterations of these correlations will skew even further towards minorities than before. 772 black Americans were killed in fatal police shootings from 2017 – July 1st 2020. The resurgence of COVID-19 three months before an expected second wave this winter is devastating, because inequality will grow even faster when lockdowns are extended and most lower-wage jobs can’t be done remotely. The fact that it took several weeks for news outlets to admit the connection, presumably because it would be unpalatable during an election year, ensured that the focus of blame would remain on the President.
Which is the greater social injustice – that 772 deaths is a tragedy or that several thousand additional minority deaths is simply a statistical means to a political end?
CH Rixey
(C) rixanalytics.com, 2020
- Using Occam’s Razor to Open Pandora’s Box: The Origin of COVID-19?
Many researchers have long believed that a lab accident is the most likely source of the COVID-19 pandemic, but China has endorsed the search for animal transmission and rejected any real investigation into the possibility. In the last six weeks, however, an increasing number of scientists have openly questioned the lack of curiosity from their peers & elected officials – but new evidence has been published that provides a simple and direct answer to the world’s biggest question. It turns out that a few details didn’t make the cut when the SARS-nCoV-2 genome was sequenced in January, but on 7/15 a pair of researchers published their analysis of a Master’s thesis describing an unknown illness that killed 3 of 6 miners after they had been infected in a cave. Spoiler Alert: the simplest answer that explains the stability of the COVID-19 virus (its lack of exponential mutations that results when a virus first transitions to human hosts) is that the virus had made the jump 7 years earlier – further evolution most likely occurred at the Wuhan Institute of Virology, where China’s “Batwoman” and a team of researchers had brought samples from the cave, 800 miles to the south, to add to their collection and conduct research in 2013. Much of the debate over provenance has been framed by the speed of virus evolution, but natural mechanisms can account for the gap with or without genetic modification (see the article dated 7/14 for specifics).
The purpose of this article is to aid in the dissemination of the findings announced by Jonathan Latham, PhD and Allison Wilson, PhD; the article is the latest of a half-dozen COVID-19 pieces published since February. I have included links for all of the papers referenced/researched in order to write this article, including ones with opposing view-points (provided at the bottom of the page).
For those who are curious about my purpose or experience, I offer a short summary of my background: I spent 14 years as a Marine in the field of Chemical, Biological, Radiological, Nuclear (CBRN) defense, with 7 total years spent under the auspices of the Department of State. In the latter capacity, I led a section of Marines tasked with training, equipping and assessing the embassy security guards’ readiness against WMD threats; my tenure included the events of the Arab Spring, Benghazi, Mumbai, the rise of ISIS/ISIL/IS and the use of chemical weapons within Syria. In between stints at DOS, I spent 3 years as a Warrant Officer Instructor & Curriculum Developer for the USMC CBRN School; re-structuring the course made me intimately familiar with the Biological Weapons Convention, the National Strategy for Pandemic Influenza, and the lessons learned from the SARS, MERS and Ebola responses.
After experiencing the onset of the pandemic in Europe during a course trip to Prague (‘Business in the EU’, one of the final requirements for my MBA) I’ve spent most of the period after 3/7 researching and analyzing the progression of the crisis, and operating a non-profit website to compile unbiased information (research articles selected from the LitCovid database of the National Institutes of Health – now over 35,000+ papers) and analytics. The quality and relevance of modern journalism, already in decline, has become so partisan that even scientific developments are stripped of context and judged by how their conclusions support or weaken political objectives. I felt compelled to take on the project in March, and this article represents the most neglected, controversial and impactful facet of COVID-19 I’ve researched; the letter at the end of the article contains my thoughts from May, but any pride stemming from the potential accuracy of my early analysis is offset by the implications for post-COVID diplomacy.
The introduction from my 5/28 response to a friend’s query:
“The ultimate question posed by _______ is the same one that many researchers have been asking themselves as this crisis has continued to play out – the question of provenance. The truth is that it’s being asked because it’s a logical conclusion that explains a variety of phenomena related to the pandemic; furthermore, scientists are scared to dig too far down the rabbit hole because they fear that their own governments might be more afraid of Chinese reprisal than the truth. After all, learning that the Chinese were negligent is probably the best-case scenario.
First, it is not unprecedented for pathogens to be accidentally released from a lab that is studying them. As CBRN Marines, we were encouraged to read a book about Lab 257, a testing facility on Plum Island, just off of the northern coast of Long Island. I now find it ironic that the book was chosen as a part of our reading list, since the US government denies several of the allegations within it. Primarily, the author accuses the lab of being responsible for the source of modern global-scale Lyme disease outbreaks, the epicenter of which can be traced to a sudden cluster of cases in Old Lyme, Connecticut in 1975. The boldness of the claim belies the simplicity of the argument – that a major outbreak of a historically rare disease began there because Old Lyme sat across 7 miles of water from Plum Island; prior to 1975, cases were usually geographically distant from each other and so rare that it was difficult to diagnose since most doctors had never seen or heard of a case. Today, Lyme disease is endemic throughout the U.S. and the world.
Therefore, when COVID-19 appeared in Wuhan in late December, it was only natural for researchers to scan the surrounding environs in order to shed light on what might have sparked its emergence in Wuhan rather than somewhere else. It’s not surprising that the Chinese government leapt at the opportunity to blame the Wuhan live-market, and by some measures the connection makes sense. However, it didn’t take long for researchers from China to determine that the theory doesn’t account for all of the identified cases, including the very first (https://pubmed.ncbi.nlm.nih.gov/31986264/).”
Pandora’s Box
When I wrote that private message on May 28th, the primary focus of origin research had centered on connecting the dots for a presumed zoonotic (animal) jump or series of jumps, because direct transmission from a bat to a human would be much less likely due to the relatively weak link between bat and human cell/immune systems – as opposed to the similarity between humans and pigs (a la swine flu). Despite a broad effort, no local coronavirus strains came close to indicating a recent ancestral connection with SARS-nCoV-2, the RNA virus that causes COVID-19 infection. The prime target species, pangolins, registered a genome similarity of 93%, which in viral terms represents a huge gulf in time and evolution, whereas the Wuhan Institute of Virology had bat samples above 96.3%; this is a correlation getting stronger in the direction of direct transmission.
However, there are at least two other major issues that have vexed scientists seeking zoonotic transmission, and the first is incredibly simple yet seemingly ignored – even if a bat managed to travel 800 miles from Yunnan Province to reach Wuhan, it would have probably been hibernating at the time a transmission took place in November. The more complex issue is based on the very low incidence of mutation observed despite more than 16 million confirmed cases; this is clear evidence that COVID-19 is already well adapted to human hosts. It’s so well adapted, in fact, that it’s statistically impossible for COVID-19’s infectivity prowess to have come via gene editing, because no simulated virus has come close to matching the complexity nature has provided.
I must note that one of the primary pieces of the Latham/Wilson hypothesis is the argument that newer techniques for nudging genome changes in viruses have been developed, and the most common option simply uses human cells to force evolutionary changes to strengthen affinity for human hosts by pairing them together over and over again. This method speeds up evolution without requiring manual editing, accomplishing similar results with zero human fingerprints.
Occam’s Razor
This article is far from a complete review of the Latham/Wilson findings, much less of the other articles I’ve included, but in order to maintain the slightest pretense of brevity I must move to the alternative proposal that the pair argues can provide far more answers than a wild goose chase for pangolins and civets in southern China.
The director of the Wuhan Institute of Virology is one of the world’s leading authorities on coronavirus research; her stature grew dramatically after her team discovered the animal source of the original SARS outbreak in 2002-2003, living within certain species of bats that inhabited a cave in Yunnan Province. 10 years later, her institute had become the epicenter and repository of coronavirus research and hundreds of different strain samples gathered over several expeditions. She led her team to Yunnan once again in 2013, and among the samples gathered were the two closest relatives of the virus that caused our global pandemic. The presence of such a close cousin was bound to intensify the natural scrutiny that emerged as a result of the laboratory’s presence within the city that sparked the pandemic.
Whispers of the 2013 cave mystery have been slowly growing in intensity, as evidenced by the 7/4 story that ran in London’s Times. Detailed versions of the ‘accidental-lab-release’ theory have become more common as well, but the 7/15 article by Latham/Wilson has provided additional evidence and the most plausible explanation by far. It’s persuasive enough that I’ve decided to publicly comment, so that their article (and 12 other related items) can begin to reach a broader audience.
Why does my CBRN/Marine/Historian/Analytics intuition find this proposal so plausible? The best answer is that China has meticulously ignored, obfuscated, erased or ‘forgotten’ many of the details within the timeline laid out by Latham and Wilson:
- The original stated purpose of the 2013 expedition was to investigate a “fungal” infection, but Dr. Zhengli Shi (“Batwoman”) personally led the sampling team; as a renowned expert on coronaviruses, there would have been no reason for her and a team of virus researchers from the WIV to travel there.
- The Chinese have also avoided referencing the 2013 miner incident despite its obvious resemblance to COVID-19 symptoms. That’s probably because most people don’t know that the RaTG13 strain (the closest relative of COVID-19) was taken during the aforementioned trip, which was undertaken specifically to investigate the earlier outbreak. RaTG13 is the strain that shared a very high affinity for the ACE2 receptor (like COVID-19), but didn’t compare as well with the original SARS-CoV from 2003.
- If not for the discovery of a master’s thesis that linked the WIV to the 2013 mystery illness investigation, we might have never known the full story behind the acquisition RaTG13 and other samples by the WIV.
- Shi partnered in publishing results of experiments involving “gain of function” by exposing coronaviruses to human, monkey and mouse cells to encourage adaptive evolution to make the affinity even greater. Her papers are readily available online.
- Many of the detractors arguing against an accidental lab release have pointed to the time needed to produce evolutionary changes that could account for the 3.7% gap between the genomes of RaTG13 & SARS-nCoV-2, estimated at 20-50 years. There is broad agreement that the genome doesn’t seem to have artificial insertions, but RaTG13 was an obvious candidate for gain-of-function experiments, and the methods used could explain the exponential condensing of evolutionary progress & the absence of evidence of human gene modification.
- In late May, China announced that the evidence no longer supported the claim that the Wuhan Live Market was the location where zoonotic transmission to humans took place.
Actions speak louder than words, especially when China isn’t saying much to begin with. Even the publication of the full gene sequence in early January was unplanned; Shi’s team had completed the task more than a week before the milestone was announced, but an unauthorized release from another research group forced the hand of the WIV. Not until January 23rd did the WIV release the full sequence of RaTG13, a virus it had held for seven years. And, ignoring the 2013 outbreak leads to greater attention being given to the search for an intermediate species; why would scientists want to focus on a less attractive theory, when the possibility exists that the first emergence of human COVID was in 2012, not 2019?
Latham and Wilson’s article (https://www.independentsciencenews.org/commentaries/a-proposed-origin-for-sars-cov-2-and-the-covid-19-pandemic/) deserves greater attention, so why haven’t more media outlets investigated the most plausible analysis of the pandemic’s genesis? China’s intransigence is unusual, because many possible outcomes could help exonerate the country from suspicions regarding the origin of the pandemic.
The alternative is that China’s silence is a natural result of being stuck in a corner, unable to offer any evidence that could clear their name because none exists. The reluctance to consider a lab accident has raised eyebrows in Europe and Australia, and the theory represents the application of Occam’s Razor to the mystery of COVID-19’s birth?
The Razor principle has highlighted a possible solution that demands a thorough investigation. Continued Chinese resistance would further imply that their unwillingness to help discover Pandora’s opened Box stems from the fear that investigators might find their fingerprints on the lid.
—C. H. Rixey
(c) rixanalytics.com, 2020
References
5/21 https://doi.org/10.1101/2020.05.21.108506
No Evidence for increased transmissibility from recurrent mutations in SARS-CoV-2
Van Dorp et al – pending review/BioRxiv
6/4* https://project-evidence.github.io/
6/4 https://www.cell.com/cell/pdf/S0092-8674(20)30820-5.pdf
Tracking Changes in the SARS-Cov-2 Spike: Evidence that D614G Increases Infectivity of the COVID-19 Virus
7/4 https://www.thetimes.co.uk/article/seven-year-covid-trail-revealed-l5vxt7jqp
7/23 https://time.com/5870481/coronavirus-origins/
My full private response of 5/28, written to a group of experienced & interested peers:
“The ultimate question posed by _______ is the same one that many researchers have been asking themselves as this crisis has continued to play out – the question of provenance. The truth is that it’s being asked because it’s a logical conclusion that explains a variety of phenomena related to the pandemic; furthermore, scientists are scared to dig too far down the rabbit hole because they fear that their own governments might be more afraid of Chinese reprisal than the truth. After all, learning that the Chinese were negligent is probably the best-case scenario.
First, it is not unprecedented for pathogens to be accidentally released from a lab that is studying them. As CBRN Marines, we were encouraged to read a book about Lab 257, a testing facility on Plum Island, just off of the northern coast of Long Island. I now find it ironic that the book was chosen as a part of our reading list, since the US government denies several of the allegations within it. Primarily, the author accuses the lab of being responsible for the source of modern global-scale Lyme disease outbreaks, the epicenter of which can be traced to a sudden cluster of cases in Old Lyme, Connecticut in 1975. The boldness of the claim belies the simplicity of the argument – that a major outbreak of a historically rare disease began there because Old Lyme sat across 7 miles of water from Plum Island; prior to 1975, cases were usually geographically distant from each other and so rare that it was difficult to diagnose since most doctors had never seen or heard of a case. Today, Lyme disease is endemic throughout the U.S. and the world.
Therefore, when COVID-19 appeared in Wuhan in late December, it was only natural for researchers to scan the surrounding environs in order to shed light on what might have sparked its emergence in Wuhan rather than somewhere else. It’s not surprising that the Chinese government leapt at the opportunity to blame the Wuhan live-market, and by some measures the connection makes sense. However, it didn’t take long for researchers from China to determine that the theory doesn’t account for all of the identified cases, including the very first (https://pubmed.ncbi.nlm.nih.gov/31986264/).
Four months later, the official position of China continues to be that COVID-19 jumped from animal to human within the live market, despite the lack of any bats available for sale there. Furthermore, there wasn’t an expected genetic marker from a intermediary species, something which could’ve substantiated that direction of investigation; instead, the evidence showed that human-to-human transmission was occurring prior to contamination in the market.
Based on that premise, the real question is figuring out where the first human case came from, but as the virus began to spread outside of mainland China the ruling party severely restricted publication or research of any information regarding the origin of the virus, and all articles are now subject to pre-approval from a government censor before they can be released.
As it stands, I don’t lean in the direction of an intentional release, because that would run counter to the regime’s long-standing goals in the region and globally. Instead, it seems far more likely that our current pandemic is the result of an ‘oops’ similar to Plum Island in 1975 – an accidental release of something actively being researched. It’s disturbingly easy to imagine that some unnamed scientist, operating within China’s brand-new (and only) BSL-4 laboratory, within mere miles of the Wuhan live market, somehow brought the virus home one night. The real story is what is spreading, not how it started.
Scientists have concluded that the current coronavirus is in fact a slightly mutated form of a strain first discovered in 2013, announced in this article from Nature: https://www.nature.com/articles/nature12711. This connection was acknowledged on the Netflix special episode regarding the COVID-19 crisis, ultimately meant to be part of a series. Researchers had been mining betacoronaviruses in bats in China ever since SARS highlighted the danger 18 years ago, and that 2013 strain in particular was notable for its receptors capable of binding to a human’s ACE2 cell proteins with high affinity, needing only a nudge to do so. Ultimately, the strain was ignored because its other features didn’t indicate potential for a near-term threat, but within two years China had successfully advocated for (and received approval) the right to build a BSL-4 laboratory. On one hand, I would’ve seen those developments as a positive, since it would mean greater collaboration and oversight amongst the scientific community, especially for a country that is certainly suspected of harboring an active biological weapons program. The ultimate result, however, is that the 2013 species came to be stored in one of the world’s largest cities, to be studied along with other coronaviruses and various samples of other high-threat pathogens.
I have no doubts that the virus originated from one of the two Wuhan laboratories, but it’s very difficult to ever determine if the genome was tweaked without access to them, and I don’t think there’s any evidence left to find (or people to testify, for that matter). I can assure you that there is zero interest amongst the members of the House Intelligence Panel to investigate anything prior to the November election, as that would run counter to their preferred narrative of Trump’s failure with COVID-19.
There’s been a lot of conjecture about vaccines, Bill Gates, etc., but I don’t see the need for any impetus beyond China’s desire to gain competitive advantage. I don’t think they had to work to tweak the genome, since the mere combining of various and humans within a research facility increased the likelihood of the jump being made – and a researcher who accidentally exposed himself would’ve been desperate to hide that knowledge from his authoritarian government.
The odds of the virus emerging from somewhere else are so small compared with the likelihood of escaping from one of the Wuhan labs that it only makes sense for China to have cut off all information leading down that pathway.”
- An Inconvenient Truth
Mixed Signals obscure the Actual danger in the “Middle”*
COVID-19 & politics is a touchy topic, but my analysis is bi-partisan – our corridors of power are infected by opportunistic vampires. How bad is COVID? As bad as it needs to be to win an election, of course.
*I feel inspired to throw in a remake of a familiar quote, which came to my fevered brain while reading the news in March (still relevant):
“You can lead a horse to water, but you cannot make him drink;
You can lead a fool to insight, but you cannot make him think.”
In April, I posted a table to illustrate expected total deaths from COVID-19, by examining a variety of possible CFR’s (Case Fatality Rates) and providing totals for each rate based upon the % of the US population infected. It has been widely understood that, if most people who contract COVID-19 never show symptoms, then the very high CFR’s from confirmed cases represent artificially inflated snapshots. The unpublicized footnote is that politicians
The frustrating reality is that humanity’s usual method for calculating such figures has been to study the evidence once an epidemic has run its course. In March, there didn’t appear to be much optimism or expectation in this effort, reminiscent of how resigned experts looked when explaining the length of time needed to produce vaccines – as if literally nothing could be done to streamline a ‘rather’ bureaucratic process.
I doubt most people are going to refrain from all of the potential candidate vaccines until June 2021, just as I imagine the FDA will magically overcome some of their typical objections to emerging medications. I fully support their courage in graciously choosing not to stand in the way just this once – because my opinion “this isn’t really the flu” hasn’t changed over the last 3 months. It’s a shame the rest of the political class can’t decide whether it’s a decent flu or some mixture of bubonic plague+ebola+anthrax; the concept of “the middle” is anathema these days, but just as with any other variety of vampire, I imagine there comes a point at which circumstances make their fear of a vegetable easier to digest.
Or maybe garlic is just that terrible, since 125,000 deaths have yet to spur consensus on the diagnosis. Thankfully, as my wife can attest, I am not encumbered by the presence of vegetables – but while Atlas refused to shrug I decided to go research the CDC’s influenza records. I didn’t have to be a scientist to spot the difference between the flu and COVID; I just counted. In the last 15 years, the average number of flu deaths has been rising because the more dangerous strains have been circulating more often than not, whereas the 3 previous decades experienced lower CFR’s and thousands of fewer deaths. The re-emergence of H1N1 in 2009 was terrifying for many experts, since death tolls for the “usual suspects” had been reaching record levels since the late 1990’s, but a year later 10,500 had died (est.), out of 57 million infections in the US.
The dire projections stemmed from the fact that the first global emergence of the H1N1 strain was in 1918; the novel influenza devastated a world without antibodies, producing 675,000 deaths in the US and 17-50 million worldwide (1-3% of infections).
Whether your ideal “safe space” is a gun range or a campus lounge, if you weren’t born before man landed on the moon (FYI: 1969), then statistically COVID-19 is like the flu. But 100% of you have parents, family members, etc. that are vulnerable; an average-sized Thanksgiving for my family (15-20) would produce 2 deaths with 100% infection. The attached 3-D graph portrays the data from my latest iteration of CFR projection (another picture below). Any column lower than the halfway point of the graph means that the US CFR and/or infection rate are higher or lower than that mark, respectively. I can make that claim because the 3rd variable is total deaths – it’s the only known variable and the absolute minimum, since CDC research continues to show far more deaths than expected in the overall mortality statistics from all causes, after accounting for confirmed cases.
For the CFR to be the same as H1N1 (.018%), the total infection number would have to reach 700 million; America is the greatest country on Earth, but even our 110% effort would be 350 million people short. The .2% typical flu CFR would only require 70 million infections, but H1N1 (highly infectious) took a year to reach 57 million – with no global lockdown, social distancing or people outside of hospitals wearing a mask.
The graph indicates that the likely answer falls somewhere in the middle, .5%-.9%, leaving us on pace for “only” 300-350K deaths before flu season. If a vaccine doesn’t fully arrive by February, only random mutations or absolute quarantine would prevent this pandemic from eclipsing the Civil War and Spanish Flu as the deadliest event in the history of the United States. Congress could just pass a law requiring all businesses to allow employees 50+ to work from home and subsidize both sides for a year, to nullify most of the negative impact.
How depressing it is, to know that our situation has not yet become scarier than a vegetable to the vampires. I can’t confirm that our current Congress is composed of soulless, blood-sucking leeches who feed off of innocent victims under the cover of darkness, but it’s clear that they managed to spend trillions of dollars in stimulus with little pause for reflection. And, now that I think about it, there’s a more obvious and understandable explanation: If I were a member of Congress, or almost any elected leader, the last thing I’d want to see is whatever was staring back at me in a mirror.
C.H. Rixey
- Hurricane Pandora: COVID-19
The latest research on how COVID-19 kills, and why it’s so effective at it.
Cautious optimism has been spreading across the world in recent weeks, as economies begin to move, people shift towards normal routines, and and communities begin to take stock of the damage left in the wake of the storm.
While 1,536 research teams work feverishly to produce vaccines or other treatments, others have been feverishly painting a picture of what makes the virus tick; the more I learn, the more convinced I become that 1,536 projects is not overkill.
First, it should be clarified that COVID-19 is a truly ‘novel’ virus – although the widespread use of face masks subconsciously reinforced the connection with the flu, scientists are learning that it is tricky to even label it as a ‘respiratory virus.’ A growing proportion of doctors and researchers now favor the argument that our current pandemic is the result of a perfect storm of infectivity characteristics and an unprecedented ability for the SARS-nCoV-2 virus to latch onto certain types of cells. The most persuasive evidence in favor of this theory is the fact that it helps explain one of the biggest mysteries of the pandemic – symptomology.
In early January, Chinese scientists sequenced the genome of a new coronavirus, having correctly identified COVID-19 as the underlying cause of a pneumonia outbreak in Wuhan. For more than a decade, epidemiologists and policymakers had been aware of the threat of a novel corona/flu virus pandemic, but the most likely scenario involved the flu, because SARS and MERS had been so deadly that they couldn’t spread fast enough to compensate, once quarantines were put in place.
COVID-19, by contrast, appears to have hit the trifecta, by being highly infectious, broad in its symptoms, able to spread in asymptomatic individuals for 2-10 days, and also a near-perfect fit with the receptors of three types of cells: epithelial, endothelial and enterocytic. The loophole is the ACE2 receptor, one of a variety of types of cell proteins that performs tasks like reducing blood pressure. So, why is the ACE2 so special?
The answer is that it isn’t – it’s found all over the body, because those cells can be found in major organs like the nasopharynx, oropharynx, lungs, stomach, small intestine, spleen, liver, kidney and brain.
One of the most puzzling elements of the pandemic has been the emerging awareness of odd symptoms appearing all over the body; most pathogens operate within relatively narrow niches, but this coronavirus appears to be more flexible. Rather than being driven by respiratory symptoms specifically, the infection seems to produce symptoms as a function of its point of entry. The first two targets are the lungs and blood vessels, and the longer the infection lasts, the more diverse one’s symptoms become. That makes COVID-19 a kind of Pandora’s Box – once opened, it will spark internal chaos until its symptoms reach the tipping point.
The ACE2 receptor theory would also explain why COVID-19 infection is so much deadlier in adults 50+ than every other age group combined. The ACE2 receptor is common among cells that line the blood vessels, pancreas, kidney & lungs – weak points for those with cardiovascular problems, diabetes and COPD. Other research indicates that ACE2 affinity makes it harder for immune systems to differentiate between SARS-nCoV-2 and the human cells around it, which can further intensify the immune response and precipitate a “cytokine storm,” an often-fatal, overwhelming immune response that ultimately delivers the final blow through organ failure and death.
Perhaps the most important takeaway from these findings is that the pandemic is still largely misunderstood, and politicians remain determined to cast blame on the opposition for the spread of the virus. The truth is that America leads the world because of demographics, not assumptions. The United States enjoys a high standard of living and relatively good healthcare. The former fuels obesity and the latter fuels longevity. It’s no coincidence then, that our number of confirmed cases leads the world; it’s a symptom of our society at large. It’s a demographic reality, not a political statement.
At the moment, it feels like we are in the eye of the storm, unable to forecast what the trailing edge of the hurricane will bring. The good news is that vaccines and treatments are in development, and many existing drugs have shown promise. ACE inhibitors (medicines that lower blood pressure) are being used in many cases, because blood pressure rises when ACE2 levels fall, thus upsetting the balance between the two.
In sum, COVID-19 is a perfect storm of chaos; infectious enough to cover the world, deadly enough to kill large numbers, with an extended incubation period and the ability to spread during that asymptomatic phase. It targets the organs where most pre-existing conditions emerge, while spreading through the ACE2-receptors in cells that help mediate blood pressure. Finally, in immunocompromised individuals, it hastens the process of the immune over-reaction.
The prospect of a vaccine in the near term is exciting, but until proven therapies emerge we should remember the lessons of the 1918 flu pandemic: as time passes, mutations appear, and that can be a blessing or a curse. In 1918, it was a summer mutation that led to devastation across the globe that winter; our best course of action is to plan for the curse and hope for a treatment blessing.
-Rixey
