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Despite Rapid Growth In Civil Rights Tourism, Montgomery Remains Firmly In The Grip Of Racist White Men

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In a tragic vote yesterday, the City Council in Montgomery, Alabama failed to pass an ordinance that would have required the use of face masks in public. This vote came after an impassioned plea from local doctors:

Jackson Hospital pulmonologist William Saliski cleared his throat as he started describing the dire situation created by the coronavirus pandemic in Montgomery to its City Council before they voted on a mandatory mask ordinance. “It’s been a long day, I apologize,” he said.

“The units are full with critically-ill COVID patients,” Saliski said. About 90% of them are Black. He said hospitals are able to manage for now, but it’s not sustainable. “This mask slows that down, 95% protection from something as easy as cloth. … If this continues the way it’s going, we will be overrun.”

More doctors followed him to the microphone, describing the dead being carried out within 30 minutes of each other, and doctors being disturbed when people on the street ask them if the media is lying about the pandemic as part of a political ploy.

There’s a lot to unpack here. Note that Salisky said that units at the hospital are full with critically ill patients. But also note especially that the newspaper adds that he said 90% of the patients are black. Finally, he said that without intervention, the hospital certainly will be overrun.

The intervention measure proposed is simple and direct. Salisky claimed 95% reduction in transmission with a mask. I’m not so sure on that number, but it is becoming increasingly clear that masks, especially when coupled with social distancing, make a huge difference in reducing transmission.

We need to set the stage properly before getting to the details of the council’s vote in order to fully appreciate it.

Montgomery has a truly sordid past. As the Equal Justice Initiative has noted, Montgomery was Alabama’s center for the slave trade. EJI erected this plaque on Commerce Street in downtown Montgomery:

That’s right. Humans were literally warehoused between auction dates in Montgomery. In a bit of rare social justice, that building, 122 Commerce Street, is now one of several Equal Justice Initiative facilities in Montgomery:

I have these photos because, as I mentioned previously, I had the opportunity in February to travel to Montgomery with a busload of people from here in the Gainesville area. We visited two EJI facilities, the National Memorial for Peace and Justice (seen in the featured image for this post) and the Legacy Museum. We also made the approximately one hour bus trip to Selma, where we experienced the Footprints to Freedom Tour which included stops at the National Voting Rights Museum and Institute, the Slavery and Civil Rights Museum and a walk across the Edmund Pettis Bridge.

It turns out we were far from alone in making this trip. In November of 2018, the Montgomery Advertiser noted a significant uptick in visits to Montgomery and traced them directly to the opening of the National Memorial and Legacy Museum that April:

Over 250,000 people have visited the Equal Justice Initiative’s downtown museum and memorial to lynching victims since the sites opened in April. More than that, the burst of international attention that came with those sites has turned the city into a destination, instead of a stop on the way to something else. That’s led more people to discover the city’s other historic sites and attractions, from Martin Luther King Jr.’s church, to the site where Rosa Parks boarded the bus.

/snip/

“EJI has put Montgomery on the world’s radar,” he said. “I think Montgomery is in the best position for tourism appeal than it has ever been.”

Now, they’re voting with dollars.

Hotel room stays in Montgomery inched up by about 5,500 in 2017, according to state figures. This year they’re up 97,579 through October, according to the Montgomery Area Chamber of Commerce’s Convention and Visitors Bureau.

Note the mention of Rosa Parks as another part of Montgomery’s role in civil rights history.  The Montgomery Bus Boycott, from December, 1955 to December, 1956 marked Rev. Dr. Martin Luther King, Jr.’s rise to national attention. This adds significantly to the historic legacy of Montgomery and civil rights.

It should also be noted that Montgomery’s demographics are 61% black and only 33% white.

So with this rich history of civil rights activism, burgeoning civil rights tourism and a population 61% black, surely Montgomery’s City Council would vote for an ordinance that would slow down a disease where one doctor characterized those hospitalized as 90% black, wouldn’t they?

Not so fast. This is, after all, still Alabama. Here’s a link to the current Montgomery City Council. In a city that has 61% black citizens and only 33% white, the City Council has five white men, three black men and one black woman. Hardly representative.

Returning to the Advertiser story on last night’s vote:

After they spoke, and before the council voted on a proposal by Councilman C.C. Calhoun to mandate mask-wearing in public in Montgomery, Councilman Brantley Lyons questioned whether masks and six-foot distancing really helps. They do, the doctors replied. Lyons was unmoved. “At the end of the day, if an illness or a pandemic comes through we do not throw our constitutional rights out the window,” Lyons said.

From the crowd, doctors called for him to visit the hospital sometime.

Instead, the council killed the ordinance after it failed to pass in a 4-4 tie, mostly along racial lines, with Councilman Tracy Larkin absent. Councilman Clay McInnis voted with three Black council members — Calhoun, Oronde Mitchell and Audrey Graham — in favor of the ordinance. Lyons, Charles Jinright, Richard Bollinger and Glen Pruitt voted against it.

Only one white man voted for the ordinance. Sadly, one of the black men on the council was absent. I haven’t seen anywhere whether there might be an attempt at a new vote with all members present, since if no members change their vote, it would have a good chance at passage.

But note especially the behavior of Brantley Lyons. He asked the doctors whether it is true the masks and distancing would help prevent spread of the disease. Even though the doctors assured him it was true, Lyons trotted out the trope that the frothy right has been spewing all through the pandemic. Trying to claim that an ordinance mandating masks somehow would “throw our constitutional rights out the window” is the same sort of stupid rhetoric that racist conservative white people have spewed for generations whenever blacks sought equal protection under the law. And that circles back perfectly on the first quote from this article, where the doctors described being upset when the public approaches them to ask if the media is lying about the pandemic as part of a political ploy.

We know exactly where the real political ploy is coming from. Donald Trump is saying the quiet part out loud to fan the flames of racism in our country and he is directly responsible for these ideas spreading rapidly through people who listen to OAN and Fox News creating the narrative that the pandemic is fake. There also is no doubt that there is a huge component of racism in this entire process. Trump doesn’t hide his, but two-bit worthless politicans like Brantley Lyons happily spew this bunk without regard to the real and ongoing danger to the black citizens of Montgomery. You can rest assured that if this disease primarily attacked old white men, those not wearing masks would risk being shot on sight.

 

 

Is COVID-19 Why Florida Has About 1300 More Pneumonia Deaths This Season Than Average Over Previous Five?

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Earlier today, I saw this tweet that suggests a huge excess of pneumonia deaths in Florida this year compared to previous years. The data in the tweet suggested that Florida has around 4000 more pneumonia deaths this year than the average for the previous five years. That sounded a little high to me, as I have spent a lot of time over the past few months poring through the data at this CDC site on weekly numbers for pneumonia and influenza deaths. Looking deeper into the tweet, it appeared to depend on a reddit post and it had a low number for Florida reported COVID-19 deaths, so it was necessary to go back to original sources.

A couple of weeks ago, I spent several hours downloading data from the CDC national database you can access at the link above and picking out just the Florida data to paste into another spreadsheet. I chose a poor strategy that day, as I only looked at the total pneumonia and influenza deaths even though the data are broken down into both categories. I few days later, I realized that I needed to go back into the data and look only at pneumonia deaths, as it seems likely that there could be quite a few deaths attributed to pneumonia in patients who were never tested for COVID-19. Also, flu deaths vary widely from year to year depending on the severity of the outbreaks and the effectiveness of that year’s vaccine, so that total number has a lot of noise year to year. Seeing the tweet today prompted me to go back and download the data again so that the 2019-2020 data would be more up to date.

As downloaded today, there are data in the spreadsheet through week number 20 for each state. For Florida, the week 20 numbers appear to be only partial totals, so for this analysis, I only went through week 19 of 2020. Each season in the data begins with week 40 of the year (so this year’s data starts at week 40 of 2019). However, since the COVID-19 outbreak is generally considered to have started in earnest in mid- to late November of 2019, I included only the last four weeks of 2019 with the first 19 weeks of 2020. I then found the totals for the same time period in each of the five previous seasons.

The totals for pneumonia deaths are:

2014-2015                 5510

2015-2016                 5214

2016-2017                 5540

2017-2018                 5792

2018-2019                 5374

2019-2020                 6772

One of these things is not like the others. The average total for the previous five years is 5486 pneumonia deaths for weeks 49 through week 19 of each season. That means that 2019-2020 has 1286 more deaths from pneumonia than the average for that period in the previous five seasons. The Florida COVID-19 dashboard right now is showing 2319 deaths from the virus. I would suggest that number is more like 3605 when the excess pneumonia deaths are included. Note also that there may well be other deaths due to the virus in patients who were not tested but died due to the other types of pathology seen by the virus that don’t manifest directly as pneumonia.

Last week, I asked how many COVID-19 deaths Ron DeSantis is hiding. We can now account for about 1300 and it seems likely there may well be more.

 

 

Pompeo’s Latest Attempts To Propel Propaganda On Lab Escape Of SARS CoV-2 Suffer Two Epic Swat-Downs

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Recall that back on April 30, I wrote about how the Trump Administration had been orchestrating a propaganda push to claim that SARS CoV-2 was accidentally released from the Wuhan Institute of Virology. Of special importance is that the New York Times article I cited on the topic specifically mentioned Mike Pompeo as one of the primary forces behind pushing the story. Recall also that a part of this propaganda effort came from “leaked” State Department cables.

Apparently, getting called out by the New York Times was not enough to deter Pompeo from this effort. He returned to the airwaves on May 3, telling ABC that there is “enormous evidence” that the virus came from the lab. And then “magically”, but in reality following the aluminum tubes playbook straight out of Cheney’s Iraq WMD playbook, a “report” came into the hands of NBC, who published it May 8. The report purportedly relied on “open source” data to make the case that some sort of accident occurred at the lab in late October, prompting officials to shut down the lab and block roads surrounding it. NBC debunked one aspect of the report in their story, noting that a conference at the lab that the report claims was cancelled in this timeframe actually took place as planned.

Yesterday, Erin Banco and colleagues at Daily Beast published what can only be described as one of the most epic slap-downs of fake intelligence I’ve ever seen. Please go read the piece in full, because summarizing cannot properly capture its full glory.

The dissection of the false intelligence in the report begins with work done by Jeffrey Lewis (one of the best follows on Twitter at @ArmsControlWonk), who utterly destroyed the report’s claims regarding satellite data:

What’s more, imagery collected by DigitalGlobe’s Maxar Technologies satellites and provided to The Daily Beast reveals a simpler, less exotic reason for why analysts believed “roadblocks” went into place around the lab after the supposed accident: road construction. The Maxar images also show typical workdays, with normal traffic patterns around the lab, after the supposedly cataclysmic event.

“This is an illustrated guide on how not to do open source analysis,” said Jeffrey Lewis, director of the East Asia Nonproliferation Program at the Center for Nonproliferation Studies, who analyzed the MACE report for The Daily Beast. “It is filled with apples-to-oranges comparisons, motivated reasoning, and a complete refusal to consider mundane explanations or place the data in any sort of context.”

That’s right. The report took images showing roads blocked for ordinary road construction and claimed they showed that a catastrophic accident in the lab meant that traffic had to be kept away to prevent exposure to the leaked virus.

But the fun doesn’t stop there. I’ll get to who MACE, who prepared the report, is a bit later. The story continues:

MACE’s analysts tried to establish a “pattern of life” at the Wuhan lab in order to reveal what they claim is an anomaly, one purportedly caused by a leak. The MACE document charts the movement of apparent Wuhan lab personnel into and out of the facility leading up to October, when the alleged leak took place. In one slide, analysts wrote that there is an “18 day gap” in which “there were no observable events” from devices at the lab between Oct. 6 and 24, supposedly suggesting an accidental leak.

In doing so, they appear to have been unaware of a key cultural factor complicating the normal course of events: a holiday. “The first week of October is a golden week in China, which is going to disrupt that pattern,” Lewis said.

Yep. The “anomaly” MACE ascribes to leak was in fact an ordinary holiday when activity would be diminished around the lab for a perfectly ordinary reason.

And the Daily Beast investigators spread the fun around, getting the folks at Bellingcat involved in investigating the claims made in the report:

The Daily Beast asked analysts at the award-winning open source investigative news outlet Bellingcat to review the MACE dossier and evaluate the quality of its conclusions. Within minutes of receiving the dossier, Bellingcat senior investigator Nick Waters disproved one of the MACE document’s claims: that a conference on biosafety lab management at the Wuhan lab scheduled for the first week of November was canceled.

But the conference did take place, as NBC first reported. Waters found a Facebook post from a Pakistani scientist who had attended the event and taken selfies there, including at the BSL-3 laboratory.

Wow. And Waters doesn’t stop there:

He also took a dig at one of the many amateurish elements in the MACE presentation. “Perhaps the authors should have spent more time testing their analysis rather than working out how to crop the eye of Sauron into a logo copy-pasted from the internet,” Waters said.

Okay, I got a huge laugh at the eye of Sauron bit. That’s because I’ve run into the folks behind MACE before. As Daily Beast points out, MACE stands for Multi Agency Collaboration Environment. And according to this link they provide, MACE is hosted at a company in Las Vegas by the name of Sierra Nevada Corporation. Way back in 2011, I wrote about a technology called Gorgon Stare, developed by Sierra Nevada Corporation, that claimed to enable real time remote viewing analysis of entire villages in Iraq or Afghanistan from imaging equipment carried by high-flying drones. Of course, this technology turned out to be a very expensive boondoggle that did nothing to help intelligence-gathering. I can’t help wondering if the eye of Sauron bit was an insider joke at Sierra Nevada that Waters understood and shot right back at them to ridicule this report and the old Gorgon Stare technology.

So, while the MACE report clearly originated in the US, what I haven’t seen yet is a clear indication of just when it surfaced, especially when it surfaced for senior Trump Administration officials and the intelligence community. It would not surprise me if it goes all the way back to the propaganda campaign in mid-April I described in my previous post. The version of the report that NBC published has the last several pages redacted with the description that this was done to protect names from being disclosed. That really makes me wonder if the specific question from John Roberts of Fox News to Trump on April 14 about an intern at the lab being infected and then spreading it to her boyfriend and the wet market was based on the redacted portion of the MACE report. All we know about timing is that the report had made its way to Congressional committees by May 8 when NBC published it.

There is another weak intelligence document, though, that this time is traced directly to the State Department. On May 7, the Sydney Morning Herald debunked a “dossier” that had been leaked from the US embassy in Canberra that the Daily Telegraph (a Rupert Murdoch paper in Australia) wrote about on May 2. The Herald says this about Australian officials  looking for the basis of the dossier:

Senior members of the Morrison government and Australian intelligence agencies at first had trouble finding the document. Eventually they found a research report, based on publicly available information including news reports, which appeared to fit the description. The research paper contained no information that was generated from intelligence gathering, according to people who have read it.

Labor MP Anthony Byrne, the deputy chair of the influential intelligence and security committee, was “incensed” by the report of the dossier. Mr Byrne, one of Parliament’s biggest supporters of the US alliance, directly raised his concerns with senior members of the Morrison government and intelligence agencies, saying Australia shouldn’t accept intelligence that doesn’t exist and fall for a “tricked-up document”.

There are now widespread suspicions within senior ranks of the Australian government and the intelligence community that the document was leaked to The Daily Telegraph by a staff member in the US embassy in Canberra. This suspicion, whether true or not, underlines how the positions between sections of Canberra and Washington national security circles have diverged over the claim. Some senior officials clearly believe the US embassy is pushing a narrative in the Australian media that could be counter to the beliefs and interests of its hosts.

The story continues:

The episode highlights the danger of mischaracterising the work of intelligence agencies. Some of the footnotes in the document contained references to US media reports that were based on unsubstantiated assertions from the US government – the same kind of circular intelligence which resulted in the “children overboard” affair in 2001.

Wow. The Herald also goes there, comparing this propaganda ploy to an Australian false information scandal of similar magnitude to the Iraq WMD operation in the US.

But again, Pompeo and those under him seem to be central to this whole operation. The Daily Telegraph story appeared just a day before Pompeo claimed “huge evidence” and likely was based on a document leaked by a US embassy. And then NBC published the MACE document a few days later. I haven’t seen anyone suggest that the document in Australia is the MACE document, but the Herald’s description and debunking of it sure would fit with them being the same or at least having the same source.

Given Pompeo’s central role in spreading propaganda that has been so easily refuted, I can’t help wondering if we will have another shoe drop on the firing of Steve Linick. Note that in his letter to Congress on the firing (which will be complete at the end of a 30 day clock starting Friday night), Trump said it was based on Pompeo’s suggestion that Linick be fired. Also note that we were first told it was because Linick was investigating Pompeo using State Department personnel to run personal errands. Today, that’s been expanded to cover the fast-tracking of arms sales to Saudi Arabia. But in their article on that, CNN notes:

But at this time, House Democrats say they do not yet know which investigation was the biggest factor behind the decision to dismiss Linick.

“I wouldn’t assign percentages,” a Democratic committee aide said.

Democrats on both the House Foreign Affairs and Senate Foreign Relations committees are interested in learning more about Linick’s investigations into Pompeo, and Engel emphasized the importance of cooperation from the administration in his statement Monday.

“The administration should comply with the probe I launched with Senator Menendez and turn over all the records requested from the Department by Friday,” he said, a reference to Sen. Bob Menendez of New Jersey, the ranking Democrat on the Senate Foreign Relations Committee.

I find it hard to believe that Pompeo would have felt truly threatened by either the investigation into using aides for personal errands or expediting the Saudi arms sales. Those just seem like garden variety Trump corruption that gets shrugged off as the next daily outrage appears. However, if Linick had started nosing around the leak of the State Department’s own Wuhan cables and/or the allegation of the leak of the report from the Canberra embassy, I think Pompeo would see a bigger danger. That would represent an investigation into an ongoing propaganda operation in which Pompeo disseminated easily disproved disinformation.

The final beautiful irony here is that if Linick had started such an investigation, it likely was based on open source information. Unlike the MACE information though, this open source information would consist of Pompeo’s own recorded media appearances and the subsequent public debunking of the propaganda. That propaganda getting debunked would be both Pompeo’s direct statements and the debunking of the “supporting” material that appears to have been released either by him or those doing his bidding.

Shi Zhengli Provides Proof SARS CoV-2 Was Not An Accidental Release From Wuhan Institute of Virology

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On Saturday, I took a deep dive into the origin of SARS CoV-2, the virus that is the cause of the deadly COVID-19 pandemic. That post was the result of several long days of deep reading and thinking. Somehow, I missed that Scientific American had put out an update on Friday of their profile of Dr. Shi Zhengli, the scientist responsible for much of what the world knows about bat coronaviruses, including isolating the bat coronavirus from Yunnan Province that is the closest relative to SARS CoV-2 that has been seen in a laboratory. Even worse, commenter Zinsky linked to the Scientific American article in one of the earliest comments on my post.

I finally got around to reading the article today. As you might imagine, this editor’s note at the top really got my attention:

Editor’s Note (4/24/20): This article was originally published online on March 11. It has been updated for inclusion in the June 2020 issue of Scientific American and to address rumors that SARS-CoV-2 emerged from Shi Zhengli’s lab in China.

I strongly urge you to read the entire article. It provides an effective look into work that Shi had been doing prior to the outbreak and then takes us along with her as she gets the news on December 30 that a novel coronavirus had been detected in two patients in Wuhan with atypical pneumonia. On instruction from the lab director, Shi left the conference she was attending in Shanghai and rushed back to Wuhan to concentrate all of her attention on the new virus.

It is important to keep in mind that Shi’s career up to the SARS CoV-2 outbreak was aimed at just such an event. In fact, she and her team had warned us. From the Scientific American article:

With growing human populations increasingly encroaching on wildlife habitats, with unprecedented changes in land use, with wildlife and livestock transported across countries and their products around the world, and with sharp increases in both domestic and international travel, pandemics of new diseases are a mathematical near certainty. This had been keeping Shi and many other researchers awake at night long before the mysterious samples landed at the Wuhan Institute of Virology on that ominous evening last December.

More than a year ago Shi’s team published two comprehensive reviews about coronaviruses in Viruses and Nature Reviews Microbiology. Drawing evidence from her own studies—many of which were published in top academic journals—and from others, Shi and her co-authors warned of the risk of future outbreaks of bat-borne coronaviruses.

With that as background, her actions in digging into the new virus make perfect sense for how a respected scientist engaged in work with dangerous viruses would seek the source of the outbreak.

She and her team jumped into work on the train trip back to Wuhan from the conference in Shanghai:

On the train back to Wuhan on December 30 last year, Shi and her colleagues discussed ways to immediately start testing the patients’ samples. In the following weeks—the most intense and the most stressful time of her life—China’s bat woman felt she was fighting a battle in her worst nightmare, even though it was one she had been preparing for over the past 16 years. Using a technique called polymerase chain reaction, which can detect a virus by amplifying its genetic material, the team found that samples from five of seven patients had genetic sequences present in all coronaviruses.

But here’s where the character of a person who has been dedicated to science her entire career comes out:

Shi instructed her group to repeat the tests and, at the same time, sent the samples to another facility to sequence the full viral genomes. Meanwhile she frantically went through her own lab’s records from the past few years to check for any mishandling of experimental materials, especially during disposal. Shi breathed a sigh of relief when the results came back: none of the sequences matched those of the viruses her team had sampled from bat caves. “That really took a load off my mind,” she says. “I had not slept a wink for days.”

Yes, months before the rumors of an accidental release from her lab started circulating, one of Shi’s very first steps was to make sure that the sequence of the virus found in patients from the wet market did not align with the sequences of any of the viruses isolated from bats that she had in her lab. She had already warned the world of the danger posed by some coronaviruses jumping from bats to humans. [Note: even though we talk about SARS CoV-2 and the bat virus RaTG13 being “closely related”, they still differ by enough that it is clear that SARS CoV-2 came from a different source than either the virus circulating in that bat population at the time it was isolated or the virus as it exists now in the lab.]

Even more importantly, she checked lab safety records and did not sleep until she could eliminate the nightmare of her lab being responsible for the outbreak.

The article goes on to detail the steps taken to confirm SARS CoV-2 as the agent for the outbreak and the use of sequencing of multiple isolates from different patients over time to indicate that it’s very likely that there was only a single introduction of the virus into humans.

Clearly, the rumors of a leak from her lab have bothered Shi, but she will not allow them to stop her:

Despite the disturbance, Shi is determined to continue her work. “The mission must go on,” she says. “What we have uncovered is just the tip of an iceberg.” She is planning to lead a national project to systematically sample viruses in bat caves, with much wider scope and intensity than previous attempts.

/snip/

“Bat-borne coronaviruses will cause more outbreaks,” Shi says with a tone of brooding certainty. “We must find them before they find us.”

Epilogue

In my post on Saturday, I posited that if we are to believe that the outbreak was the product of an accidental release from Wuhan Institute of Virology, we would have to claim that China has removed from the record any evidence of workers from the lab, or the family or other close contacts, being infected or dying.

Now, after the details that Shi has provided, we would have to believe that a scientist with a long history of top-notch peer reviewed research would be involved in such a lie and would further fabricate the story that none of the previous isolates in her lab match the outbreak.

A scientist of this caliber would know that such a lie would eventually be uncovered. That Shi intends to continue her work unabated is very strong evidence that she is being truthful and can rightfully proceed with a clear conscience.

Those considerations prompted me to return to the “evidence” that was presented to suggest an accidental release. Recall that in my post Saturday, I was perplexed by what looked like the outlines of an information operation. First, the specificity, out of the blue, of the question from John Roberts of Fox about an intern at the lab being infected. I still haven’t heard any others make this same suggestion, so that still stands out as suspicious.

But then I went back and looked at the Josh Rogin column from the same day, where Rogin concentrated on two State Department cables from 2018 about Wuhan Institute of Virology. Here’s the setting Rogin provided for the cables:

In January 2018, the U.S. Embassy in Beijing took the unusual step of repeatedly sending U.S. science diplomats to the Wuhan Institute of Virology (WIV), which had in 2015 become China’s first laboratory to achieve the highest level of international bioresearch safety (known as BSL-4). WIV issued a news release in English about the last of these visits, which occurred on March 27, 2018. The U.S. delegation was led by Jamison Fouss, the consul general in Wuhan, and Rick Switzer, the embassy’s counselor of environment, science, technology and health. Last week, WIV erased that statement from its website, though it remains archived on the Internet.

What the U.S. officials learned during their visits concerned them so much that they dispatched two diplomatic cables categorized as Sensitive But Unclassified back to Washington. The cables warned about safety and management weaknesses at the WIV lab and proposed more attention and help. The first cable, which I obtained, also warns that the lab’s work on bat coronaviruses and their potential human transmission represented a risk of a new SARS-like pandemic.

And yet, even though Rogin says he got a copy of the first cable, this is the only money quote he chose to put into his column:

“During interactions with scientists at the WIV laboratory, they noted the new lab has a serious shortage of appropriately trained technicians and investigators needed to safely operate this high-containment laboratory,” states the Jan. 19, 2018, cable, which was drafted by two officials from the embassy’s environment, science and health sections who met with the WIV scientists. (The State Department declined to comment on this and other details of the story.)

Rogin then adds what I think is the most important part:

The Chinese researchers at WIV were receiving assistance from the Galveston National Laboratory at the University of Texas Medical Branch and other U.S. organizations, but the Chinese requested additional help. The cables argued that the United States should give the Wuhan lab further support, mainly because its research on bat coronaviruses was important but also dangerous.

Really? The scariest language that Rogin could lift from the cable warned of a “shortage of appropriately trained technicians and investigators needed to safely operate”, but then he grudgingly had to note that this was in fact tied to a request from the lab for more outside assistance in getting that training. When we couple that thought with the failure, so far, of Rogin or anyone else to have actually published the full cables, I am more convinced than ever that the whole cable story is part of a coordinated information operation where Roberts asked the specific question and then Rogin took information that had been twisted inside-out from a cable asking for help with training at the lab to try to turn it into a potential whistle-blowing event.

One more bit. I did some digging. Rick Switzer, the “embassy’s counselor of environment, science, technology and health” is not a scientist:

Rogin says the cable he saw was written by “two officials  from the embassy’s environment, science and health sections who met with the WIV scientists”. One would hope that there was at least one actual scientist among those two officials.

Research Misinfo/Disinfo: Ain’t No Sunshine Kill COVID-19 Gone

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[Check the byline, thanks! /Rayne]

I thought this series would end after three posts but clearly the misinfo/disinfo related to research studies on COVID-19 continues.

This time Department of Homeland Security is one of the problem children.

By now you know about Trump’s wrong-headed comments about light and disinfectants used in and on humans’ bodies to eliminate SARS-CoV-19. You’ve also heard he gaslighted the public by claiming he was being sarcastic during Thursday’s briefing about light and disinfectants, followed by even more dog-ate-my-homework excuses.

You may have heard speculation that bleach as a COVID-19 therapy specifically may have been the result of communications with Trump by some crackpot who sells this re-labeled chlorine dioxide product as a miracle cure-all.

What you probably haven’t seen is the DHS’s “study” which may also have spurred Trump’s idiotic remarks about light or sunlight. Yahoo News reported about the “study” a week ago, sharing a link to the DHS document it received outlining DHS’s findings.

It’s not a paper. It’s a goddamned slide presentation of which stability of SARS-CoV-19 on surfaces was only a portion.

No peer-reviewed study has been published by DHS in any of the articles since Trump’s ridiculously inappropriate comments last evening.

News outlets have been all over Trump’s remarks, which as Marcy said elicited justifiable uproar. But outlets are doing a pissy job covering the sources of Trump’s practice of medicine without a license at the podium.

Newsweek offers a great example:

Fortunately, CNN got it right:

If DHS’s science and technology advisor Bill Bryan isn’t qualified to make declarative statements relying on research, who is?

Who did the research and where’s their data and output?

Why did the American public have to hear what DHS learned filtered through Trump who has proven himself to be incapable of understanding science let alone demonstrate respect for it?

We need to see the work because there are other studies which do not appear to agree with DHS’s presentation.

This widely cited piece tested the viability of SARS-CoV-2 on different surfaces after exposure to aerosolized virus. The temperature of the study was comparable to a nice spring day — 21-23 degrees Celsius or 69-73 degrees Fahrenheit — with 40% relative humidity.

Aerosol and Surface Stability of SARS-CoV-2 as Compared with SARS-CoV-1
van Doremalen N, Bushmaker T, Morris DH, et al.
March 17, 2020
DOI: 10.1056/NEJMc2004973
https://www.nejm.org/doi/full/10.1056/NEJMc2004973

SARS-CoV-2 is quite stable in conditions one might find in an air-conditioned indoor setting according to this study. This much agrees with what DHS presented.

This study looked at viability of the virus over time at different increasing temperatures and exposure to ultraviolet light — like solar radiation.

Stability of SARS-CoV-2 in different environmental conditions
Alex W.H. Chin, Julie T.S. Chu, Mahen R.A. Perera, Kenrie P.Y. Hui, Hui-Ling Yen, Michael C.W. Chan, Malik Peiris, Leo L.M. Poon
https://www.medrxiv.org/content/10.1101/2020.03.15.20036673v2.full.pdf

Here’s a table from the study addressing viability of SARS-CoV-2 at different temperatures:

You can see the virus is viable at 37 degrees C — that’s coincidentally 98.6F, the old average temperature for humans. The virus is stable at that temp for as long as a day. It’s not stable for long at 56C (132.8F) and not at all at 70C (158F) but then neither are humans.

Unsurprisingly, disinfectants disinfect according to the study’s results shown in the table above. Only one little burp with hand soap solution — one of three attempts showed some viability.

This study looked at the differences in number of outbreaks over time in a particular region of China, as the season changed and both temperature and amount of sunlight increased.

No Association of COVID-19 transmission with temperature or UV radiation in Chinese cities
Ye Yao, Jinhua Pan, Zhixi Liu, Xia Meng, Weidong Wang, Haidong Kan, Weibing Wang
Published online April 8, 2020.
European Respiratory Journal 2020, 2000517; DOI: 10.1183/13993003.00517-2020
https://erj.ersjournals.com/content/early/2020/04/01/13993003.00517-2020

These researchers hypothesized that COVID-19 transmission may decrease or even disappear when the temperature and UV radiation increase in the summer.

They collected the confirmed case numbers of 224 cities from China’s National Health Commission, the daily mean temperature and relative humidity collected from the China Meteorological Data Sharing Service System, and daily erythemally-weighted daily dose of UV radiation data extracted from the Dutch-Finnish Ozone Monitoring Instrument aboard NASA’s Aurora satellite. After adjustment for relative humidity and UV, they found temperature held no significant associations with cumulative incidence rate, and that UV was not significantly associated with cumulative incidence rate after adjustment for temperature and relative humidity.

These studies — though some are pre-print and in peer review — do not agree with what DHS’s Bill Bryan or the DHS presentation published a week ago said.

And none of them match what Trump said, whatsoever.

Media outlets really need to have a science reporter covering Trump’s briefings rather than the usual White House correspondents — people who are already highly versed in COVID-19 research and are able to put Trump on the spot.

Or the media needs to give up covering Trump’s briefings live if they can’t do real time pushback and demand better of the guy occupying the White House. Carrying his unfiltered bullshit will get somebody killed and damage businesses which are doing their best to operate under the strain of pandemic conditions.

~ ~ ~

We know now from the Washington Post that Trump’s unacceptable remarks on light and disinfectant therapy for treatment of COVID-19 may have been inspired by a briefing about a DHS study:

Trump’s commentary seemed to be inspired by a presentation from a Department of Homeland Security official about a promising but still inconclusive government study exploring the possibility of heat, humidity and light to kill the virus, as well as the effectiveness of disinfectants in killing it on surfaces such as tables, countertops and office workspaces.

Emphasis mine. An in-fucking-conclusive study, the same one on which Bill Bryan gave a presentation. Why was it offered at all? To provide happy talk for the daily propaganda program?

William Bryan, the department’s acting undersecretary for science and technology, first shared the study with members of the White House coronavirus task force on Wednesday and returned Thursday. He said his department had studied the virus in an air chamber and never said chemicals or UV light had been studied on humans nor suggested they be used in humans, according to several administration officials.

Why did he come back? Did some asshat on the White House coronavirus task force think Bryan could finesse this inconclusive report?

Others on the task force, including Birx, White House chief of staff Mark Meadows, as well as McEnany and others in the communications and press shops, were concerned that the Department of Homeland Security study had not been thoroughly vetted. “It was not ready at all to go to the president,” the senior official said. “There was no guideline. There was no data. There was nothing.”

Oh. Now we have sources named. At least one of these people and/or Dr. Fauci are most likely to have said this “study” was not ready to go to Trump. If these three and Dr. Fauci didn’t think it was ready, how did it end up getting in front of Trump?

Still, Vice President Pence and his team wanted Bryan to present the information to the president and to the public, eager to have something positive to share. They hoped the study would help encourage people to spend more time outdoors and to disinfect their homes, aides said.

Oh great — Mr. HIV-outbreak-of Indiana Pence with a history of ignoring public health officials’ advice to the public’s detriment, probably ignored the opinions of task force members who felt the DHS “study” was not ready for Trump’s propaganda show.

This time Pence’s bad decision-making resulted in an onslaught of calls to poison control center numbers and at least 20 people in New York alone who ingested bleach or disinfectant.

No word yet as to whether someone has fried themselves crispy outdoors in an effort to get rid of SARS-CoV-2 using ultraviolet light having relied on the misinfo/disinfo served up by the idiocracy in the White House.

Digging Through The Science—And The Noise—On What Is Known About The Origin Of SARS CoV-2

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Update: In a new post we find that Shi Zhingli of Wuhan Institute of Virology has provided convincing evidence to Scientific American that SARS CoV-2 is the result of a natural jump to humans from an animal host and was not accidentally released from her lab, which had no isolates of any viruses that match closely enough to be the outbreak virus.

Although it seems that all of this has been going on forever at this point, it’s important to realize that the COVID-19 pandemic outbreak probably began less than six months ago. In the context of how we develop an understanding of a disease like this one, and the virus that causes it, SARS CoV-2, that means that we really have only just begun our analysis. Nevertheless, because of the ongoing disastrous impact on global public health as well as the global economy, it is imperative that we learn as much as we can as fast as we can.

In this post, I want to take a deep dive into what virologists and epidemiologists have pieced together on the emergence of SARS CoV-2. The problem is that what might initially appear to be straightforward scientific and public health questions eventually get muddled by accusations of disinformation, accusations of hiding data and offerings of potential leaks of intelligence that also have a chance to be disinformation. These noisy battles relate to basic facts that have a direct bearing on our understanding of the virus’ origin.

As a result, it needs to be stated from the outset that because some of the needed basic information may be hidden or some of what we think we know might be wrong. Therefore, this analysis will be unable to come to a definite conclusion. With any luck, the discussion will help us to have a framework within which we can proceed as more facts become verified.

Overview Derived From SARS CoV-2 Genetic Sequence

I want to start with the science.  The very helpful graphic below is lifted from this paper in Current Biology. It is in three sections. The section on the left illustrates what we know from the genetic sequence of the virus when that is compared to other known viruses. What it shows is that the closest overall relative to SARS CoV-2, with a sequence identity of 96%, is RaTG13, another coronovirus isolated from a bat:

Let’s move to this Nature Medicine article from March 17 and this Cell article from April 16 for the narrative on diving into the distinguishing features of SARS CoV-2 from its genetic sequence.

From the Nature Medicine article, we get a description of the features of SARS CoV-2 that distinguish it from other known viruses (these features are what the center and right panels of the graphic address):

Our comparison of alpha- and betacoronaviruses identifies two notable genomic features of SARS-CoV-2: (i) on the basis of structural studies and biochemical experiments, SARS-CoV-2 appears to be optimized for binding to the human receptor ACE2; and (ii) the spike protein of SARS-CoV-2 has a functional polybasic (furin) cleavage site at the S1–S2 boundary through the insertion of 12 nucleotides, which additionally led to the predicted acquisition of three O-linked glycans around the site.

To translate some of the terms and clarify a bit, there are four genera of coronaviruses, with alpha and beta infecting mammals and delta and gamma infecting birds. The genome is the genetic sequence of the virus. I would usually say the DNA sequence, but coronaviruses are RNA viruses. There has been much discussion of ACE2 on this blog in the comments, so for now let’s just say ACE stands for angiotensin converting enzyme and ACE2 is present on the surface of many cell types found in many different tissues within the body. So what stands out here is that the structure of the virus spike protein, as determined from its genetic sequence and tests in the lab, allows it to bind exceptionally well to ACE2 when compared to other coronaviruses.

The middle panel of the graphic shows us that although the overall sequence of SARS CoV-2 is very closely aligned to the bat virus, when we narrow it down to only compare the region where the spike protein binds to ACE2, it is a perfect match of that part of a pangolin virus, while it is very different from the bat virus. For the important stretch of the spike protein (these amino acids are not next to each other when the gene sequence is read from start to finish, but once the protein is assembled from amino acids, the amino acids are close to each other from the way the protein assumes its three dimensional structure), the gene encodes a string of five amino acids in the protein that matches exactly with the pangolin virus sequence but in only the first of the five positions on the bat virus sequence.

But that final panel and the second half of the Nature Medicine snippet goes further in what is different about this virus. The gene for the spike protein encodes two subunits, S1 and S2. Remarkably, SARS CoV-2 has acquired a site where the two subunits can be separated using a enzyme called furin that is found in mammalian cells. The right panel shows us that neither the bat sequence nor the pangolin sequence has a furin cleavage site.

The Cell paper tells us that a furin cleavage site has not been seen in the betacoronaviruses closely related to SARS CoV-2. It has been seen in other human coronaviruses, though. Of further significance is that a furin cleavage site also appears in the more pathogenic bird flu viruses.

Not A Lab Construct

From the Nature Medicine article, we get one of the most convincing arguments I’ve seen against the virus being created in a lab:

While the analyses above suggest that SARS-CoV-2 may bind human ACE2 with high affinity, computational analyses predict that the interaction is not ideal and that the RBD sequence is different from those shown in SARS-CoV to be optimal for receptor binding. Thus, the high-affinity binding of the SARS-CoV-2 spike protein to human ACE2 is most likely the result of natural selection on a human or human-like ACE2 that permits another optimal binding solution to arise. This is strong evidence that SARS-CoV-2 is not the product of purposeful manipulation.

So, in other words, if someone in the lab wanted to set out to make a virus with the best possible ACE2 binding site, this is not the sequence the computer or the literature would have given them. That suggests that this very good binding sequence is a product of natural evolution instead. The Nature Medicine article also further noted that the genetic sequence of SARS CoV-2 differs too much from that of any other known coronavirus sequence for one of the known viruses to have been used as a starting point in engineering this stronger pathogen.

The Species Jump

Perhaps the most important step in the emergence of SARS CoV-2 is the jump from its initial host species to humans. This could have happened directly, or as in the case of MERS CoV, which went from bats to camels to humans, with an intermediate host. Note that MERS still has not adapted to efficient human to human transmission, and so when we see it, it’s usually from multiple camel to human events.

The problem here is that we don’t have proof of the host from which humans were first infected with SARS CoV-2. In other words, no virus isolated from an animal so far is related closely enough at the sequence level to SARS CoV-2 that we can say this is where humans were first infected, as we can tell from the MERS jumps from camels to humans. As we will discuss below, and as you are well aware, early suspicion on the origin of human infection centered on the wet market in Wuhan. Remarkably, authors of the Cell paper visited the market and took these pictures in October 2014 because they were concerned that wet markets in general, and this one in particular, represent a particularly large risk for bringing humans into contact with less commonly encountered hosts of potentially deadly viruses:

The caption properly notes that many early cases are linked to the market, but we don’t yet have proof of where and how the first human infection(s) took place. In discussing the jump and subsequent outbreak, the Cell authors continue:

The emergence and rapid spread of COVID-19 signifies a perfect epidemiological storm. A respiratory pathogen of relatively high virulence from a virus family that has an unusual knack of jumping species boundaries, that emerged in a major population center and travel hub shortly before the biggest travel period of the year: the Chinese Spring Festival.

/snip/

While our past experience with coronaviruses suggests that evolution in animal hosts, both reservoirs and intermediates, is needed to explain the emergence of SARS-CoV-2 in humans, it cannot be excluded that the virus acquired some of its key mutations during a period of “cryptic” spread in humans prior to its first detection in December 2019. Specifically, it is possible that the virus emerged earlier in human populations than envisaged (perhaps not even in Wuhan) but was not detected because asymptomatic infections, those with mild respiratory symptoms, and even sporadic cases of pneumonia were not visible to the standard systems used for surveillance and pathogen identification. During this period of cryptic transmission, the virus could have gradually acquired the key mutations, perhaps including the RBD and furin cleavage site insertions, that enabled it to adapt fully to humans. It wasn’t until a cluster of pneumonia cases occurred that we were able to detect COVID-19 via the routine surveillance system. Obviously, retrospective serological or metagenomic studies of respiratory infection will go a long way to determining whether this scenario is correct, although such early cases may never be detected.

So, the sequence information comes to a dead end here until the details of the epidemiology are reconstructed. As the authors note, it likely will prove impossible to sample many of the most important animals and humans that would clarify the route and timing. It is further worth noting that the bat from which the RaTG13 sequence is derived was found in Yunnan province, a very long way from Wuhan.

Epidemiology

It appears that as of this writing, the earliest known infection may have been a shrimp seller in the wet market who first developed symptoms on November 17. Also, this Lancet article provides further details on some of the early studies showing a high concentration of cases affiliated with the market in December. The Lancet graphic suggests a case on December 1 not affiliated with the market and the start of the market cluster on the tenth, with 27 of the 41 early patients considered here being associated with the wet market. If that were indeed the earliest case, we might think we’ve seen the index case. But if the South China Post article is to be believed, the shrimp seller fell ill on November 17 and, according to the article, one to five people a day from that day forward had the disease. If we believe that information, then the virus appears to have already been circulating before the middle of November.

It is when we start getting into this information that accusations of hiding information are thrown about. Were there earlier cases that China suppressed or that simply went undetected? We have no way of knowing at this point.

A further point that comes from the Cell paper is that SARS CoV-2 has been circulating long enough that minor variations in the gene sequence are arising that don’t affect pathogenicity but allow for tracing of various lineages of the virus in its spread around the globe. They also note that the lineages allow them to go back in time over the evolution of those sequences and the diversity diminishes a lot as they get back to the early isolates from Wuhan. This is further confirmation for Wuhan being essential in the earliest part of the outbreak.

Accidental Release

It is here that the noise gets really loud. If we accept the really strong evidence that SARS CoV-2 was not deliberately made in a laboratory, there remains the possibility that the virus could have escaped from a laboratory that studies potential pandemic agents.

As long ago as 2004, Rutgers scientist Richard Ebright spoke out against the massive amount of funding that was funneled into research on bioweapons after the 2001 anthrax attacks. From the New York Times:

Dr. Ebright disagrees with much of the security community about how best to protect the nation from attacks with biological weapons.

The government and many security experts say one crucial step is to build more high-security laboratories, where scientists can explore the threats posed not only by deadly natural germs, but also by designer pathogens — genetically modified superbugs that could outdo natural viruses and bacteria in their killing power. To this end, the Bush administration has earmarked hundreds of millions of dollars to erect such laboratories in Boston; Galveston, Tex.; and Frederick, Md., among other places, increasing eightfold the overall space devoted to the high-technology buildings.

Dr. Ebright, on the other hand, views the plans as a recipe for catastrophe. The laboratories, called biosafety level 4, or BSL-4, are costly, unnecessary and dangerous, he says.

”I’m concerned about them from the standpoint of science, safety, security, public health and economics,” he added in an interview. ”They lose on all counts.”

Ebright continues:

The labs, Dr. Ebright says, are a perilous overreaction to an inflated threat and will do more harm than good.

Although the threat of biological warfare is real, the weapons used by terrorists are unlikely to be the next-generation agents that the high-security labs are intended to study, he says. Yet by increasing the availability of such pathogens, Dr. Ebright argues, the labs will ”bring that threat to fruition.”

”It’s arming our opponents,” he said.

In addition, he says, the laboratories could leak. They could put deadly pathogens into irresponsible hands and they will divert money from other worthy endeavors like public health and the frontiers of biology. Moreover, their many hundreds of new employees would become a pool of deadly expertise that could turn malevolent, unleashing lethal germs on an unsuspecting public.

Note the “leak” bit. The article goes on:

But Dr. Ebright noted that the deadly SARS virus recently escaped from BSL-4 and BSL-3 labs in Taiwan, Singapore and Beijing, in each case setting off minor epidemics that killed or sickened people.

This 2014 paper from the Center for Arms Control goes into detail on two separate escapes of SARS from the same laboratory in Beijing,  along with four other documented cases of releases of possibly pandemic pathogens if you care to read further. Suffice it to say that Ebright was right that with the proliferation of these new labs, there would be leaks. So far, they’ve all been accidental instead of the type feared by Ebright where someone from inside a laboratory deliberately releases a pathogen.

With regard to the SARS CoV-2 outbreak, rumors from nearly the very beginning swirled about a lab in Wuhan. There is in fact a level 4 containment lab in Wuhan and there is also a level 2 lab as well, that I believe is very close to the wet market.

Should there have been an accidental release from either of these labs, at this point we would have to postulate that China has specifically quashed all information relating to this event and kept the laboratory personnel and any close family or other contacts who may have been infected out of the databases of patients.

But that hasn’t stopped the noise. Some aspects of the noise even begin to look to me like an information operation of sorts. Of course, since we don’t know the originator of the operation, we don’t know if it is actual intelligence being leaked or if it is disinformation being sown to add to the chaos.

At any rate, this April 2 column from David Ignatius put the idea of an accidental leak from a Wuhan lab into the Washington Post. Those who follow intelligence community news know that Ignatius is often thought of as a mouthpiece for information the CIA wants disseminated. Are they his source here? Was some other information operative his source?

Then things really heated up on April 15. Here is John Roberts of Fox News asking Trump a question during the April 15 “press conference”:

Wow. That’s an incredibly specific question. It assumes a female intern at the lab who infected a boyfriend and then she (or did he, not clear to me from Roberts’ phrasing) went to the market. Even though this was April 15, I’ve seen no further pushing of this specific version of the story.

But Trump’s response is a bit concerning. Note that he says they’re “hearing that story a lot”, but then makes a really big deal of the word “sources”. Given Trump’s history of spilling classified intelligence, and the constant warnings to him about such leaks compromising “sources and methods”, I almost wonder if that’s a genuine response of his lizard brain to all those warnings. We simply have no way of knowing that or knowing if perhaps those “sources” happen to lie outside the intelligence community and among circle of wingnuts who have the ears of Trump and Fox News and he’s really proud of them but doesn’t want to divulge them.

That same day, Josh Rogin put out a Washington Post column pushing the leak from a lab story, this time tying it directly to the State Department cables in 2018 about lax biosecurity protocols at the level 4 containment lab in Wuhan that Roberts mentioned. But Rogin didn’t include the specifics about the intern.

I’ve heard nothing further on the intern question, but the general idea of an escape from a Wuhan lab still gets tossed around. Ignatius returned to the idea of an accidental release on April 23. He even talked to Ebright:

“Science is not going to shift this from a ‘could have been’ to a ‘probably was,’ ” messaged Richard H. Ebright, a leading biosafety expert at Rutgers. “The question whether the outbreak virus entered humans through an accidental infection of a lab worker . . . can be answered only through a forensic investigation, not through scientific speculation.” Ebright told me the Chinese government should launch a forensic investigation by reviewing “facilities, samples, records, and personnel.”

Given Ebright’s history of predicting just such an accidental release, I find it very reassuring that he isn’t ready to say that’s what happened. As he rightfully points out, we can only know what happened when detailed information is assembled on the epidemiology of the earliest cases. Only Chinese medical investigators can know whether any laboratory personnel, and especially whether any family or other close contacts of them appear on the timeline of the early infections. It is also crucial to know where any such infections, if they exist, fall on the timeline in relation to cases affiliated with the wet market.

My gut feeling is that the evidence still very strongly points to the virus originating through the wet market, but I also think the index case there likely goes back even earlier than the November 17 case discussed above, since there are suggestions there were other cases appearing daily by then. Also, it’s hard to imagine that if the official intelligence community had a story as specific as the intern story and had evidence to back it up, that Trump wouldn’t be trumpeting it on a daily basis to deflect the criticism being heaped on his response to the outbreak.

Stay tuned. I suspect the story will take several more turns before we ever reach any level of certainty.

Understanding Covid-19 for Viral Newbies

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These days we’re drowning in information about the pandemic, but without much context for understanding the virus causing it. With a never-before-seen virus, the best place to get that context is from looking at the history of previous diseases, and by understanding what they’ve done to our biology and society, as we try to figure out what this one does to our biology and society.

People lining up for a market in San Francisco’s Mission District

One of the first and most important questions is how Covid-19 infects people, and this disease is pretty damn infectious. Not as bad as diseases like Measles, Mumps, and Rubella, but worse than most flus. (The most infectious diseases tend to become the diseases of childhood because you’re born, and BAM! you get them, they’re so infectious.) Transmission is measured with the R₀ (“R-naught”) we keep seeing in news stories, measuring how many people one infected person will infect in a given time period. But it’s not a number that just exists without context — lowering that number is why so many of us are staying at home, trying to figure out how we’re going to pay the bills right now. But without the social distancing, Covid-19 is more infectious than anything most of us have experienced in our lives.

What makes Covid-19 infectious has a lot to do with how well the particular virus that causes it, SARS-CoV-2, survives in the world, along with how good SARS-CoV-2 is at finding the kind of cell it uses as a host and then invading it.

To contrast Covid-19 with the most recent nasty pandemic, AIDS, it is much more likely to spread and much less likely to kill those it spreads to. HIV, the virus that causes AIDS, is a delicate virus, despite causing a nasty disease. HIV dies if you blow on it.

The only fomite (the word for inanimate objects that can pass infections) that transmits HIV in the normal course of life is a needle full of HIV-infected blood, and that’s not easy to accidentally infect yourself with on your way to a restaurant. Other than direct blood transmission, it has to be transmitted person to person through intimate contact.

HIV is also good, but not great, at finding and infecting its target cells, and it happens to use the same kind of cells that Yersinia pestis, better known as the plague, and one of the worst pandemics ever, likes to invade. (This fact becomes very important in the story of contemporary civilization, hold on to your hats.)

So the limits to HIV spreading come from how hard it is for the virus to survive when it’s not in an ideal environment, and how hard it is to invade certain immune cells, its host of choice. This is why it is much easier to catch it from needle/blood transfer than anything else, and why some sex is more likely to transmit it than other sex is. For all the gay plague talk, the absolute safest sexually active group in the AIDS epidemic was lesbians. (I guess God loves lesbians the most?)

HIV is not passed via the respiratory system. The entrance to the respiratory system is the leaky liquidy parts of your face: eyes, nose, and mouth. This is an extremely important point. If HIV was transmitted that way, if it was a little hardier and could live in droplets you expel from your face, everything, and I do mean everything, would be terrible.

This isn’t because a respiratory infection couldn’t do what HIV does – there is a respiratory version of the plague that’s completely horrific. Pneumonic plague is in that category of diseases so bad that they burn themselves out by being so horrible and deadly that they run out of hosts, if not for the fact that it has other ways to spread, namely fleas. (Y. pestis is the worst.)

HIV budding out of an immune cell (NIAID)

So while HIV is terrible and has cost the world immeasurably, it’s not the plague. Also, because of the plague, HIV is considerably worse at infecting immune cells in populations that were genetically impacted by the plague. HIV uses a receptor on immune cells called CCR5. The “receptor” here is a little protein lock that opens up a cell. A bit like a tiny door with lock and doorknob. Seven hundred years before HIV came around, Y. pestis, despite being a bacterium rather than a virus, was using the same CCR5 to get inside immune cells. It killed somewhere around half of Europe and came back and kept killing for hundreds of years until the human genome declared FUCK THIS and mutated CCR5 out of service in a portion of the population, a portion that then had the chance to have more kids.

 

This is why despite having similar chances to spread, HIV is less prevalent in European populations that went through that plague-induced genetic narrowing than in sub-Saharan Africa, which was probably never seriously afflicted by Y. pestis in the way Europe, western Asia, and North Africa were. This made them far more vulnerable to HIV, with the tragic results we see now.

To bring it back to our current bug: SARS-CoV-2’s infectiousness is closer to pneumonic plague than HIV in infectiousness, but also different because there’s no insect vector.

This little bugger can hang on in the environment. SARS-CoV-2 can survive for days on common surfaces like steel or plastic. It survives for four hours on copper. Copper is basically the Purell of metals. That’s not good.

SARS-CoV-2 is very good at accessing and infecting its target cells, which are generally surface tissue (epithelial) cells with ACE2 protein receptors, analogous to the CCR5 that Y. pestis and HIV use. Anything with that ACE2 receptor will work for SAR-CoV-2, but lung cells are the tissues they most likely encounter when someone breathes in the virus. It’s harder for it to get to those same receptors in your intestines from your nose. But it’s entirely possible that for the people who do experience intestinal symptoms like diarrhea, SARS-CoV-2 got to those ACE2 receptors as well.

You can think of the ACE2 receptor as a little locked door on the surface of the cell. In order for the useful things that the cell makes to get out, or for the cell to get a useful thing it needs to get in, other cells will come by with the key that fits into the receptor and unlock it.

A coronavirus is a small ball of fat and protein covered in lock picks, which in this case are little “spike” proteins that fit into the ACE2 receptor and open the door for the virus’s RNA to come in.

A 3D print of just the spike protein from a SARS-CoV-2 virus. This is the “lockpick” for the ACE2 receptor.

That’s it, that’s how it works. It’s amazing how much, when you get biology down to the micro level, bodies work like legos and tinker toys, but wet.

The thing about this virus, which makes it more infectious than the flu or even classic SARS or MERS, is that the spike protein on the surface of SARS-CoV-2 picks the lock of the ACE2 receptor very well. As soon as it hits it, it locks in. That means fewer viruses are needed to infect a person.

See more here.

That, along with how well it survives and travels in droplets, is what stopped the world.

The good news is for most people Covid-19 doesn’t do much. In many cases, it does even less than the flu or a normal cold. It’s good news for people who get Covid-19, but not great news for a planet trying to find and isolate asymptomatic cases. You win some, you lose some.

There are two kinds of immune systems at play in responding to anything that threatens the body: the innate immune system, and the adaptive immune system.

The innate is your first level of defense, looking for and eliminating baddies like SARS-CoV-2. But the innate system isn’t where you get immunity. Immunity comes from a process where the innate system reacts to a novel bug it has never seen, and learns about it. Then a certain kind of innate immune cell, called a dendritic cell, presents the shape of a coronavirus, or whatever other nasty pathogen the body is fighting, to the T and B cells of the adaptive immune system, which then go all Terminator and hunt down and kill whatever is shaped like the thing they got from the innate system.

That process is what we call acquiring immunity, and it’s why no one can, by definition, be immune to a novel virus, including this one. Immune is not the same as showing no symptoms, even though many people, including journalists, keep using those terms interchangeably. That is a dangerous mistake, so let me repeat this: the only people on our beloved blue-green world who are immune to Covid-19 are those who have had it and recovered from it, and we’re not even sure how immune they are. So why do some people seem immune?

Covid-19 seems to have some way of calming down some innate immune responses (mechanisms which seem work strangely in children, that’s still unclear). It doesn’t usually win against the learned immune response in most people who get infected, who clear out the virus and become immune. Of course, this isn’t how it goes for everyone… but thankfully for most of us, it’s mild to asymptomatic.

The problem is with the virus calming the innate immune response is that the innate immune system is what gives you symptoms. Viruses don’t give you fevers and headaches, coughs, aches, and the desire to stay in bed, your immune response does that.

Without those symptoms infected people spread this very hardy virus all over until the immune system catches up with making them feel sick. We don’t know how long asymptomatic carriers shed virus this way. It could be a day, it could be two weeks.

In the end, it’s likely most of us are either going to get Covid-19 or get a vaccine. With this much global spread, the disease is headed to be the next coronoavirus to be endemic in humanity (the common cold is caused by other coronaviruses between 15-20% of the time).

Endemic means this is a disease the floats around the population, with pretty much one infected person infecting one more person (R=1). Many endemic diseases in history are nasty, like Smallpox, which in its prime regularly killed a third of children in Europe.

Endemic diseases can also flare into epidemics, when they encounter a large group of people without immunity, and then calm down again once they’ve done their damage. Diseases going from epidemic to endemic don’t just change our lifestyles and our societies, they change us at the genetic level, and we change them back.

We see that with the HIV and plague connection, and with European explorers accidentally (mostly) wiping out the vast majority of the new world, for whom the Smallpox virus was, like Covid-19, novel, and consequently far more deadly.

I hope we get the vaccine, and the news is good there, so far. SARS-CoV-2 doesn’t seem to be a fast mutator, unlike HIV, which has dodged all of our attempts to vaccinate for it.

Covid-19 might be treatable with some kind of antiviral medications, which would be nice, but that needs to go through trials first before any more unscrupulous doctors and incompetent politicians make up things about malaria meds, and people start eating fish tank cleaner en masse.

But in general, this is a bit like plague-level nightmare transmission, but with novel influenza lethality. Not great, but it could be much worse. At its most terrible, Y. pestis could kill up to 80% of its victims. (Y. pestis is the worst.)

How long we stay immune is another question, and we are far from answering it.

There’s two factors at play – one is that some immunity (like Smallpox) is for life, but for some other diseases, the adaptive immune system forgets about them after enough time passes. The second factor is how much the virus changes as it mutates going through hosts. The more people it infects, the more chances there are for the virus’s genes to drift as it reproduces. That makes more chances for it to become different enough that the body has to learn about it again, which unfortunately gets done by getting re-infected. It’s early days, but so far SARS-CoV-2 doesn’t seem to be prone to drifting.

Genomic changes in SARS-CoV-2 as it infects the world, tracked by Nextstrain.

SARS-CoV-2’s apparent genetic stability is some of the best news we’ve had for beating this disease in the long term, but it’s still early days. When bugs become endemic, they tend to lose some of their virulence as well. Killing your hosts isn’t very adaptive for a parasite, and dying isn’t very adaptive for us. But that is generations away.

For now, keep washing your hands and staying home for everything but essential work, store runs, exercise, and medical care. This is going to be very hard for everyone, but humanity will get through it together.

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Research Misinfo/Disinfo: Check Experts’ Homework

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[Check the byline, thanks. /~Rayne]

This is the first of two posts about research information and the disease COVID-19. I want to point out upfront I’m not a scientist/medical professional/public health expert. However I spend a lot of time reading fine print.

One thing I should set straight here is that we tend to use COVID-19 to refer to the disease and to the virus which causes it. This isn’t really accurate; I’ll be referring to SARS-CoV-2 as the virus underlying the disease called COVID-19 in this post.

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Family members shared with me a link they received from a health care professional we know and trust. This professional told my family a Stanford researcher said “heat and sunshine will help to diminish the virus that causes COVID-19.”

You can imagine my family members’ concern because they’re in Florida where it’s quite warm already and yet COVID-19 cases continue to mount.

This situation provides a good example of how experts misunderstand and/or misuse research information and how lay people can be further misled or confused.

Direct link to video: https://youtu.be/xUGwGgV7r5Y

Note the researcher Dr. Lin’s background, Associate Professor in Neurology and Bioengineering at Stanford. He’s degreed in biochemistry and neurobiology, did postdoctoral work in fluorescent protein engineering. Sharp guy, great CV, but he isn’t a virologist or an epidemiologist.

At 6:45 in the video he refers to the outside of the virus as a “plasma membrane” — that’s just another less frequently-used term referring to a cell membrane. Virologists are more specific when discussing the coronavirus which causes COVID-19; it’s an RNA virus with a lipid membrane, attacked readily by soap though he does mention detergents.

When talking about sunshine or UV effects he discusses coronaviruses as a class, not SARS-CoV-2 specifically; he actually uses the word “estimate” with regard to timing.

Here is the first PubMed study Dr. Lin referred to in his video:

Photochem Photobiol. 2007 Sep-Oct;83(5):1278-82.
Inactivation of influenza virus by solar radiation.
Sagripanti JL, Lytle CD.
https://www.ncbi.nlm.nih.gov/pubmed/17880524

Emphasis mine. It’s not a study about *any* coronaviruses at all.

This is the second PubMed doc he cited:

J Virol. 2005 Nov;79(22):14244-52.
Predicted inactivation of viruses of relevance to biodefense by solar radiation.
Lytle CD, Sagripanti JL.
https://www.ncbi.nlm.nih.gov/pubmed/16254359

This study doesn’t even mention coronaviruses and was published *before* the MERS outbreak — another SARS-like variant of coronavirus which was first identified in 2012 in the Middle East, which I’ll point out is both sunny and hot compared to the northern U.S.

When Dr. Lin discussed temperature he referred to this study on the specific corona virus which causes the disease SARS:

Adv Virol. 2011;2011:734690. doi: 10.1155/2011/734690. Epub 2011 Oct 1.
The Effects of Temperature and Relative Humidity on the Viability of the SARS Coronavirus.
Chan KH, Peiris JS, Lam SY, Poon LL, Yuen KY, Seto WH.
https://www.ncbi.nlm.nih.gov/pubmed/22312351

Emphasis mine. Note this is a study of the virus which causes SARS, not the viruses which cause influenza or COVID-19. This is the abstract:

The main route of transmission of SARS CoV infection is presumed to be respiratory droplets. However the virus is also detectable in other body fluids and excreta. The stability of the virus at different temperatures and relative humidity on smooth surfaces were studied. The dried virus on smooth surfaces retained its viability for over 5 days at temperatures of 22-25°C and relative humidity of 40-50%, that is, typical air-conditioned environments. However, virus viability was rapidly lost (>3 log(10)) at higher temperatures and higher relative humidity (e.g., 38°C, and relative humidity of >95%). The better stability of SARS coronavirus at low temperature and low humidity environment may facilitate its transmission in community in subtropical area (such as Hong Kong) during the spring and in air-conditioned environments. It may also explain why some Asian countries in tropical area (such as Malaysia, Indonesia or Thailand) with high temperature and high relative humidity environment did not have major community outbreaks of SARS.

38C = 100F degrees.

People avoid being tightly clustered in confined spaces at that temperature. Note especially the first sentence about inhaled droplets. It’s not just that the virus may lose viability in a shorter period of time which reduces cases but the proximity of humans during the time the virus is active. Temperature alone is not a factor in reducing transmission rates.

The second study about temperature he cited:

Biomed Environ Sci. 2003 Sep;16(3):246-55.
Stability of SARS coronavirus in human specimens and environment and its sensitivity to heating and UV irradiation.
Duan SM, Zhao XS, Wen RF, Huang JJ, Pi GH, Zhang SX, Han J, Bi SL, Ruan L, Dong XP; SARS Research Team.
https://www.ncbi.nlm.nih.gov/pubmed/14631830

Emphasis mine — this is yet another study of the virus which causes SARS. This is a fairly early study dated 2003; the SARS outbreak began in 2002 with the first epidemic ending in June 2003. Here’s the results in the abstract:

RESULTS:
The results showed that SARS coronavirus in the testing condition could survive in serum, 1:20 diluted sputum and feces for at least 96 h, whereas it could remain alive in urine for at least 72 h with a low level of infectivity. The survival abilities on the surfaces of eight different materials and in water were quite comparable, revealing reduction of infectivity after 72 to 96 h exposure. Viruses stayed stable at 4 degrees C, at room temperature (20 degrees C) and at 37 degrees C for at least 2 h without remarkable change in the infectious ability in cells, but were converted to be non-infectious after 90-, 60- and 30-min exposure at 56 degrees C, at 67 degrees C and at 75 degrees C, respectively. Irradiation of UV for 60 min on the virus in culture medium resulted in the destruction of viral infectivity at an undetectable level.

37C = 98.6F (This made me laugh – it’s the temperature used for many years as a baseline for the average healthy human.)

Sure, heat deactivates the SARS coronavirus at temperatures fatal to humans, but it’s active at least a couple hours at temperatures in which humans live.

The last study cited was:

Aerosol and Surface Stability of SARS-CoV-2 as Compared with SARS-CoV-1
March 17, 2020
DOI: 10.1056/NEJMc2004973
https://www.nejm.org/doi/full/10.1056/NEJMc2004973
https://www.ncbi.nlm.nih.gov/pubmed/32182409

I’ve referred to this several times in comments with regard to hang time of the aerosolized virus. This study is a pre-print, not peer reviewed I should point out. It’s worth reading this study in particular because it’s about SARS-CoV-2 not SARS-CoV-1 and the findings have been misreported or misused a number of times in the media.

Rely on that last study the most because it’s about SARS-CoV-2, not SARS-CoV-1. It confirms that like the virus which causes SARS that SARS-CoV-2 can hang in the air as aerosol, and in this case the study showed it was viable for 3 hours:

SARS-CoV-2 remained viable in aerosols throughout the duration of our experiment (3 hours), with a reduction in infectious titer from 103.5 to 102.7 TCID50 per liter of air. This reduction was similar to that observed with SARS-CoV-1, from 104.3 to 103.5 TCID50 per milliliter (Figure 1A).

A friend sent me a link to this new pre-print study, not peer reviewed yet, published Friday March 27:

Stability of SARS-CoV-2 in different environmental conditions
Alex W.H. Chin, Julie T.S. Chu, Mahen R.A. Perera, Kenrie P.Y. Hui, Hui-Ling Yen, Michael C.W.
Chan, Malik Peiris, Leo L.M. Poon
https://www.medrxiv.org/content/10.1101/2020.03.15.20036673v2.full.pdf

This work confirms the viability of SARS-CoV-2 virus drops with increases in temperature and over time, but do note the data table provided in the study.

What the March 17 and March 27 studies say is that SARS-CoV-2 does weaken and become inactive with heat and over time.

What these and the other studies above do NOT say is that “heat and sunshine will diminish the virus.” There haven’t been any studies about SARS-CoV-2 viability over time with exposure to UV that I’m aware of . And while heat does speed the inactivation of SARS-CoV-2, the virus is still active for 2-3 hours in aerosolized form.

Like exhalation from infected humans, whether symptomatic or not.

It’s critically important that the public understands this virus SARS-CoV-2 is different from its relative, SARS-CoV-1. We can see this difference in both the ease with which it spreads and its much lower case fatality rate. Using studies of SARS and SARS-CoV-1 to extrapolate what SARS-CoV-2 will do has limits because of these key differences.

The same goes for anyone claiming SARS-CoV-2 is just another flu bug, that COVID-19 is just another influenza. It’s definitely not — anecdotal evidence of dead Americans by the truckloads tell you this is not just another flu. This difference is so obvious you should reject any such claims as propaganda. And any researcher making claims about SARS-CoV-2’s viability under certain conditions based on influenza viruses isn’t helping the public.

It’s as unhelpful as telling people erroneously that “heat and sunshine will help to diminish the virus that causes COVID-19.”

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The bottom line: STAY HOME because aerosolized virus from asymptomatic and pre-symptomatic carriers in closed spaces has resulted in a significant number of confirmed cases versus fomite transmission — virus left on surfaces — though fomite transmission is still possible.

I’ll point to the story the Los Angeles Times published this week — sharing The Daily Beast’s summary because the LAT article is behind a paywall:

The Los Angeles Times reports that 45 out of 60 Skagit Valley Chorale who gathered at the Mount Vernon Presbyterian Church have tested positive. Three have been hospitalized and two have died.
https://www.thedailybeast.com/coronavirus-strikes-45-of-60-people-who-went-to-mount-vernon-washington-choir-practice

These people were careful; they observed social distancing techniques and heightened hygiene. But aerosolized virus got them, and it can get to others even when the weather is warm.

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Next: the lack of solid research behind a particular off-label therapy.