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COMMENT: An interesting piece in “The Atlantic” describes how the SARS-CoV‑2 virus that causes COVID-19 differs from other coronaviruses known to infect humans. We present this as supplemental to discussion of DARPA research into bat-borne coronaviruses. Note that:
- The virus appears to have been a bat virus and the random mutations seen are unlikely to be natural: ” . . . . What are the odds that a random bat virus had exactly the right combination of traits to effectively infect human cells from the get-go, and then jump into an unsuspecting person? ‘Very low,’ [Kristian] Andersen [of the Scripps Research Translational Institute] says . . . . ”
- The SARS-CoV‑2 (Covid-19) virus is unusual in that it infects both the upper and lower respiratory tracts. The ‘spike’ part of the SARS-CoV‑2 virus is unusually good at latching into a protein called ACE2 which is found on the exterior of the cells in human airways. This ability appears to be fundamental to the virus’s ability to infect the upper respiratory tract. The virus appears to infect the upper airways first and then, as cells in them die and are sloughed off, it makes its way down to the lower respiratory tract and lungs where the deadly infections occur. This sequential pattern of infecting the upper respiratory tract prior to making its way down to the lungs enables it to silently spread asymptomatically before turning more lethal in the lower respiratory tract.
- We note that the ACE2 protein appears to manifest more heavily in the lung tissue of East-Asians. As indicated in the Whitney Webb article, genetic modification has been envisioned as applicable to biological warfare to create “ethno-specific” biological weapons.
- Another key feature of the virus’s ability to infect humans concerns a protein bridge connecting two halves of the virus’s spike. Activation of this spike causes the virus injects its nucleic acid into the cell. Activating the spike requires the cleavage of a protein bridge connecting the two halves of the spike. That cleavage is precipitated by the enzyme furin which is ubiquitous in human cells. In contrast, the coronavirus which caused SARS had a protein bridge that was less likely to be cleaved. SARS-CoV‑2 first latches onto to human upper airway cells and, once there, has the protein bridge linking the halves of the spike severed by the furin enzyme.
- Perhaps the most notable observation made about this virus thus far: it doesn’t appear to be mutating in evolutionarily significant ways. Of the 100-plus mutations observed in the virus so far, none has emerged as evolutionarily dominant–unusual for a virus that only recently jumped to humans. and has spread prolifically. It’s as though the virus is already evolutionarily optimized for spreading among humans and there are no ‘gain-of-fuction’ mutations left for it acquire. As Lisa Gralinski, a coronavirus expert at the University of North Carolina Chapel Hill, described it, “The virus has been remarkably stable given how much transmission we’ve seen . . . . there’s no evolutionary pressure on the virus to transmit better. It’s doing a great job of spreading around the world right now.”
- Gralinsky works closely with Ralph Baric’s lab. Recall that Baric is the researcher who constructed a chimeric virus out of a SARS virus and horseshoe bat coronavirus in 2015. When Gralinski observes that the virus wouldn’t feel any evolutionary pressure to spread because it’s already doing such a good job that is VERY significant. Evolution doesn’t stop just because the status quo of an organism is already effective. A mutation allowing the virus to spread even more readily would be expected. And normally such an event does happen. But it hasn’t happened so for SARS-CoV‑2 because it is already at something of a “coronavirus evolutionary peak”.
In addition, an article in Science Direct characterizes the advent of the furin-like cleavage site as a “gain-of-function” phenomenon. “Gain of Function” is a mechanism of action of an “Enhanced Potential Pandemic Pathogen.” “. . . . Strikingly, the 2019-nCoV S‑protein sequence contains 12 additional nucleotides upstream of the single Arg↓ cleavage site 1 (Fig. 1, Fig. 2) leading to a predictively solvent-exposed PRRAR↓SV sequence, which corresponds to a canonical furin-like cleavage site (Braun and Sauter, 2019; Izaguirre, 2019; Seidah and Prat, 2012). This furin-like cleavage site, is supposed to be cleaved during virus egress (Mille and Whittaker, 2014) for S‑protein “priming” and may provide a gain-of-function to the 2019-nCoV for efficient spreading in the human population compared to other lineage b betacoronaviruses. This possibly illustrates a convergent evolution pathway between unrelated CoVs. Interestingly, if this site is not processed, the S‑protein is expected to be cleaved at site 2 during virus endocytosis, as observed for the SARS-CoV. . . .”
1. “Why the Coronavirus Has Been So Successful” Ed Yong; The Atlantic; 03/20/2020
One of the few mercies during this crisis is that, by their nature, individual coronaviruses are easily destroyed. Each virus particle consists of a small set of genes, enclosed by a sphere of fatty lipid molecules, and because lipid shells are easily torn apart by soap, 20 seconds of thorough hand-washing can take one down. Lipid shells are also vulnerable to the elements; a recent study shows that the new coronavirus, SARS-CoV‑2, survives for no more than a day on cardboard, and about two to three days on steel and plastic. These viruses don’t endure in the world. They need bodies.
But much about coronaviruses is still unclear. Susan Weiss, of the University of Pennsylvania, has been studying them for about 40 years. She says that in the early days, only a few dozen scientists shared her interest—and those numbers swelled only slightly after the SARS epidemic of 2002. “Until then people looked at us as a backward field with not a lot of importance to human health,” she says. But with the emergence of SARS-CoV‑2—the cause of the COVID-19 disease—no one is likely to repeat that mistake again.
To be clear, SARS-CoV‑2 is not the flu. It causes a disease with different symptoms, spreads and kills more readily, and belongs to a completely different family of viruses. This family, the coronaviruses, includes just six other members that infect humans. Four of them—OC43, HKU1, NL63, and 229E—have been gently annoying humans for more than a century, causing a third of common colds. The other two—MERS and SARS (or “SARS-classic,” as some virologists have started calling it)—both cause far more severe disease. Why was this seventh coronavirus the one to go pandemic? Suddenly, what we do know about coronaviruses becomes a matter of international concern.
The structure of the virus provides some clues about its success. In shape, it’s essentially a spiky ball. Those spikes recognize and stick to a protein called ACE2, which is found on the surface of our cells: This is the first step to an infection. The exact contours of SARS-CoV‑2’s spikes allow it to stick far more strongly to ACE2 than SARS-classic did, and “it’s likely that this is really crucial for person-to-person transmission,” says Angela Rasmussen of Columbia University. In general terms, the tighter the bond, the less virus required to start an infection.
There’s another important feature. Coronavirus spikes consist of two connected halves, and the spike activates when those halves are separated; only then can the virus enter a host cell. In SARS-classic, this separation happens with some difficulty. But in SARS-CoV‑2, the bridge that connects the two halves can be easily cut by an enzyme called furin, which is made by human cells and—crucially—is found across many tissues. “This is probably important for some of the really unusual things we see in this virus,” says Kristian Andersen of Scripps Research Translational Institute.
For example, most respiratory viruses tend to infect either the upper or lower airways. In general, an upper-respiratory infection spreads more easily, but tends to be milder, while a lower-respiratory infection is harder to transmit, but is more severe. SARS-CoV‑2 seems to infect both upper and lower airways, perhaps because it can exploit the ubiquitous furin. This double whammy could also conceivably explain why the virus can spread between people before symptoms show up—a trait that has made it so difficult to control. Perhaps it transmits while still confined to the upper airways, before making its way deeper and causing severe symptoms. All of this is plausible but totally hypothetical; the virus was only discovered in January, and most of its biology is still a mystery.
The new virus certainly seems to be effective at infecting humans, despite its animal origins. The closest wild relative of SARS-CoV‑2 is found in bats, which suggests it originated in a bat, then jumped to humans either directly or through another species. (Another coronavirus found in wild pangolins also resembles SARS-CoV‑2, but only in the small part of the spike that recognizes ACE2; the two viruses are otherwise dissimilar, and pangolins are unlikely to be the original reservoir of the new virus.) When SARS-classic first made this leap, a brief period of mutation was necessary for it to recognize ACE2 well. But SARS-CoV‑2 could do that from day one. “It had already found its best way of being a [human] virus,” says Matthew Frieman of the University of Maryland School of Medicine.
This uncanny fit will doubtlessly encourage conspiracy theorists: What are the odds that a random bat virus had exactly the right combination of traits to effectively infect human cells from the get-go, and then jump into an unsuspecting person? “Very low,” Andersen says, “but there are millions or billions of these viruses out there. These viruses are so prevalent that things that are really unlikely to happen sometimes do.”
Since the start of the pandemic, the virus hasn’t changed in any obviously important ways. It’s mutating in the way that all viruses do. But of the 100-plus mutations that have been documented, none has risen to dominance, which suggests that none is especially important. “The virus has been remarkably stable given how much transmission we’ve seen,” says Lisa Gralinski of the University of North Carolina. “That makes sense, because there’s no evolutionary pressure on the virus to transmit better. It’s doing a great job of spreading around the world right now.”
There’s one possible exception. A few SARS-CoV‑2 viruses that were isolated from Singaporean COVID-19 patients are missing a stretch of genes that also disappeared from SARS-classic during the late stages of its epidemic. This change was thought to make the original virus less virulent, but it’s far too early to know whether the same applies to the new one. Indeed, why some coronaviruses are deadly and some are not is unclear. “There’s really no understanding at all of why SARS or SARS-CoV‑2 are so bad but OC43 just gives you a runny nose,” Frieman says.
Researchers can, however, offer a preliminary account of what the new coronavirus does to the people it infects. Once in the body, it likely attacks the ACE2-bearing cells that line our airways. Dying cells slough away, filling the airways with junk and carrying the virus deeper into the body, down toward the lungs. As the infection progresses, the lungs clog with dead cells and fluid, making breathing more difficult. (The virus might also be able to infect ACE2-bearing cells in other organs, including the gut and blood vessels.)
The immune system fights back and attacks the virus; this is what causes inflammation and fever. But in extreme cases, the immune system goes berserk, causing more damage than the actual virus. For example, blood vessels might open up to allow defensive cells to reach the site of an infection; that’s great, but if the vessels become too leaky, the lungs fill even more with fluid. These damaging overreactions are called cytokine storms. They were historically responsible for many deaths during the 1918 flu pandemic, H5N1 bird flu outbreaks, and the 2003 SARS outbreak. And they’re probably behind the most severe cases of COVID-19. “These viruses need time to adapt to a human host,” says Akiko Iwasaki of the Yale School of Medicine. “When they’re first trying us out, they don’t know what they’re doing, and they tend to elicit these responses.”
During a cytokine storm, the immune system isn’t just going berserk but is also generally off its game, attacking at will without hitting the right targets. When this happens, people become more susceptible to infectious bacteria. The storms can also affect other organs besides the lungs, especially if people already have chronic diseases. This might explain why some COVID-19 patients end up with complications such as heart problems and secondary infections.
But why do some people with COVID-19 get incredibly sick, while others escape with mild or nonexistent symptoms? Age is a factor. Elderly people are at risk of more severe infections possibly because their immune system can’t mount an effective initial defense, while children are less affected because their immune system is less likely to progress to a cytokine storm. But other factors—a person’s genes, the vagaries of their immune system, the amount of virus they’re exposed to, the other microbes in their bodies—might play a role too. In general, “it’s a mystery why some people have mild disease, even within the same age group,” Iwasaki says.
Coronaviruses, much like influenza, tend to be winter viruses. In cold and dry air, the thin layers of liquid that coat our lungs and airways become even thinner, and the beating hairs that rest in those layers struggle to evict viruses and other foreign particles. Dry air also seems to dampen some aspects of the immune response to those trapped viruses. In the heat and humidity of summer, both trends reverse, and respiratory viruses struggle to get a foothold.
Unfortunately, that might not matter for the COVID-19 pandemic. At the moment, the virus is tearing through a world of immunologically naive people, and that vulnerability is likely to swamp any seasonal variations. After all, the new virus is transmitting readily in countries like Singapore (which is in the tropics) and Australia (which is still in summer). And one recent modeling study concluded that “SARS-CoV‑2 can proliferate at any time of year.” “I don’t have an immense amount of confidence that the weather is going to have the effect that people hope it will,” Gralinski says. “It may knock things down a little, but there’s so much person-to-person transmission going on that it may take more than that.” Unless people can slow the spread of the virus by sticking to physical-distancing recommendations, the summer alone won’t save us.
. . . . Based on its genome sequence, 2019-nCoV belongs to lineage b of Betacoronavirus (Fig. 1A), which also includes the SARS-CoV and bat CoV ZXC21, the latter and CoV ZC45 being the closest to 2019-nCoV. . . .
. . . . Since furin is highly expressed in lungs, an enveloped virus that infects the respiratory tract may successfully exploit this convertase to activate its surface glycoprotein (Bassi et al., 2017; Mbikay et al., 1997). Before the emergence of the 2019-nCoV, this important feature was not observed in the lineage b of betacoronaviruses. However, it is shared by other CoV (HCoV-OC43, MERS-CoV, MHV-A59) harbouring furin-like cleavage sites in their S‑protein (Fig. 2; Table 1), which were shown to be processed by furin experimentally (Le Coupanec et al., 2015; Mille and Whittaker, 2014.
Strikingly, the 2019-nCoV S‑protein sequence contains 12 additional nucleotides upstream of the single Arg↓ cleavage site 1 (Fig. 1, Fig. 2) leading to a predictively solvent-exposed PRRAR↓SV sequence, which corresponds to a canonical furin-like cleavage site (Braun and Sauter, 2019; Izaguirre, 2019; Seidah and Prat, 2012). This furin-like cleavage site, is supposed to be cleaved during virus egress (Mille and Whittaker, 2014) for S‑protein “priming” and may provide a gain-of-function to the 2019-nCoV for efficient spreading in the human population compared to other lineage b betacoronaviruses. This possibly illustrates a convergent evolution pathway between unrelated CoVs. Interestingly, if this site is not processed, the S‑protein is expected to be cleaved at site 2 during virus endocytosis, as observed for the SARS-CoV. . . .
The Future: Technology, Theocracy and the Thousand Year Reich
Sure you’ve already seen these but on the off chance that you’ve not:
Tiergartenstrasse4 for the 21st century?:
https://www.usatoday.com/story/news/nation/2020/03/26/coronavirus-crisis-people-with-disabilities-discriminate/5082197002/
https://www.nytimes.com/2020/03/24/upshot/coronavirus-rationing-decisions-ethicists.html
“Capitalist colony collapse”:
https://www.cnbc.com/2020/03/18/bill-ackman-pleads-to-trump-to-increase-closures-to-save-the-economy-shut-it-down-now.html
Investor Bill Ackman urged President Donald Trump and corporate America in an impassioned plea on CNBC to shut down the country for 30 days to contain the fast-spreading coronavirus, calling it the only option to rescue the economy.
“What’s scaring the American people and corporate America now is the gradual rollout,” Ackman told Scott Wapner on “Halftime Report” on Wednesday. “We need to shut it down now. ... This is the only answer.”
“America will end as we know it. I’m sorry to say so, unless we take this option,” he said. Ackman added that if Trump saves the country from the coronavirus, he will get reelected in November.
Ackman urged U.S. companies to stop their buyback programs because “hell is coming.” The biggest U.S. banks have already halted repurchasing stocks to put their capital to use helping consumers and businesses.
Black swans and black eagles?
https://www.forbes.com/sites/kenrapoza/2020/01/10/dont-discount-a-black-swan-event-for-china/
https://www.cnn.com/2019/12/15/investing/stocks-week-ahead/index.html
@Peter Pandemic: There’s an interesting following controversy related to Bill Ackman’s CNBC appearance where he warned that “America will end as we know it” unless President Trump shuts the US economy down for 30 days to get the spread of COVID-19 under control: The markets started tanking even more aggressively during Ackman’s apocalyptic interview. CNBC’s Stephanie Fuuhle later chastised Ackman for being wildly irresponsible with his comments and causing the circuit-breakers to trigger. This prompted a number of observers to point out that Ackman’s firm, Pershing Square Capital, happened to have disclosed on March 3 that it had opened up a number of aggressive short positions in the market that were designed to profit from a destabilization of the credit markets. This led to accusations that Ackman decision to call into CNBC and make his apocalyptic comments was intended to further destabilize the markets and profit from those short positions.
Ackman defends himself against these accusations by suggesting that he had actually become bullish due to his belief that a US lockdown was coming soon and that this defeat the virus. It’s not exactly a compelling defense.
Ackman also pointed out that Pershing Square Capital had actually already started buying up stocks in areas like hotel and travel stocks as the market was declining. During that interview he warned that hotel stocks would go to zero if the 30 day lockdown didn’t happen soon. by pointing out that he was already starting to buy up the hotel stocks that had already been hammered, Ackman appeared to be arguing that he wouldn’t have had an incentive to drive down the market since his hedge fund was already long on the very types of stocks he was warning would “go to zero” during the CNBC call. It’s not exactly a compelling defense since going long on those stocks implies that the hedge fund thinks they’ll be going even higher in the future so there’s actually an incentive to temporarily drive the stocks even lower so you can buy them even cheaper. For example, let’s say the value of HotelX chain had fallen from $100/share to $80/share duing a period when Pershing Square Capital was buying the stock. That would suggest the fund expects HotelX’s stock to be above $100 at some point in the future. And if that’s the case, Pershing Square Capital would have had an incentive to drive HotelX’s stock down as low as possible to buy up more shares for even cheaper. Driving HotelX’s stock down to $50/share would only make it even more tempting a buy if you think it’s going to go back above $100, especially if you’re already shorting the markets and protecting against those losses.
But the big story here doesn’t really have to do with Pershing Square Capital. The big story is about just how wildly profitable those short positions were as an example of how much money someone could have if they made big bets on a large destabilization of the economy before it was clear this virus was going to shut down the global economy: Ackman’s firm made $2.6 billion on short positions that it spent $27 million on. That’s a ~100-fold return.
It sounds like, net, Pershing Square Capital’s short positions basically covered the losses it’s made on its long positions. At least for the time being. If the market recovers there’s presumably going to be quite a profit on those stocks the fund has been buying on the way down. But you have to wonder how many other firms out that didn’t simply cover their losses but actually made large net returns shorting the markets in a similar fashion
Ok, first, here’s an article where Ackman attempts to defend himself against accusations that he was intentionally driving down the market. Ackman asserts that, contrary to what everyone is saying, he was actually being bullish in his comments. Plus, since his fund was buying up stocks on the way down that means the accusations he was trying to drive down the market was absurd. So his warnings about hotel stocks “going to zero” were actually bullish because he was buying upon those very same plummeting stocks he was warning would go to zero Which is a pretty absurd defense but that’s what he’s arguing:
“Pershing Square Capital manager Bill Ackman defended his emotional CNBC appearance last week after his fund announced a few days later that it made more than $2 billion on bets against the markets. The investor warned in the interview that “hell is coming” and that hotel stocks could go to zero.”
“Hell is coming” and hotel stocks could go to zero, unless Trump imposes a 30 day lockdown. That was message 10 days ago during the CNBC interview. But the way Ackman describes it, he was actually bullish at the time and had started buying up cheap hotel stocks because he was confident the entire US would soon go into lockdown soon. And then he also notes that his fund had already unwound most, but not all, of its short positions by the time of the interview. It’s not exactly a compelling defense:
And now here’s an article that points out just how wildly profitable those short positions really were: $2.6 billion on $27 million. That’s how prescient the bet was that Pershing Square Capital made back in February. The specific bet was far ‘out of the money’ protection against investment-grade and high-yield bond indexes. So, basically, that $27 million was unlikely to make any money at all unless there was a large disruption in the corporate credit markets at which point they could be worth quite a bit. It was a high-payout/low-probabilty bet which means those shorts were going to be extra cheap. Implicitly, it also means the rest of the market was not betting on the level of financial upheaval that unfolded. That’s why the options were so cheap and what allowed for the 100-fold payout and why it’s now deemed to be a highly prescient bet.
In the case of Pershing Square Capital this bet is seen as being even more prescient than it would be for other hedge funds because Pershing Square almost exclusively makes long bets on a handful of holdings. That’s the fund’s general strategy: find seven or eight companies that Ackman has faith in and make $500-to-$1 billion investments in those companies. The fund isn’t known for taking short positions. But So you have to wonder just who else made similar out of the money bets wih 100-fold returns over the past month
“Most of the time Ackman’s fund, Pershing Square, is almost 100% long by way of an ultra-concentrated portfolio of large stock holdings. His current style is to find about seven-or-eight companies he believes strongly in and bet between $500 million and $1 billion on each.”
Ackman’s hedge fund is almost 100% long in ultra-concentrated positions in just seven or eight companies. That’s part of what made this short position unusual. But it was a position that was still just a tiny fraction of the fund’s $6.5 billion portfolio: only $27 million was spent on these far “out of the money” short positions that increased in value if the spread between low risk and high risk lending jumped. It was basically an economic doomsday bet that paid off:
And note it also sounds like Pershing invested in a new coronavirus antibody test kit company, Covaxx. Keep in mind that widespread antibody tests are actually extremely important for dealing with the current pandemic and allowing economies to normalize. It’s those kinds of tests that will allow us to know who has been exposed to the virus and hopefully has immunity. So if Covaxx does end up developing a workable test that becomes part of the solution...well, at least in that case it will be a decent way to profit from this economic nightmare:
But also keep in mind that being an investor in a company that’s working to provide one of the key components of reopening economies is possibly going to provide Pershing Square Capital future opportunities for massive “out of the money” bets of this nature. If Covaxx was to announce soon that it has an approve antibody test that could be delivered soon at scale, that announcement alone would probably move the markets dramatically upwards. What kinds of options trading might give 100-fold returns following that kind of announcement? We can probably be sure someone at Pershing Square Capital is trying to answer that question.
So the take away message from this whole story is that when we have historic market swings like we’ve seen, massive fortunes can be made in short order. Some of those massive fortunes might come from luck, others from keen foresight, and are inevitably going to involve insider information and knowledge of key upcoming events and policies. It’s a particularly important aspect of this crisis to keep in mind given that we have the ’emoluments clauses don’t apply to us’ Trump administration that’s going to be making a lot of those key market-moving decisions. What kinds of insights about upcoming market-moving policies might notorious short-seller J. Kyle Bass receive from his close friend Tommy Hicks Jr. who just happens to be Donald Trump Jr.‘s hunting buddy? Who knows, but given that the coronavirus pandemic was preceded by a pandemic of epic corruption with the US ruling class that has culminated in the presidency of someone like Donald Trump, these are the kinds of questions we unfortunately need to be asking at the same time we’re asking the basic question of how to deal with this pandemic. Massive overnight fortunes predicated on insider knowledge and the crafting of sober pandemic responses aren’t a great mix.
Why was the federal ban on production of lethal viruses lifted in 2017? https://www.nytimes.com/2017/12/19/health/lethal-viruses-nih.html
Why was funding to CDC personnel assigned to China cut in 2018?
https://mobile.twitter.com/JuddLegum/status/1232051346796371968
Was there an unusual spike in livestock sales from USDA to China since early 2018 corresponding to the beginning of the “trade war”?
Is it possible to take a genetically modified virus, then generationally harvest and mutate “natural” genes? https://www.sciencemag.org/news/2011/11/scientists-brace-media-storm-around-controversial-flu-studies#
Biological warfare agents are mostly invisible to the human eye and naturally present in the environment. One of the advantages of using biological warfare could be “an optimal death to cost ratio; they are virtually undetectable; and they offer the potential for mass panic.”56 This is a positive motivation for nations, groups, and individuals to pursue genetically engineered pathogens as a weapon of choice. *Biological warfare attacks may resemble a natural disease outbreak phenomenon and it would be very difficult to trace back to the source, thereby discounting the perpetrator’s actions.* BIOTECHNOLOGY: GENETICALLY ENGINEERED PATHOGENS Lt Col Joel Almosara, BSC, USAF June 2010
Two breeches of containment at Ft. Detrick. [This could have been a related ‘warning — something big is coming’ type event]
https://www.military.com/daily-news/2019/11/24/cdc-inspection-findings-reveal-more-about-fort-detrick-research-suspension.html
According to a Georgetown University, and Erasmus Medical Center University Netherlands study the virus may have originated as early as 18 September 2019 and not of “wet market” origin.
Then we have Steve Bannon’s increasingly hostile regime change rhetoric around this time; and more recently, Bill Gates’ maniacal laughter on CNN. But I’m sure you’ve got that covered.
https://www.bbc.com/news/world-us-canada-52194018
Stark statistics from Chicago health officials have underscored the heavy toll of coronavirus on black Americans.
Black Chicagoans account for half of all coronavirus cases in the city and more than 70% of deaths, despite making up 30% of the population.
Other cities with large black populations, including Detroit, Milwaukee, New Orleans and New York, have become coronavirus hotspots.
The US has recorded nearly 370,000 virus cases and almost 11,000 deaths.
Globally there have been nearly 75,000 deaths and more than 1.3m cases total.
What do Chicago’s statistics show?
As of 5 April, 1,824 out of Chicago’s 4,680 confirmed Covid-19 cases were black residents, said city officials on Monday.
That compared with 847 white, 478 Hispanic and 126 Asian Chicagoans.
Chicago has seen a total of 98 deaths as of Sunday, with 72% of them black residents.
The disparity is reflected across the state, where black people account for 41% of Covid-19 deaths, despite making up 14% of the population of Illinois.
Chicago public health commissioner Dr Allison Arwady told reporters that black city residents already lived on average about 8.8 years less than their white counterparts.
Mayor Lori Lightfoot said the coronavirus was “devastating black Chicago”.
She said city inspectors would be sent into shops to ensure everyone was adhering to social distancing guidelines.
Mayor Lightfoot also raised the possibility of curfews in areas where people gathered outside liquor stores, reports the Chicago Sun-Times.
What’s the picture nationally?
Though the coronavirus has been called the “great equalizer”, data suggests that vulnerability to the infection may vary by neighbourhood. [ed. note: It’s curious that they use ‘neighborhood’ while the entire article focuses on “race”.]
In Michigan, African Americans make up 14% of the population, but they account for 33% of the coronavirus cases and 41% of deaths, figures from the state health department showed on Monday.
White residents account for about 23% of recorded cases in Michigan and 28% of deaths, according to the data.
Detroit, Michigan, is about 80% black, and the city together with its surrounding suburbs accounts for around 80% of confirmed coronavirus cases.
A similar disparity has emerged in Milwaukee, Wisconsin, one of the most segregated cities in the US.
African Americans made up almost half of Milwaukee Country’s nearly 1,000 cases as of last Friday and 81% of its 27 deaths, despite black people accounting for 26% of the population there, according to a study by ProPublica.
Some 40% of Louisiana’s coronavirus deaths have occurred in the New Orleans area, where the majority of residents are black.
Health officials have previously said the Big Easy’s residents suffer from rates of obesity, diabetes and hypertension that are higher than the national average, making them more vulnerable to Covid-19.
What’s behind the disparity in Chicago?
Mayor Lightfoot said diabetes, heart disease and respiratory illness were “really prevalent” in black communities.
Dr Arwady told reporters that even if everyone in the city did have access to a doctor, “we would still see significant health disparities because of food deserts and lack of walkable streets”.
Dr Cameron Webb, an African-American physician who is running for Congress in the US state of Virginia, told BBC News that US racial and economic disparities were being amplified by the pandemic.
“It really exposes our society’s fault lines,” he said.
Alderman Jason Ervin, who chairs Chicago council’s black caucus, told the Chicago Tribune that “rates of non-compliance in some parts of the city with the stay-at-home orders” might also be contributing to the statistics.
THIS IS WHAT PRESIDENT TOXIC DUMP IS DOING TO DESTROY THE BLUE STATES BY ONLY HELPING ONLY THE RED STATES IN THIS PANDEMIC.
Hospitals say feds are seizing masks and other coronavirus supplies without a word
https://www.latimes.com/politics/story/2020–04-07/hospitals-washington-seize-coronavirus-supplies
10,000 Cases And 500 Deaths In Africa. Health Officials Say It’s Just The Beginning
April 8, 20206:27 PM ET
Pien Huang
Kola Sulaimon/AFP via Getty Images
Coronavirus case counts are rising exponentially in Africa. Since the continent saw its first case, in Egypt in mid-February, some 10,000 cases and 500 deaths have been confirmed.
Public health officials think this is just the beginning, and they worry that the situation in the coming weeks will get much worse. “COVID-19 has the potential not only to cause thousands of deaths, but to also unleash economic and social devastation,” Dr. Matshidiso Moeti, WHO regional director for Africa, said in a statement Wednesday.
There are several reasons why health officials are especially concerned about the impact of COVID-19 in African countries.
First, countries in sub-Saharan Africa carry some of the world’s heaviest burdens of serious underlying conditions such as HIV, which limits immune function, and tuberculosis, which often scars the lungs. Malnutrition compromises the health of more than 50 million children in the region.
Then there’s the limited access to quality care. Numbers vary by country, but on average across the region, there’s about one doctor and five nurses for every 5,000 people. A consult with a doctor could be far away and prohibitively expensive.
And when it comes to specialized equipment like ventilators that can help severely ill patients breathe, there just aren’t enough of them. “We talk about surging to 75,000 ventilators in New York City, and yet we have whole countries that only have one or two ventilators,” says Joia Mukherjee, chief medical officer for the global health nonprofit Partners in Health.
“I fully expect that when [COVID-19] hits, if it hits in a big way in impoverished countries, it could have a four to five times higher mortality” than in other countries so far, Mukherjee says.
In Nigeria, public health officials are working to get local manufacturers to produce various types of ventilators, putting up prefabricated isolation centers and turning hotels and convention centers into hospital beds. Some 20,000 hospital beds will be added to Nigeria’s capacity by week’s end, says Dr. Adaeze Oreh, a senior official with the Nigerian Ministry of Health.
The primary strategy, though, is to try and prevent as many infections as possible. “We’ve seen the increase in the rates of spread across Africa,” Oreah says, “We are trying to be proactive in trying to stop that kind of massive spread in the communities.”
Last week, Nigeria locked down the cities of Lagos and Abuja, telling more than 20 million residents to stay at home.
That’s especially hard in a country where half the population is below the poverty line, and many people work every day to earn their daily bread.
But Nigeria is betting that the unchecked spread of COVID-19 would be worse.
https://www.npr.org/sections/coronavirus-live-updates/2020/04/08/830209940/10–000-cases-and-500-deaths-in-africa-health-officials-say-its-just-the-beginnin
OPINION/CHINA
A new cold war in Africa
Increasing tensions between China and the US will be detrimental to African prosperity and peace.
Mehari Taddele Maru by Mehari Taddele Maru
1 Jul 2019
https://www.aljazeera.com/indepth/opinion/cold-war-africa-190630102044847.html
Last week, the 12th US-Africa Business Summit, a high-level event attended by 11 African heads of state and government and some 1,000 business leaders, was held in Maputo, Mozambique. During the three-day event, US officials unveiled a $60bn investment agency which will seek to invest in low and middle-income countries, with a special focus on Africa.
The announcement came six months after National Security Advisor John Bolton presented the Trump administration’s “New Africa Strategy”. According to the document: “Great power competitors, namely China and Russia, are rapidly expanding their financial and political influence across Africa. They are deliberately and aggressively targeting their investments in the region to gain a competitive advantage over the United States.”
Although both China and Russia are mentioned, over the past few months, the US has demonstrated that it is mainly concerned about the former. In fact, it already appears that Africa is set to become yet another battleground for the escalating trade war between Beijing and Washington.
With increasing foreign military presence and growing diplomatic tensions, the continent is already witnessing the first signs of an emerging new cold war. And just like the previous one devastated Africa, fuelling wars and forcing African governments to make economic choices not in their best interests, this one will also be detrimental to African development and peace.
Economic war
China’s approach to Africa has always been trade oriented. The continent became one of the top destinations for Chinese investment after Beijing introduced the so-called “Go Out” policy in 1999 which encouraged private and state-owned business to seek economic opportunities abroad.
As a result, Chinese trade with Africa has increased 40-fold over the past two decades; in 2017, it stood at $140bn. Between 2003 and 2017, Chinese foreign direct investment (FDI) flows have also jumped more close to 60-fold to $4bn a year; FDI stocks stand at $43bn — a significant part of which has gone to infrastructure and energy projects.
China has significantly expanded African railways, investing in various projects in Kenya, Ethiopia, Djibouti, Angola and Nigeria; it is currently building a massive hydropower plant in Angola and have built Africa’s longest railway connecting Ethiopia and Djibouti; it has built the headquarters of the African Union in Addis Ababa and the West African regional bloc ECOWAS in Abuja.
By contrast, for a long time the US has viewed Africa as a battlefield where it can confront its enemies, whether the Soviets during the Cold War, terrorists after 9/11 or now the Chinese. Washington has never really made a concerted effort to develop its economic relations with the continent.
As a result, trade between the US and Africa has decreased from $120bn in 2012 to just over $50bn today. US FDI flows have also slumped from $9.4bn in 2009 to around $330m in 2017. The new $60bn investment fund announced last week is a welcome initiative from the US but it will not be able to challenge Chinese economic presence on the continent. Just last year Chinese President Xi Jinping pledged $60bn too but dedicated it solely to investment in Africa.
The US has repeatedly accused China of using “debt to hold states in Africa captive to [its] wishes and demands” and has warned African states to avoid Chinese “debt diplomacy” which is supposedly incompatible with the independence of African nations and civil society and poses “a significant threat to US national security interests”.
Yet, Africa is only the fourth-biggest recipient of Chinese FDI after Europe (mainly Germany, UK and Netherlands), the Americas (mainly the US and Canada), and Asia. The US has also borrowed heavily from China; currently its debt to its rival stands at $1.12 trillion. By contrast, Africa owes China around $83bn.
Africans are fully aware of and concerned about high indebtedness, trade imbalances, the relatively poor quality of Chinese goods and services and Beijing’s application of lower standards of labour and environmental practices. But many do not share the American perspective that their economic relationship with China is to their detriment and rather see it as an opportunity that provides much-needed unconditional funding and that takes into account local priorities.
As Djibouti’s President Ismail Omar Guelleh has pointed out, “The reality is that no one but the Chinese offers a long-term partnership.”
The pressure the US is currently exerting on African countries to move away from partnerships with China could hurt African economies. It could force African countries into making choices that are not in their best economic interests and miss out on important development projects or funding.
Meanwhile, the US-China trade war is already affecting the continent. According to the African Development Bank, it could cause as much as a 2.5 percent decrease in GDP for resource-intensive African economies and a 1.9 percent dip for oil-exporting countries.
Militarisation
The escalating tensions between the US and China could also end up threatening the security of the continent. Both countries are militarily involved in Africa.
Over the past 15 years, the Chinese People’s Liberation Army has been engaged in a number of security missions across the continent, making modest auxiliary troop contributions to peacekeeping operations in Sudan, South Sudan, Liberia, Mali and the Democratic Republic of Congo. It has also contributed millions of dollars of peacekeeping equipment to the African Union Mission in Somalia and provided significant funding to the Intergovernmental Authority on Development for its mediation in South Sudan.
In 2017, the first Chinese overseas military base was opened in Djibouti. The facility, which currently hosts some 400 staff and troops, and has the capacity to accommodate 10,000, is officially supposed to provide support for the ongoing anti-piracy operations of the Chinese navy, but it also plays a role in securing maritime routes, part of the Belt and Road Initiative. There has also been speculation that this is the first of a number of planned bases meant to secure Chinese interests in Africa.
China’s military presence in Africa, however, pales in comparison to that of the US. Over the past few years, US Africa Command has run some 36 different military operations in 13 African countries, including Burkina Faso, Cameroon, Central African Republic, Chad, Democratic Republic of Congo, Kenya, Libya, Mali, Mauritania, Niger, Somalia, South Sudan and Tunisia. It has more than 7,000 troops deployed on the continent.
It has a large base in Djibouti — the biggest and only permanent US military base in Africa — but it also runs at least 34 other military outposts scattered across the west, east and north of the continent where US troops are deployed and military operations (including drone attacks) are launched from.
The US also directly supports the armies of Egypt, Nigeria, Ethiopia, Mali, Niger and others as well as the G5 Sahel force tasked with counterterrorism.
While a direct confrontation between US and Chinese forces in Africa is unlikely, their growing presence is becoming an increasingly destabilising factor. Already Washington’s strategy to contain Chinese influence over Africa is playing out at different conflict and social upheaval hotspots across the continent. The fallout of the US-Chinese competition is particularly apparent in the strategic Red Sea region, through which passes one of the most important maritime routes.
Countries in the region are not only feeling growing US and Chinese pressure to take one side or the other, but are also increasingly exposed to outside interference by various regional powers.
Growing regional tensions
Djibouti has recently found itself at the centre of US-Chinese diplomatic confrontation. Being a host to military bases of both superpowers, the small country has had to play a difficult balancing game.
In 2018, Djibouti seized control of its Doraleh Container Terminal from the Emirati company DP World, claiming its operation of the facility was threatening its sovereignty. The Djibouti authorities had feared that the UAE’s investment in the nearby Port of Berbera in the autonomous Somali region of Somaliland could challenge its position as the main maritime hub for Ethiopia’s large economy.
Its decision to terminate the contract with DP World, however, triggered a sharp reaction from Washington, a close Emirati ally. The Trump administration fears that Djibouti could hand over control of the terminal to China.
Bolton has warned: “Should this occur, the balance of power in the Horn of Africa — astride major arteries of maritime trade between Europe, the Middle East, and South Asia — would shift in favour of China. And, our US military personnel at Camp Lemonnier could face even further challenges in their efforts to protect the American people.”
Djibouti was forced to declare publicly that it would not allow China to take over the terminal but that has not assuaged US fears. Ever since, the US sought to secure a possible alternative location for its African military base: neighbouring Eritrea.
It encouraged regional actors, including Saudi Arabia and the UAE, to pull Eritrea out of its decades-long isolation. In a matter of months, long-time enemies Ethiopia and Eritrea concluded a peace agreement to end their 20-year-old cold conflict, while the UN lifted sanctions on Asmara. As a result, Eritrea could emerge as a strategic rival to Djibouti, offering its coast for foreign military and economic facilities. The UAE, for example, has already set up a military base near the port of Assab.
Sudan, to the north, has also been the battleground of the ongoing superpower turf war. China had been a long-term supporter of President Omar al-Bashir. Under his rule, Beijing came to dominate its oil industry, buying some 80 percent of its oil and thus providing Khartoum with much-needed cash to wage war against various rebel groups. It was also one of the few countries, along with Russia, that would break the UN arms embargo and sell weapons to al-Bashir’s regime.
After South Sudan gained independence in 2011, China continued to be a close partner of the Sudanese regime, remaining its main trading partner. Sudan in fact became the biggest beneficiary of the $60bn Africa investment package China pledged in 2018, having some $10bn in Chinese debt written off. The Chinese government also made a lot of plans to develop facilities in Port Sudan, where it already operates an oil terminal. Qatar and Turkey also signed deals with al-Bashir for various facilities in the port city.
When mass protests erupted in December last year, Beijing stood by al-Bashir, who it saw as the main guarantor of stability in the country, which falls on strategic routes, part of its Belt and Road Initiative.
Meanwhile, the US had repeatedly demonstrated that it did not want al-Bashir running for another term. His removal was approved in Washington, which has since appeared to back the interests of Saudi Arabia and the UAE in the country.
The two Gulf states currently hope to install another strongman sympathetic to their regional politics, who would maintain Sudan’s participation in the war in Yemen and curb Turkish and Qatari influence. At this point, it seems China is at risk of being sidelined by the significant sway the UAE and Saudi Arabia have with Sudan’s Transitional Military Council (TMC).
Apart from Djibouti and Sudan, various other countries in the region have felt the consequences of the US bid to contain China. This political confrontation has also added to the already rising tensions between other players in the region, including Egypt, Gulf countries, Iran and Turkey.
The Trump administration has particularly favoured Emirati, Saudi and Egyptian interests which have emboldened these three countries in their efforts to shape regional dynamics to their advantage.
Thus, in the long-term, given the pre-existing faultlines and conflicts in the region, the US-China cold war could have a detrimental effect, not only on its economy but also on its security.
At this point, to preserve its interests and its peace, Africa has only one option: to reject pressures to swear allegiance to either of the two powers. African countries should uphold their sovereignty in policy and decision-making and pursue the course that is in the best interests of their nations.
If the US wants to compete with China on the continent, it should do so in good faith. It can gain a competitive advantage by offering African countries better, more credible and principled alternatives to those put forward by China. But that can only happen if the US develops a strategy that focuses on Africa itself, not on containing and undermining the business of a third party.
The views expressed in this article are the author’s own and do not necessarily reflect Al Jazeera’s editorial stance.
ABOUT THE AUTHOR
Mehari Taddele Maru Mehari Taddele Maru
Dr Mehari Taddele Maru is a scholar of peace and security, law and governance, and human rights and migration issues.
@ drmehari
OPINION/CORONAVIRUS PANDEMIC
Medical colonialism in Africa is not new
Remarks about testing coronavirus drugs on Africans part of pattern where some bodies are dehumanised, others protected.
Karsten Noko by Karsten Noko
8 Apr 2020
https://www.aljazeera.com/indepth/opinion/medical-colonialism-africa-200406103819617.html
Last Wednesday, a French doctor caused controversy when he proposed that vaccines for the COVID-19 pandemic be tried on Africans because they lack masks and other personal protective equipment.
By Friday, after widespread accusations of racism, he was forced to apologise for what he then called his “clumsily expressed” remarks.
But the type of thinking exposed by his words is nothing new. Neither is it exceptional to this doctor. It is part of a trend that for generations has seen the dehumanising of some people because of the superiority complex of others.
In early March 2020, as coronavirus cases began an exponential growth curve, some people asked why African countries were not recording higher numbers of COVID-19 cases.
The tone of these queries had the impact of questioning if Africans were somehow genetically immune to the new virus. But why would this question even be raised if we know the biological set-up of all humans is similar?
The dehumanisation of people from the Global South was one of the driving forces behind the slave trade and colonialism. It is inconceivable that anyone could fathom the thought of trading in human beings unless they regarded that person as inferior.
Joseph Conrad, in his book Heart of Darkness writing in 1899, grappled with the question of whether the people he had met in Africa were really human. He opines: “No they were not inhuman. Well, you know, that was the worst of it — this suspicion of their not being inhuman.”
It is the naturalness of someone even posing such questions that cements these ideas; the acceptance of a “second-class humanity” that allows the dispossession and trade in human lives to be so easily explained away.
Dehumanised in life, fetishised in death
Saartjie Baartman, or Sarah Baartman as she is commonly called, was a Khoikhoi woman born in what is present-day South Africa. In 1810, she was abducted and taken to Europe where she was turned into an object of an exhibition for European audiences because of her body and her perceived large buttocks.
Many of the audience members came to see her because they thought that she was not human. When she died, a French surgeon dissected her body and concluded that she had ape-like features.
In 2002, the South African government finally managed to retrieve her body from the French National Museum in Paris where her remains had stood in exhibit for more than 150 years. Baartman was dehumanised in life, and fetishised in death, in pursuit of a scientific theory that sought to draw biological and scientific differences between white and black people.
Two centuries after Baartman’s death, the dehumanisation of certain races is not put on display in such an obvious way. But the trend of using some bodies for the benefit of others continues in different forms.
In the 2014 West Africa Ebola outbreak, for instance, more than 250,000 blood samples were collected from patients by laboratories in France, the UK and the US among others — often with no informed consent — as patients underwent testing and treatment for Ebola, to help researchers create new vaccines and medicines.
Today, South African, French and American researchers refuse to disclose how many of these samples they still hold, citing “national security” as an excuse. As one patient remarked, “They are using it to make research, make billions of dollars … That medicine they produce will not be free. It will be something that you will sell.”
Because the affected communities are poorer and people lack the information that will help protect them from such researchers, their samples are taken, and used at will to produce medicine for people who will pay for treatment — often without their knowledge.
A long history of medical trials
In 1996, Kano State in Nigeria was the epicentre of a huge meningitis outbreak. At the time, Pfizer, one of the largest research pharmaceutical companies in the world, decided to conduct clinical trials to test a drug it was developing.
Pfizer neglected to acquire informed consent from the parents of the patients, who were, anyway, too stressed to make rational decisions. It was only in 2009 that Pfizer settled out-of-court and paid $75 million to the Kano State government and $175,000 to the parents of four of the children who had died during the outbreak and clinical trials.
Although Pfizer argued in its legal defence that the children had been killed by the disease and not their drugs, the out-of-court settlement robbed us of an opportunity to have the medical facts established before a court of law.
Similar trials and tests were conducted in Zimbabwe in 1994 with the drug AZT — projects funded by the US-based CDC and NIH resulted in adverse effects for patients. In Namibia in the early 1900s, sterilisation tests were done on Herero women by German doctors who sought to provide “scientific” backing to ban mixed-race marriages.
Researchers know only too well that conducting such research in the Global North is more onerous and has too much red tape. In the Global South, big pharmaceuticals, often with the complicit support of bribed government officials, have it easy.
As they chase huge profits, the lives of often uninformed patients are far from a main consideration. For many people from the affected communities, the work of researchers is clearly meant to serve the financial interests of those who pretend to be kind-hearted or philanthropic.
What remains curious is how diseases like TB, malaria and hepatitis continue to kill millions every year, and yet the amount of energy and resources being put into eradicating them is nowhere near the efforts against COVID-19 and Ebola. It would appear that certain diseases get more attention because of the people they affect or potentially threaten.
Imagined suspicion?
In 2011, the CIA, under the cover of an international NGO, collected DNA samples in Pakistan in a fake vaccination campaign as they trailed Osama bin Laden. The move had the impact of straining an already complicated relationship between the US and Pakistan, but it also had the much wider impact of providing proof to the sceptics who always suspected there was a hidden agenda in the delivery of medical services from the Global North.
In the race to contain the coronavirus pandemic, the last thing overburdened health practitioners need is some so-called “clumsy” remarks from a fellow medic.
But when a French doctor suggests that Africa must be included as part of a vaccine trial, it is not surprising that suspicions and anger are reignited — especially when there are relatively fewer cases on the continent than there are in Europe and the US.
Given the history of medical colonialism in Africa, and the current realities around the spread of COVID-19, how do we begin to persuade anyone that those remarks were something other than the continuation of a racist, dehumanising approach that sees some humans as expendable?
How are Africans expected to not react to yet another attempt to use them as guinea pigs to develop drugs that would serve the Global North, whose well-funded health systems can afford the hefty-priced life-saving medication that Africans themselves often die without?
The views expressed in this article are the author’s own and do not necessarily reflect Al Jazeera’s editorial stance.
ABOUT THE AUTHOR
Karsten NokoKarsten Noko
Karsten Noko is a Zimbabwean lawyer and humanitarian working across sub-Saharan Africa.
@ KarstenNoko
Coronavirus destroys lungs. But doctors are finding its damage in kidneys, hearts and elsewhere.
By
Lenny Bernstein,
Carolyn Y. Johnson,
Sarah Kaplan and
Laurie McGinley
April 15, 2020 at 7:00 AM EDT
The new coronavirus kills by inflaming and clogging the tiny air sacs in the lungs, choking off the body’s oxygen supply until it shuts down the organs essential for life.
But clinicians around the world are seeing evidence that suggests the virus also may be causing heart inflammation, acute kidney disease, neurological malfunction, blood clots, intestinal damage and liver problems. That development has complicated treatment for the most severe cases of covid-19, the illness caused by the virus, and makes the course of recovery less certain, they said.
The prevalence of these effects is too great to attribute them solely to the “cytokine storm,” a powerful immune-system response that attacks the body, causing severe damage, doctors and researchers said.
Almost half the people hospitalized because of covid-19 have blood or protein in their urine, indicating early damage to their kidneys, said Alan Kliger, a Yale University School of Medicine nephrologist who co-chairs a task force assisting dialysis patients who have covid-19.
Even more alarming, he added, is early data that shows 14 to 30 percent of intensive-care patients in New York and Wuhan, China — birthplace of the pandemic — have lost kidney function and require dialysis, or its in-hospital cousin, continuous renal replacement therapy. New York intensive care units are treating so much kidney failure, he said, they need more personnel who can perform dialysis and have issued an urgent call for volunteers from other parts of the country. They also are running dangerously short of the sterile fluids used to deliver that therapy, he said.
“That’s a huge number of people who have this problem. That’s new to me,” Kliger said. “I think it’s very possible that the virus attaches to the kidney cells and attacks them.”
But in medicine, logical inferences often do not prove true when research is conducted. Everyone interviewed for this story stressed that with the pandemic still raging, they are speculating with much less data than is normally needed to reach solid clinical conclusions.
Many other possible causes for organ and tissue damage must be investigated, they said, including respiratory distress, the medications patients received, high fever, the stress of hospitalization in an ICU and the now well-described impact of cytokine storms.
Still, when researchers in Wuhan conducted autopsies on people who died of covid-19, they found nine of 26 had acute kidney injuries and seven had particles of the coronavirus in their kidneys, according to a paper by the Wuhan scientists published April 9 in the medical journal Kidney International.
“It does raise the very clear suspicion that at least a part of the acute kidney injury that we’re seeing is resulting from direct viral involvement of the kidney, which is distinct from what was seen in the SARS outbreak in 2002,” said Paul M. Palevsky, a University of Pittsburgh School of Medicine nephrologist and president-elect of the National Kidney Foundation.
One New York hospital recently had 51 ICU patients who needed 24-hour kidney treatment but had just 39 machines to do it, he said. The hospital had to ration the care, keeping each patient on the therapy less than 24 hours a day, he said.
The virus also may be damaging the heart. Clinicians in China and New York have reported myocarditis, an inflammation of the heart muscle, and, more dangerous, irregular heart rhythms that can lead to cardiac arrest in covid-19 patients.
“They seem to be doing really well as far as respiratory status goes, and then suddenly they develop a cardiac issue that seems out of proportion to their respiratory issues,” said Mitchell Elkind, a Columbia University neurologist and president-elect of the American Heart Association. “This seems to be out of proportion to their lung disease, which makes people wonder about that direct effect.”
One review of severely ill patients in China found that about 40 percent suffered arrhythmias and 20 percent had some form of cardiac injury, Elkind said. “There is some concern that some of it may be due to direct influence of the virus,” he said.
The new virus enters the cells of people who are infected by latching onto the ACE2 receptor on cell surfaces. It unquestionably attacks the cells in the respiratory tract, but there is increasing suspicion that it is using the same doorway to enter other cells. The gastrointestinal tract, for instance, contains 100 times more of these receptors than other parts of the body, and its surface area is enormous.
“If you unfurl it, it’s like a tennis court of surface area — this tremendous area for the virus to invade and replicate itself,” said Brennan Spiegel, co-editor in chief of the American Journal of Gastroenterology.
In a subset of covid-19 cases, researchers have found, the immune system battling the infection goes into hyperdrive. The uncontrolled response leads to the release of a flood of substances called cytokines that, in excess, can result in damage to multiple organs. In some severely ill covid-19 patients, doctors have found high levels of a pro-inflammatory cytokine called interleukin‑6, known by the medical shorthand IL‑6.
The unfettered response, also called “cytokine release syndrome,” has long been recognized in other patients, including those with autoimmune diseases such as rheumatoid arthritis or in cancer patients undergoing certain immunotherapies.
For covid-19 patients, cytokine storms are a major reason that some require intensive care and ventilation, said Jeffrey S. Weber, deputy director of the Perlmutter Cancer Center at NYU Langone Medical Center.
“When your cytokines are systemically out of control, bad stuff happens,” he said. “It can be a complete disaster.” It isn’t clear why cytokine storms occur in some patients and not others, though genetic factors may play a role, some doctors say.
To treat cytokine storms, some doctors are using anti-IL‑6 drugs such as tocilizumab, which is approved for cancer patients who develop cytokine storms as a result of immunotherapy.
Another odd, and now well-known, symptom of covid-19 is loss of smell and taste. Claire Hopkins, president of the British Rhinological Society, said studies of patients in Italy and elsewhere have shown that some lose their sense of smell before they show signs of being sick.
“The coronavirus can actually attack and invade olfactory nerve endings,” Hopkins said. When these aroma-detecting fibers are disrupted, they can’t send odors to the brain.
Anosmia — the medical term for the inability to smell — was not initially recognized as a symptom of covid-19, Hopkins said. Doctors were so overwhelmed by patients with severe respiratory problems, she said, that “they didn’t ask the question.”
But subsequent data from a symptom-tracking app has shown that 60 percent of people later diagnosed with covid-19 reported losing their senses of smell and taste. About a quarter of participants experienced anosmia before developing other symptoms, suggesting it can be an early warning sign of infection.
Intriguingly, Hopkins said, people who lose their sense of smell don’t seem to develop the same severe respiratory problems that have made covid-19 so deadly. But a very small number of patients have experienced confusion, low blood oxygen levels and even lost consciousness — a sign that the virus may have traveled along their olfactory nerve endings straight to the central nervous system.
“Why you get this different expression in different people, nobody knows,” she said.
There are also reports that covid-19 can turn people’s eyes red, causing pinkeye, or conjunctivitis, in some patients. One study of 38 hospitalized patients in Hubei province, China, found that a third had pinkeye.
But like many of the non-respiratory effects of the virus, this symptom may be relatively uncommon — and may develop only in people already severely ill. The fact that the virus has been found in the mucus membrane that covers the eye in a small number of patients, however, does suggest that the eye could be an entryway for the virus — and is one reason that face shields and goggles are being used to protect health-care workers.
The virus also is having a clear impact on the gastrointestinal tract, causing diarrhea, vomiting and other symptoms. One study found that half of covid-19 patients have gastrointestinal symptoms, and specialists have coined a Twitter hashtag, #NotJustCough, to raise awareness of them.
Studies suggest that patients with digestive symptoms will also develop a cough, but one may occur days before the other.
“The question is, is it kind of behaving like a hybrid of different viruses?” Spiegel said. “What we’re learning is, it seems anyway, that this virus homes in on more than one organ system.”
Reports also indicate that the virus can attack the liver. A 59-year-old woman in Long Island came to the hospital with dark urine, which was ultimately found to be caused by acute hepatitis. After she developed a cough, physicians attributed the liver damage to a covid-19 infection.
Spiegel said he has seen more such reports every day, including one from China on five patients with acute viral hepatitis.
A particular danger of the virus appears to be its tendency to produce blood clots in the veins of the legs and other vessels, which can break off, travel to the lung and cause death by a condition known as pulmonary embolism.
An examination of 81 patients hospitalized with pneumonia caused by covid-19 in Wuhan found that 20 had such events and that eight of them died. The peer-reviewed data was published online April 9 in the Journal of Thrombosis and Hemostasis.
Across New York City, blood thinners are being used with covid-19 patients much more than expected, said Sanjum Sethi, an interventional cardiologist and assistant professor of medicine at Columbia University’s Irving Medical Center.
“We’re just seeing so many of these events that we have to investigate further,” he said.
https://www.washingtonpost.com/health/coronavirus-destroys-lungs-but-doctors-are-finding-its-damage-in-kidneys-hearts-and-elsewhere/2020/04/14/7ff71ee0-7db1-11ea-a3ee-13e1ae0a3571_story.html
AFA #39:
https://spitfirelist.com/anti-fascist-archives/afa-39-the-world-will-be-plunged-into-an-abyss/
From the original 1982 version of “A Higher Form of Killing” is an excerpt from testimony before a House appropriations subcommittee which said:
Peer Reviewed Paper:
https://www.nature.com/articles/s41423-020‑0424‑9.pdf
Coronavirus Could Attack Immune System Like HIV by Targeting Protective Cells, Warn Scientists
April 12, 2020
https://www.scmp.com/news/china/society/article/3079443/coronavirus-could-target-immune-system-targeting-protective
@Mother Muckraker–
Thanks for this! I have heard casual discussion on not-very-credible forums about this dynamic, but this is a scholarly treatment.
Sheeeyit!
There are many and varied symptoms of infected people: heart trouble, clotting, skin rashes, kidney problems in addition to the respiratory symptoms.
As AIDS cued various types of illness by nuking the immune system, this, too might account for the varied immune reacions.
Note a very important Pterrafractyl contribution, noting that significant numbers of infected and recovered people showed very little antibody presence in their bloodstream.
That would make the DARPA-funded Moderna Inc.‘s messenger RNA vaccine problematic at best and worthless or counter-productive at worst.
Best,
Dave
@Dave and @Mother Muckraker: Regarding that previous study out of China that found the low (or undetectable) antibody levels in 30 percent of the recovered COVID-19 patients they tested, it’s worth noting that T cells play an important role in antibody production so it would be interesting to know if the patients with low antibody counts also had low T cell counts. The study found that the patients with low antibody levels skewed towards the younger patients, prompting the researchers to speculate that their bodies were fighting off the virus using the non-targeting parts of the immune system that don’t involve T‑Cells and antibodies. They also found that antibody levels rose with age, suggesting that the bodies of the elderly were more reliant on the targeted immune response that uses antibodies and T cells. So the ability of the virus to kill off T cells at the same time younger healthier immune systems can defeat the virus without relying on T cells might make this virus even more selectively deadly to the elderly and immunologically compromised than we previously recognized.
Now, regarding that research that found the virus attacks and kills T cells, it’s also worth noting how this finding might tie into other studies that have found the virus is capable of infecting and damaging a large number of organs like the heart, kidneys, blood vessels, but and brain. NOT just the lungs and respiratory tract. The researchers who found ability to infect T cells also discovered was that the virus doesn’t NEED a target cell to have high numbers of ACE2 receptors. The ACE2 receptor certainly helps because the virus is built to build to that receptor but they found cell lines expressing low levels of ACE2 still getting infected by SARS-CoV‑2. And guess what cell types don’t express high levels of ACE2: the T cells in their experiments that were getting infected. This led to their speculation that some other receptor is playing a role in mediating that membrane fusion step. Some other receptor that happens to be on the surface of T cells. This ability to infect cells without ACE2 receptors appears to be due to another features on the virus’s S‑protein...a protein that’s turning out to have a lot of ‘features’ in this virus!
Now, it’s worth noting that MERS can infect lymphocytes like T cells. MERS is a in the same genera as SARS-CoV‑2 (they’re both Beta coronaviruses) but a different lineage (MERS is linage C and SARS-CoV‑2 is B). The original SARS-CoV virus from 2003 — which is the most closely related to SARS-CoV‑2 genetically and in the B lineage — did not have this feature. A feature that turns out to crucial for the virus’s ability to attack and kill the part of the immune system the elderly rely on to kill the virus. So SARS-CoV‑2 wouldn’t be unique among human coronaviruses in this respect but it’s not a feature found in other B lineage viruses (<a href=””>like of like that cannonical furin cleavage site on the S‑protein).
Now, there is a bit of good new all this. As we’ll see in a paper published by this same research team a week earlier, they’ve been studying for year the part of the coronavirus that play a key role in this step in the delivery of the viral RNA payload into the cell. After the virus’s S‑protein binds to an ACE2 receptor (or perhaps another mystery receptor), the protein complex consisting of 6 helices — known as the six-helix bundle (6‑HB) — is formed and shifts in its conformation to interact with the target cell’s member. The formation and conformational shift of the 6‑HB bundle causes a fusion of the viral and cell membranes, allowing for the deposition of the viral RNA content in the cell. They’ve been studying this process for years and have previously actually developed drugs to block the interaction of the 6‑HB structure with the target cell membrane which stops the replication of the virus. More recently, the team compared SARS-CoV-2’s 6‑HB bundle to the original SARS-CoV and found three novel mutations that presumably play a role in SARS-CoV-2’s ability to fuse with the target cell membrane. They then designed a new drug to block this fusion step in SARS-CoV‑2 and found a potentially very potent candidate drug. It was a bit of good news amid the avalanche of bad news, although we’ll still presumably have to wait years for this drug to go through human clinical testing. But hey, it’s progress.
First, here’s the letter written by that team to Nature describing their findings. Findings like an apparent ability of the virus to infect T cells without relying on binding to ACE2 receptors first:
“To assess if SARS-CoV‑2 enters T lymphocytes through non-receptor-mediated endocytosis, we used EK1 peptide which has been shown to inhibit SARS-CoV‑2 spike protein (S) mediated cell–cell fusion and pseudovirus infection.7,10 Specifically, it inhibits receptor-mediated infection by interacting with HR1 to block the formation of the six-helix bundle (6‑HB), further inhibiting fusion between viral and target cell membranes. We found that the EK1 peptide had significant inhibitory activity against SARS-CoV‑2 pseudoviruses on MT‑2 cells (Fig. 1d), suggesting that virus entry depends on receptor-mediated fusion. However, only a high concentration (40 µM) of EK1 had inhibitory activity on MT‑2 cells. Meanwhile, the IC50 value of EK1 was 2.38 µM on 293T/ACE2 cells.10 These results suggest that SARS-CoV‑2 can also enter T lymphocytes through the receptor-mediated endocytosis pathway. To clarify, we performed a SARS-CoV‑2 S‑mediated cell–cell fusion assay according to previous studies.7,10 After 48 h of coculture, 293T cells expressing SARS-CoV‑2 S protein fused with MT‑2 cells. Compared with unfused cells, the fused cells clustered together and appeared as a large faint green fluorescent mass. In contrast, no fused cells were found in the SARS-CoV coculture (Fig. 1e). Therefore, it can be concluded that SARS-CoV‑2 might infect T cells through S protein-mediated membrane fusion.”
It’s the ‘little S‑protein that could’. We’ve already learned about the S‑protein’s cannonical furin-cleavage site that makes it extra easy for the virus to get activated after attaching to a cell not found in its closest viral relatives. And now we’re learning that the S‑protein has features that appear to allow it to infect cells that don’t even have ACE2 receptors. Cells like T cells.
Fortunately, there’s one features this virus doesn’t have (yet): it can infect T cells but can’t replicate in them like HIV. This was also found with MERS, a human coronavirus that is in the same genera as SARS-CoV‑2 (they’re both Beta coronaviruses) but a different lineage (SARS-CoV‑2 is in the B lineage, MERS is in C). Recall how SARS-CoV-2’s furin cleavage site has never been seen in other B lineage Beta coronaviruses. So this ability to infect T cells via this enhanced interaction with target cell membrane is another example of a feature that’s found in other coronaviruses but not found in other B lineage Beta coronaviruses. It’s like SARS-CoV‑2 got all the ‘best’ features from its more distant coronavirus cousins:
Finding out the identify of that novel cell receptor that might mediate entry into the T cells. Let’s hope that receptor isn’t being expressed by a lot of other tissues because those tissues will potentially be viral targets too.
Ok, now here’s a paper published by the same team a week before the above letter to nature where they describe their previous work designing drugs to block this viral-cell membrane fusion step. That drug, EK1, is the same drug they used in the above study to establish that membrane fusion was indeed required for the mysterious infections of T cells. The study also mentions they found three novel mutations in SARS-CoV‑2 in one part of its 6‑HB complex that carries out membrane fusion step. Those mutations are presumably playing a role in the ability to infect T cells. Finally, they mention their success in designing a new drug based on EK1 that is far more effective at blocking the membrane fusion step not just on SARS-CoV‑2 but other human coronaviruses. So it’s actually a potentially exciting development in terms of the quest for an effective drug.
They mention that the Receptor Binding Domain (RBD) of the S‑protein of SARS-CoV‑2 has a 10-to-20 fold greater affinity to binding to the ACE2 receptor on the target cells than the original SARS-CoV. It’s one of the other ‘features’ of this virus’s S‑protein. So SARS-CoV‑2 is not only extra good at binding to ACE2 receptors (then then getting activated by the furin cleavage-site after binding) but it’s also adept at entering cells without relying on ACE2 receptors:
“The recent outbreak of coronavirus disease (COVID-19) caused by SARS-CoV‑2 infection in Wuhan, China has posed a serious threat to global public health. To develop specific anti-coronavirus therapeutics and prophylactics, the molecular mechanism that underlies viral infection must first be defined. Therefore, we herein established a SARS-CoV‑2 spike (S) protein-mediated cell–cell fusion assay and found that SARS-CoV‑2 showed a superior plasma membrane fusion capacity compared to that of SARS-CoV. We solved the X‑ray crystal structure of six-helical bundle (6‑HB) core of the HR1 and HR2 domains in the SARS-CoV‑2 S protein S2 subunit, revealing that several mutated amino acid residues in the HR1 domain may be associated with enhanced interactions with the HR2 domain. We previously developed a pan-coronavirus fusion inhibitor, EK1, which targeted the HR1 domain and could inhibit infection by divergent human coronaviruses tested, including SARS-CoV and MERS-CoV. Here we generated a series of lipopeptides derived from EK1 and found that EK1C4 was the most potent fusion inhibitor against SARS-CoV‑2 S protein-mediated membrane fusion and pseudovirus infection with IC50s of 1.3 and 15.8 nM, about 241- and 149-fold more potent than the original EK1 peptide, respectively. EK1C4 was also highly effective against membrane fusion and infection of other human coronavirus pseudoviruses tested, including SARS-CoV and MERS-CoV, as well as SARSr-CoVs, and potently inhibited the replication of 5 live human coronaviruses examined, including SARS-CoV‑2. Intranasal application of EK1C4 before or after challenge with HCoV-OC43 protected mice from infection, suggesting that EK1C4 could be used for prevention and treatment of infection by the currently circulating SARS-CoV‑2 and other emerging SARSr-CoVs.”
A drug that might be effective against not just ARS-CoV‑2 but future emerging “SARSr-CovSs” (bat coronavirueses). That’s what this team may have developed, based on their previous research on the mechanisms of how related coronaviruses infect cells during this membrane fusion step. In particular, research on the original SARS-CoV appears to be particularly important because SARS-CoV‑2 and SAR-CoV have an 89.8% genetic sequence similarity for the S‑protein S2 subunits. And when we do that comparison we find that SARS-CoV-2’s ability to bind to the ACE2 receptor is 10-to-20 times greater than SARS-CoV, although that ACE2 RBD is in the S1 subunit of the S‑protein. It’s in the S2 subunit of the S‑protein where, where SARS-CoV and SARS-CoV‑2 are 89.8% similar, that we find the 6‑HB bundle of helices form after the finding of the S1 subunit to ACE2. That 6‑HB bundle is what fuses with the target cell membrane. And here we find several amino acid mutations in SARS-CoV-2’s 6‑HB bundles that appear to enhance the formation and stability of the bundle resulting in what they described as a “much higher capacity of membrane fusion than SARS-CoV”. So SARS-CoV‑2 had the kinds of mutations in its genetic sequence that resulted in actual changes in its protein amino acid sequences and those amino acid mutations appear to have made SARS-CoV‑2 much better at fusing with human cells than the original SARS-CoV virus:
So that’s one of example of this virus having a remarkable ability to interact with human cells not found in its closest viral cousins. It would be interesting to know if the mutations found in the SARS-CoV-2’s 6‑HB helix bundle were also found MERS since MERS also appears to have a similar capacity to infect T cells. In other words, are we seeing a feature found elsewhere showing up in this new virus or is this a totally new feature?
But at least it sounds like they do have some very potent candidate drug that might not only work on SARS-CoV‑2 to treat current COVID-19 victims but future coronaviruses too. Let’s hope this drug doesn’t end up having too many side effects. And, of course, let’s also hope knowledge of how this drug works doesn’t make it easy to design a drug-resistance version of the virus.
@Pterrafractyl–
Excellent work!
We can but wonder, though, how much of this was engineered?
Again, these viruses were the focal point of some very powerful, capable, and well-funded interests:
https://spitfirelist.com/news/disturbing-article-about-darpa-and-bat-borne-coronaviruses/
And note other “bio-occurrences” that have happened to China in the recent past:
https://www.globalresearch.ca/china-coronavirus-shocking-update/5705196
” . . . . Just for information
In the past two years (during the trade war) China has suffered several pandemics:
February 15, 2018: H7N4 bird flu. Sickened at least 1,600 people in China and killed more than 600. Many chickens killed. China needs to purchase US poultry products.
June, 2018: H7N9 bird flu. Many chickens killed. China needs to purchase US poultry products.
August, 2018: outbreak of African swine flu. Same strain as Russia, from Georgia. Millions of pigs killed. China needs to purchase US pork products.
May 24, 2019: massive infestation of armyworms in 14 province-level regions in China, which destroy most food crops. Quickly spread to more than 8,500 hectares of China’s grain production. They produce astonishing numbers of eggs. China needs to purchase US agricultural products – corn, soybeans.
December, 2019: Coronavirus appearance puts China’s economy on hold.
January, 2020:China is hit by a “highly pathogenic” strain of bird flu in Hunan province. Many chickens died, many others killed. China needs to purchase US poultry products.”
Best,
Dave