scientificamerican--2020-09-07--Costa Rica Readies Horse Antibodies for Trials as an Inexpensive COVID-19 Therapy

Editor ’ s Note ( 9/4/20 ) : Drugmakers worldwide are working overtime to produce vaccines for COVID-19 .
If delays emerge , they may need to rely on costly biotech such as monoclonal antibodies .
In this article , Scientific American details another approach making progress in Costa Rica , where inexpensive horse antibodies are being developed against the novel coronavirus .
Development of the hundreds of vaccines and therapies for COVID-19 is by no means confined to metro areas surrounding San Francisco , Boston or Washington , D.C .
Borrowing from decades of experience in producing snake antivenoms @ @ @ @ @ @ @ a scientific and technical institute in Costa Rica have labored nonstop in recent months to produce a therapeutic formulation of equine antibodies against SARS-CoV-2 , the coronavirus that causes COVID-19 .
Similar efforts are underway in Brazil and Argentina to tide these countries over until the arrival of an effective vaccine .
In late March , after the first case of COVID-19 was diagnosed in Costa Rica , Román Macaya—a biochemist and public health expert who heads the Costa Rican Social Security Fund , which runs the nation ’ s public clinics and @ @ @ @ @ @ @ to join the fight against the then nascent pandemic .
“ Our response to COVID-19 could not be only a health care response , ” Macaya says .
“ It had to be a scientific response as well.
” In making his plea for help , he singled out the antivenom specialists at the University of Costa Rica ’ s Clodomiro Picado Institute , which is named after a renowned Costa Rican scientist .
“ The very next day we got a letter from Henning Jensen , then rector of the University of @ @ @ @ @ @ @ re in .
Let 's get together and work on this , ’ ” Macaya recalls .
The effort ’ s objective was to harness the technology and experience the Clodomiro Picado Institute has acquired in its work using horse antibodies to fabricate antivenoms for snake bites during the past five decades .
Every year , the antivenoms with purified equine antibodies produced at the institute save more than 500 people in Costa Rica and thousands more in other countries around the world .
The Clodomiro Picado Institute has more than 100 horses @ @ @ @ @ @ @ venoms after being inoculated with small quantities of toxins over a period of weeks to months .
Besides their use in antivenoms for snakes , scorpions and spiders , for decades , pharmaceutical preparations of equine antibodies have been employed worldwide as a treatment for rabies , botulism and diphtheria .
Clinical trials of the institute ’ s antivenoms conducted in Colombia , Nigeria and Papua New Guinea have shown that these antibodies are safe in humans and rarely induce severe adverse reactions .
More recently , equine immunoglobulin therapy has emerged as @ @ @ @ @ @ @ viruses that have limited therapeutic options .
Among them are the highly pathogenic avian influenza viruses H5N1 and H7N9 and the coronavirus that causes Middle East Respiratory Syndrome ( MERS ) .
“ All this inspired several research groups to find ways to produce safe and effective COVID-19 equine immunoglobulins , ” explains Fan Hui Wen , a researcher and project manager at the Butantan Institute in Brazil , which also has long experience in manufacturing such antibodies .
She was not involved with the research at the Clodomiro Picado Institute .
The @ @ @ @ @ @ @ familiarity .
“ The idea behind the antibody therapy for patients with COVID-19 is similar to that of treating patients suffering from snakebite poisoning , ” says Alberto Alape Girón , a microbiologist and lead researcher of the COVID-19 project at the Clodomiro Picado Institute .
“ We want to generate specific antibodies against viral structures in horses , purify the antibodies and give them to patients who are starting to fight the infection but whose immune system still does not produce enough antibodies to clear the viral particles , ” he adds @ @ @ @ @ @ @ with the research donated six horses to the institute .
The animals were inoculated with engineered proteins of the SARS-CoV-2 virus .
Three of the horses received only S1 , a portion of the protein that makes up the protruding spikes that stick out from the pathogen ’ s surface .
The other three animals received a combination of four proteins from the coronavirus , including S1 .
After four rounds of inoculations administered every two weeks , the horses produced the desired level of antibodies .
At this point , their blood @ @ @ @ @ @ @ cells were separated from the plasma and returned to the horses .
“ Plasma is a very complex mixture that has hundreds of proteins , ” Alape-Girón says .
“ Antibodies are one of the most abundant proteins , but there are others.
” At the pharmaceutical plant , researchers used a technology developed by the Clodomiro Picado Institute to separate the antibodies from other proteins in the plasma and then purified them to obtain the therapeutic formulation for human testing .
In total , the plant produced 1,000 10-milliliter vials of purified @ @ @ @ @ @ @ antibodies against the S1 protein , and the other half contained the four proteins present in the coronavirus .
“ Just one 10-mL vial has about 80 times the quantity of antibodies you can find in 800 mL of convalescent plasma , which is the plasma donated by someone who has overcome an infection of SARS-CoV-2 , ” Alape-Girón says .
To test the efficacy of the equine antibodies , a few vials were shipped to George Mason University ’ s National Center for Biodefense and Infectious Diseases ( NCBID ) .
“ @ @ @ @ @ @ @ virus could be neutralized by the horse-produced antibodies , ” says Charles Bailey , a professor of biology and executive director of the NCBID .
“ The test we performed on the samples is called a plaque reduction neutralization test , PRNTest .
We exposed the antibodies produced in horses , at various dilutions , to the SARS-CoV-2 virus growing on cell culture .
The virus was neutralized.
” The results of the research are expected to be published in the near future .
The next step—testing the equine antibodies in COVID-19 patients—will @ @ @ @ @ @ @ month .
The antibodies ’ safety and efficacy will be examined in a group of 26 patients with COVID-19 who have been hospitalized but not placed in an intensive care unit .
The results are expected by the end of September .
If they are positive , the research will then move to a large-scale trial with hundreds of patients .
And if the equine antibodies are shown to be effective , the Clodomiro Picado Institute could immunize more horses to scale up and produce enough of them to cover Costa Rica ’ @ @ @ @ @ @ @ .
It received a $ 500,000 grant on Aug. 13 from the Central American Bank for Economic Integration to move ahead with equine antibody research .
Unlike monoclonal antibodies , which are being developed to target a specific molecular region , or epitope , on the surface of SARS-CoV-2 to elicit an immune response , horse polyclonal antibodies against SARS-CoV-2 recognize multiple epitopes .
The lower specificity translates into a more inexpensive manufacturing process .
Alape-Girón estimates that a vial of equine antibodies will cost $ 100 to produce , whereas a treatment @ @ @ @ @ @ @ more expensive .
“ It ’ s not the highest technology , ” Macaya says .
“ It ’ s not a monoclonal antibody , but it allows us the benefit of speed , and it ’ s a very pragmatic approach.
” Further , “ if this were a monoclonal antibody , you would need a big factory to produce them , ” he adds .
“ Here , the horses are the factories—at least for the production part .
Then comes the purification part , which is an industrial process , @ @ @ @ @ @ @ that infrastructure.
” Fan says this description mirrors her experience at the Butantan Institute in Brazil .
“ Polyclonal antibody products can be made in large quantities , and cost-effectively , to respond to large-scale pandemic situations , such as the infection by SARS-CoV-2 ” , she says .
Currently , the Butantan Institute is preparing horses to be immunized with portions of inactivated SARS-COV-2 virus , which were isolated , cultured and purified , using its expertise in the production of influenza virus vaccines .
Even though the development protocols differ at @ @ @ @ @ @ @ Fan predicts their antibodies “ will have equivalent efficiency and safety in the treatment of COVID-19 patients.
” Even farther south in South America , scientists in Argentina are also developing a potential therapy for COVID-19 patients using equine antibodies , while other researchers worldwide are exploring antibodies against SARS-CoV-2 from llamas and cows .
The objective behind all of these projects is the same : to save lives while waiting for a vaccine to become available .
Costa Rica has more than 28,000 cases of COVID-19 .
`` We have over 100 @ @ @ @ @ @ @ says .
`` And our ICU capacity , as with any country , is limited . ''
His hope is that equine antibodies will prove to be “ a very valuable tool in keeping our health care system from collapsing at the ICU level and , obviously , preventing deaths .
That ’ s the ultimate goal.
” Read more about the coronavirus outbreak from Scientific American here .
And read coverage from our international network of magazines here .

Editor’s Note (9/4/20): Drugmakers worldwide are working overtime to produce vaccines for COVID-19. If delays emerge, they may need to rely on costly biotech such as monoclonal antibodies. In this article, Scientific American details another approach making progress in Costa Rica, where inexpensive horse antibodies are being developed against the novel coronavirus.
Development of the hundreds of vaccines and therapies for COVID-19 is by no means confined to metro areas surrounding San Francisco, Boston or Washington, D.C. Borrowing from decades of experience in producing snake antivenoms, scientists, veterinarians and technicians at a scientific and technical institute in Costa Rica have labored nonstop in recent months to produce a therapeutic formulation of equine antibodies against SARS-CoV-2, the coronavirus that causes COVID-19. Similar efforts are underway in Brazil and Argentina to tide these countries over until the arrival of an effective vaccine.
In late March, after the first case of COVID-19 was diagnosed in Costa Rica, Román Macaya—a biochemist and public health expert who heads the Costa Rican Social Security Fund, which runs the nation’s public clinics and hospitals—issued a call for the research community to join the fight against the then nascent pandemic. “Our response to COVID-19 could not be only a health care response,” Macaya says. “It had to be a scientific response as well.”
In making his plea for help, he singled out the antivenom specialists at the University of Costa Rica’s Clodomiro Picado Institute, which is named after a renowned Costa Rican scientist. “The very next day we got a letter from Henning Jensen, then rector of the University of Costa Rica saying, ‘We’re in. Let's get together and work on this,’” Macaya recalls.
The effort’s objective was to harness the technology and experience the Clodomiro Picado Institute has acquired in its work using horse antibodies to fabricate antivenoms for snake bites during the past five decades. Every year, the antivenoms with purified equine antibodies produced at the institute save more than 500 people in Costa Rica and thousands more in other countries around the world.
Equine antibodies made at The Clodomiro Picado Institute’s production plant. Credit: Jenniffer Jiménez Oficina de Divulgación, Universidad de Costa Rica
The Clodomiro Picado Institute has more than 100 horses that have developed strong immunity to snake venoms after being inoculated with small quantities of toxins over a period of weeks to months. Besides their use in antivenoms for snakes, scorpions and spiders, for decades, pharmaceutical preparations of equine antibodies have been employed worldwide as a treatment for rabies, botulism and diphtheria. Clinical trials of the institute’s antivenoms conducted in Colombia, Nigeria and Papua New Guinea have shown that these antibodies are safe in humans and rarely induce severe adverse reactions.
More recently, equine immunoglobulin therapy has emerged as a potential treatment for a range of viruses that have limited therapeutic options. Among them are the highly pathogenic avian influenza viruses H5N1 and H7N9 and the coronavirus that causes Middle East Respiratory Syndrome (MERS). “All this inspired several research groups to find ways to produce safe and effective COVID-19 equine immunoglobulins,” explains Fan Hui Wen, a researcher and project manager at the Butantan Institute in Brazil, which also has long experience in manufacturing such antibodies. She was not involved with the research at the Clodomiro Picado Institute.
The Costa Rican project has an air of familiarity. “The idea behind the antibody therapy for patients with COVID-19 is similar to that of treating patients suffering from snakebite poisoning,” says Alberto Alape Girón, a microbiologist and lead researcher of the COVID-19 project at the Clodomiro Picado Institute. “We want to generate specific antibodies against viral structures in horses, purify the antibodies and give them to patients who are starting to fight the infection but whose immune system still does not produce enough antibodies to clear the viral particles, ” he adds.
Private citizens who wanted to help with the research donated six horses to the institute. The animals were inoculated with engineered proteins of the SARS-CoV-2 virus. Three of the horses received only S1, a portion of the protein that makes up the protruding spikes that stick out from the pathogen’s surface. The other three animals received a combination of four proteins from the coronavirus, including S1.
After four rounds of inoculations administered every two weeks, the horses produced the desired level of antibodies. At this point, their blood was extracted, and the red blood cells were separated from the plasma and returned to the horses. “Plasma is a very complex mixture that has hundreds of proteins,” Alape-Girón says. “Antibodies are one of the most abundant proteins, but there are others.” At the pharmaceutical plant, researchers used a technology developed by the Clodomiro Picado Institute to separate the antibodies from other proteins in the plasma and then purified them to obtain the therapeutic formulation for human testing.
In total, the plant produced 1,000 10-milliliter vials of purified equine antibodies. Half of them had antibodies against the S1 protein, and the other half contained the four proteins present in the coronavirus. “Just one 10-mL vial has about 80 times the quantity of antibodies you can find in 800 mL of convalescent plasma, which is the plasma donated by someone who has overcome an infection of SARS-CoV-2,” Alape-Girón says.
To test the efficacy of the equine antibodies, a few vials were shipped to George Mason University’s National Center for Biodefense and Infectious Diseases (NCBID). “We wanted to determine if the SARS-CoV-2 virus could be neutralized by the horse-produced antibodies,” says Charles Bailey, a professor of biology and executive director of the NCBID. “The test we performed on the samples is called a plaque reduction neutralization test, PRNTest. We exposed the antibodies produced in horses, at various dilutions, to the SARS-CoV-2 virus growing on cell culture. The virus was neutralized.” The results of the research are expected to be published in the near future.
The next step—testing the equine antibodies in COVID-19 patients—will begin with an accelerated clinical trial this month. The antibodies’ safety and efficacy will be examined in a group of 26 patients with COVID-19 who have been hospitalized but not placed in an intensive care unit. The results are expected by the end of September. If they are positive, the research will then move to a large-scale trial with hundreds of patients. And if the equine antibodies are shown to be effective, the Clodomiro Picado Institute could immunize more horses to scale up and produce enough of them to cover Costa Rica’s demand—and probably that of its neighbors. It received a $500,000 grant on Aug. 13 from the Central American Bank for Economic Integration to move ahead with equine antibody research.
Unlike monoclonal antibodies, which are being developed to target a specific molecular region, or epitope, on the surface of SARS-CoV-2 to elicit an immune response, horse polyclonal antibodies against SARS-CoV-2 recognize multiple epitopes. The lower specificity translates into a more inexpensive manufacturing process. Alape-Girón estimates that a vial of equine antibodies will cost $100 to produce, whereas a treatment with monoclonal antibodies could be 10 times more expensive.
“It’s not the highest technology,” Macaya says. “It’s not a monoclonal antibody, but it allows us the benefit of speed, and it’s a very pragmatic approach.” Further, “if this were a monoclonal antibody, you would need a big factory to produce them,” he adds. “Here, the horses are the factories—at least for the production part. Then comes the purification part, which is an industrial process, but the Clodomiro Picado Institute already has that infrastructure.”
Fan says this description mirrors her experience at the Butantan Institute in Brazil. “Polyclonal antibody products can be made in large quantities, and cost-effectively, to respond to large-scale pandemic situations, such as the infection by SARS-CoV-2”, she says.
Currently, the Butantan Institute is preparing horses to be immunized with portions of inactivated SARS-COV-2 virus, which were isolated, cultured and purified, using its expertise in the production of influenza virus vaccines. Even though the development protocols differ at the Brazilian and Costa Rican institutes, Fan predicts their antibodies “will have equivalent efficiency and safety in the treatment of COVID-19 patients.”
Even farther south in South America, scientists in Argentina are also developing a potential therapy for COVID-19 patients using equine antibodies, while other researchers worldwide are exploring antibodies against SARS-CoV-2 from llamas and cows. The objective behind all of these projects is the same: to save lives while waiting for a vaccine to become available.
Costa Rica has more than 28,000 cases of COVID-19. "We have over 100 patients in the ICU," Macaya says. "And our ICU capacity, as with any country, is limited." His hope is that equine antibodies will prove to be “a very valuable tool in keeping our health care system from collapsing at the ICU level and, obviously, preventing deaths. That’s the ultimate goal.”
Read more about the coronavirus outbreak from Scientific American here. And read coverage from our international network of magazines here.


scientificamerican--2020-09-07--An Immune Protein Could Prevent Severe COVID-19--if It Is Given at the Right Time

Editor ’ s Note ( 9/4/20 ) : Understanding how the immune system goes awry in COVID-19 may help prevent the most severe and deadly cases .
Earlier this year Scientific American explained how administering an antiviral protein called interferon at just the right time may help .
When the immune system fights viruses , timing is key .
And this maxim may be especially true for its defense against the deadly severe form of COVID-19 .
Several new studies of immune response to SARS-CoV-2 , the virus that causes the disease , suggest timing could be critical for a @ @ @ @ @ @ @ which are being researched as potential treatments .
These immune proteins suppress viral replication early in disease .
Yet if they are active later , some scientists think they can exacerbate the harmful inflammation that forces some COVID-19 patients onto life support .
Interferons are “ a double-edged sword , ” says immunologist Eui-Cheol Shin of the Korea Advanced Institute of Science and Technology .
Researchers have been looking at both of that sword ’ s edges .
About a decade ago , when Shin was studying the viral disease hepatitis C , @ @ @ @ @ @ @ .
But examinations of some conditions suggested they should not be employed .
For example , researchers in Paris found that too much of the proteins can lead to a diseases known as children ’ s interferonopathies .
In a sense , each of these two perceptions of interferons is correct .
And understanding when , and to what extent , using them is warranted could be a critical factor in treating COVID-19 .
The researchers in Paris analyzed blood from 50 people with varying COVID-19 severity and 18 healthy controls .
They @ @ @ @ @ @ @ overall counts of lymphocytes ( a type of white blood cell ) .
Using techniques to analyze broad-based gene activity and measure specific proteins , two trends stood out : Compared with patients with milder forms of the disease , people with severe COVID-19 had an exaggerated inflammatory response , coupled with a marked decrease in interferons .
And among severe COVID-19 patients , the interferon deficiency was worse in those who died versus those who stabilized , the team reported on July 13 in Science .
“ We were surprised , ” @ @ @ @ @ @ @ Cochin Hospital in Paris , who was co-senior author of the study .
“ It was not our hypothesis.
” An analysis published in the May 28 issue of Cell by researchers at the Icahn School of Medicine at Mount Sinai turned up a similar dual signature : low interferon levels and elevated inflammatory proteins .
Meanwhile , in another new study , Shin and his colleagues used single-cell RNA sequencing to analyze gene activity in immune cells .
They analyzed blood samples from eight patients with mild or severe COVID-19 , four @ @ @ @ @ @ @ influenza—more than 59,000 cells in total .
The researchers employed computer algorithms to compare individual cells ’ RNA , and they expected patterns to cluster by cell type .
That is , they anticipated that T cells , lymphocytes that coordinate an immune response or kill invading pathogens , would look a lot alike , whether they were taken from patients with COVID-19 or influenza .
But that was not the case .
Instead the cellular profiles grouped by disease .
For example , T cells from COVID-19 patients did not resemble those @ @ @ @ @ @ @ looked more like COVID-19 B cells , Shin says .
This curious observation prompted his team to search for molecules that might serve as a common mediator influencing various immune cells .
Comparing gene activity profiles , the researchers first noticed a flu-COVID dichotomy : influenza cells showed higher activity in genes regulated by interferons , whereas inflammatory genes driven by so-called tumor necrosis factor ( TNF ) and interleukin-1 beta ( IL-1β ) predominated in COVID-19 .
They then compared severe versus mild COVID-19 samples and focused on a specific pool of @ @ @ @ @ @ @ COVID-19 patients , these first-defender cells had increased activity in interferon-stimulated genes in addition to the TNF/IL-1β inflammatory genes .
But mild COVID-19 monocytes only had the TNF/IL-1β signature , Shin and his colleagues reported on July 10 in Science Immunology .
At first glance , the recent French and South Korean papers seemed to reach contradictory conclusions—with severely ill COVID-19 patients showing weaker interferon responses in Terrier and his colleagues ’ analysis and more interferon activity in Shin and his colleagues ’ study .
The difference could come down to technique and @ @ @ @ @ @ @ in samples containing mixtures of immune cells , whereas the South Korean team sequenced RNA in individual cells and observed interferon differences in monocytes .
But because monocytes make up just a tenth of total make up less than a tenth of white blood cells , an increased signal in this population could be obscured by other cells in the French team ’ s bulk samples , Shin suggests .
There is another side to the coin , however .
Multiple immune cells produce interferons and are presumably influenced by the proteins .
@ @ @ @ @ @ @ profiling only looked at interferons ’ effect on monocytes .
“ What is the impact of a change in one small cell population on the whole system ?
It ’ s really complicated to interpret , ” Terrier says .
“ The interferon response is a little bit tricky , ” says Rudragouda Channappanavar , a viral immunologist at the University of Tennessee Health Science Center , who was not involved with the new studies .
The response protects the body from infections by thwarting viral replication .
“ The body needs it @ @ @ @ @ @ @ says .
“ But viruses are smart .
They have several proteins that can antagonize and suppress early interferon responses.
” One of SARS-CoV-2 ’ s own defenders , a viral protein called Nsp1 , can shut down the host cell ’ s production of immune molecules , including interferons , researchers in Munich reported on July 17 in Science .
In earlier studies with Stanley Perlman of the University of Iowa , Channappanavar analyzed mouse models for the coronaviruses that cause severe acute respiratory syndrome ( SARS ) and Middle East respiratory @ @ @ @ @ @ @ showed that “ if the interferon response begins before viral replication peaks , we will have protective immunity , ” he says .
If the viruses thwart this antiviral defense , however , the delayed interferon response becomes pathogenic—summoning too many monocytes , which secrete inflammatory molecules and cause tissue damage .
“ It ’ s the relative timing of interferon with virus replication that ’ s the key , ” Channappanavar says .
Therapeutically , the findings suggest that interferons matter in the initial phase of infection .
“ If you give @ @ @ @ @ @ @ the antiviral response .
This is where you gain the most , ” says Miriam Merad , who directs the Precision Immunology Institute at the Icahn School of Medicine at Mount Sinai and was not involved with the new research .
If a person with COVID-19 has already progressed to having inflammation , “ and you go in and give interferon , you are going to make things worse , ” she says .
In an open-label preprint study in China , interferon nasal drops prevented the disease in at-risk medical staff who @ @ @ @ @ @ @ data from COVID-19 patients hospitalized in the U.K. suggest that interferons inhaled directly into the lungs shortened hospital stays and increased odds of recovery .
And a randomized trial in Iran is testing whether the proteins can enhance a base therapeutic regimen in moderate to severe COVID-19 patients .
Read more about the coronavirus outbreak from Scientific American here .
And read coverage from our international network of magazines here .

Editor’s Note (9/4/20): Understanding how the immune system goes awry in COVID-19 may help prevent the most severe and deadly cases. Earlier this year Scientific American explained how administering an antiviral protein called interferon at just the right time may help.
When the immune system fights viruses, timing is key. And this maxim may be especially true for its defense against the deadly severe form of COVID-19.
Several new studies of immune response to SARS-CoV-2, the virus that causes the disease, suggest timing could be critical for a class of proteins known as interferons, which are being researched as potential treatments. These immune proteins suppress viral replication early in disease. Yet if they are active later, some scientists think they can exacerbate the harmful inflammation that forces some COVID-19 patients onto life support. Interferons are “a double-edged sword,” says immunologist Eui-Cheol Shin of the Korea Advanced Institute of Science and Technology.
Researchers have been looking at both of that sword’s edges. About a decade ago, when Shin was studying the viral disease hepatitis C, interferons were used as a standard treatment. But examinations of some conditions suggested they should not be employed. For example, researchers in Paris found that too much of the proteins can lead to a diseases known as children’s interferonopathies. In a sense, each of these two perceptions of interferons is correct. And understanding when, and to what extent, using them is warranted could be a critical factor in treating COVID-19.
The researchers in Paris analyzed blood from 50 people with varying COVID-19 severity and 18 healthy controls. They determined that severely ill patients had lower overall counts of lymphocytes (a type of white blood cell). Using techniques to analyze broad-based gene activity and measure specific proteins, two trends stood out: Compared with patients with milder forms of the disease, people with severe COVID-19 had an exaggerated inflammatory response, coupled with a marked decrease in interferons. And among severe COVID-19 patients, the interferon deficiency was worse in those who died versus those who stabilized, the team reported on July 13 in Science.
“We were surprised,” says Benjamin Terrier, a clinician-researcher at Cochin Hospital in Paris, who was co-senior author of the study. “It was not our hypothesis.” An analysis published in the May 28 issue of Cell by researchers at the Icahn School of Medicine at Mount Sinai turned up a similar dual signature: low interferon levels and elevated inflammatory proteins.
Meanwhile, in another new study, Shin and his colleagues used single-cell RNA sequencing to analyze gene activity in immune cells. They analyzed blood samples from eight patients with mild or severe COVID-19, four healthy donors and five people with severe influenza—more than 59,000 cells in total. The researchers employed computer algorithms to compare individual cells’ RNA, and they expected patterns to cluster by cell type. That is, they anticipated that T cells, lymphocytes that coordinate an immune response or kill invading pathogens, would look a lot alike, whether they were taken from patients with COVID-19 or influenza. But that was not the case. Instead the cellular profiles grouped by disease. For example, T cells from COVID-19 patients did not resemble those from people with influenza. Rather they looked more like COVID-19 B cells, Shin says.
This curious observation prompted his team to search for molecules that might serve as a common mediator influencing various immune cells. Comparing gene activity profiles, the researchers first noticed a flu-COVID dichotomy: influenza cells showed higher activity in genes regulated by interferons, whereas inflammatory genes driven by so-called tumor necrosis factor (TNF) and interleukin-1 beta (IL-1β) predominated in COVID-19. They then compared severe versus mild COVID-19 samples and focused on a specific pool of immune cells called monocytes. In severe COVID-19 patients, these first-defender cells had increased activity in interferon-stimulated genes in addition to the TNF/IL-1β inflammatory genes. But mild COVID-19 monocytes only had the TNF/IL-1β signature, Shin and his colleagues reported on July 10 in Science Immunology.
At first glance, the recent French and South Korean papers seemed to reach contradictory conclusions—with severely ill COVID-19 patients showing weaker interferon responses in Terrier and his colleagues’ analysis and more interferon activity in Shin and his colleagues’ study. The difference could come down to technique and timing. The French researchers analyzed RNA in samples containing mixtures of immune cells, whereas the South Korean team sequenced RNA in individual cells and observed interferon differences in monocytes. But because monocytes make up just a tenth of total make up less than a tenth of white blood cells, an increased signal in this population could be obscured by other cells in the French team’s bulk samples, Shin suggests.
There is another side to the coin, however. Multiple immune cells produce interferons and are presumably influenced by the proteins. Yet the Korean team’s single-cell profiling only looked at interferons’ effect on monocytes. “What is the impact of a change in one small cell population on the whole system? It’s really complicated to interpret,” Terrier says.
“The interferon response is a little bit tricky,” says Rudragouda Channappanavar, a viral immunologist at the University of Tennessee Health Science Center, who was not involved with the new studies. The response protects the body from infections by thwarting viral replication. “The body needs it, without a doubt,” he says. “But viruses are smart. They have several proteins that can antagonize and suppress early interferon responses.” One of SARS-CoV-2’s own defenders, a viral protein called Nsp1, can shut down the host cell’s production of immune molecules, including interferons, researchers in Munich reported on July 17 in Science.
In earlier studies with Stanley Perlman of the University of Iowa, Channappanavar analyzed mouse models for the coronaviruses that cause severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS). Those studies showed that “if the interferon response begins before viral replication peaks, we will have protective immunity,” he says. If the viruses thwart this antiviral defense, however, the delayed interferon response becomes pathogenic—summoning too many monocytes, which secrete inflammatory molecules and cause tissue damage. “It’s the relative timing of interferon with virus replication that’s the key,” Channappanavar says.
Therapeutically, the findings suggest that interferons matter in the initial phase of infection. “If you give interferon early, you can really increase the antiviral response. This is where you gain the most,” says Miriam Merad, who directs the Precision Immunology Institute at the Icahn School of Medicine at Mount Sinai and was not involved with the new research. If a person with COVID-19 has already progressed to having inflammation, “and you go in and give interferon, you are going to make things worse,” she says. In an open-label preprint study in China, interferon nasal drops prevented the disease in at-risk medical staff who had treated infected individuals. Early unpublished data from COVID-19 patients hospitalized in the U.K. suggest that interferons inhaled directly into the lungs shortened hospital stays and increased odds of recovery. And a randomized trial in Iran is testing whether the proteins can enhance a base therapeutic regimen in moderate to severe COVID-19 patients.
Read more about the coronavirus outbreak from Scientific American here. And read coverage from our international network of magazines here.


scientificamerican--2020-09-07--The Idea that a Scientific Theory can be 'Falsified' Is a Myth

J.B.S .
Haldane , one of the founders of modern evolutionary biology theory , was reportedly asked what it would take for him to lose faith in the theory of evolution and is said to have replied , “ Fossil rabbits in the Precambrian.
” Since the so-called “ Cambrian explosion ” of 500 million years ago marks the earliest appearance in the fossil record of complex animals , finding mammal fossils that predate them would falsify the theory .
But would it really ?
The Haldane story , though apocryphal , is one of many in the scientific folklore @ @ @ @ @ @ @ characteristic of science .
As expressed by astrophysicist Mario Livio in his book Brilliant Blunders : `` [ E ] ver since the seminal work of philosopher of science Karl Popper , for a scientific theory to be worthy of its name , it has to be falsifiable by experiments or observations .
This requirement has become the foundation of the ‘ scientific method.
’ ” But the field known as science studies ( comprising the history , philosophy and sociology of science ) has shown that falsification can not work even in @ @ @ @ @ @ @ result is not a simple fact obtained directly from nature .
Identifying and dating Haldane 's bone involves using many other theories from diverse fields , including physics , chemistry and geology .
Similarly , a theoretical prediction is never the product of a single theory but also requires using many other theories .
When a “ theoretical ” prediction disagrees with “ experimental ” data , what this tells us is that that there is a disagreement between two sets of theories , so we can not say that any particular theory @ @ @ @ @ @ @ other philosophy of science—is not necessary for the actual practice of science .
The physicist Paul Dirac was right when he said , `` Philosophy will never lead to important discoveries .
It is just a way of talking about discoveries which have already been made.
” Actual scientific history reveals that scientists break all the rules all the time , including falsification .
As philosopher of science Thomas Kuhn noted , Newton 's laws were retained despite the fact that they were contradicted for decades by the motions of the perihelion of @ @ @ @ @ @ @ .
It is the single-minded focus on finding what works that gives science its strength , not any philosophy .
Albert Einstein said that scientists are not , and should not be , driven by any single perspective but should be willing to go wherever experiment dictates and adopt whatever works .
Unfortunately , some scientists have disparaged the entire field of science studies , claiming that it was undermining public confidence in science by denying that scientific theories were objectively true .
This is a mistake since science studies play vital roles @ @ @ @ @ @ @ that it gives scientists a much richer understanding of their discipline .
As Einstein said : `` So many people today—and even professional scientists—seem to me like somebody who has seen thousands of trees but has never seen a forest .
A knowledge of the historic and philosophical background gives that kind of independence from prejudices of his generation from which most scientists are suffering .
This independence created by philosophical insight is—in my opinion—the mark of distinction between a mere artisan or specialist and a real seeker after truth . ''
The @ @ @ @ @ @ @ in inspiring more confidence in science , not less .
The second is that this knowledge equips people to better argue against antiscience forces that use the same strategy over and over again , whether it is about the dangers of tobacco , climate change , vaccinations or evolution .
Their goal is to exploit the slivers of doubt and discrepant results that always exist in science in order to challenge the consensus views of scientific experts .
They fund and report their own results that go counter to the scientific consensus in @ @ @ @ @ @ @ argue that they have falsified the consensus .
In their book Merchants of Doubt , historians Naomi Oreskes and Erik M. Conway say that for these groups “ [ t ] he goal was to fight science with science—or at least with the gaps and uncertainties in existing science , and with scientific research that could be used to deflect attention from the main event.
” Science studies provide supporters of science with better arguments to combat these critics , by showing that the strength of scientific conclusions arises because credible experts use @ @ @ @ @ @ @ consensus judgments about whether a theory should be retained or rejected in favor of a new one .
These consensus judgments are what have enabled the astounding levels of success that have revolutionized our lives for the better .
It is the preponderance of evidence that is relevant in making such judgments , not one or even a few results .
So , when anti-vaxxers or anti-evolutionists or climate change deniers point to this or that result to argue that they have falsified the scientific consensus , they are making a meaningless statement @ @ @ @ @ @ @ produce a preponderance of evidence in support of their case , and they have not done so .
Falsification is appealing because it tells a simple and optimistic story of scientific progress , that by steadily eliminating false theories we can eventually arrive at true ones .
As Sherlock Holmes put it , “ When you have eliminated the impossible , whatever remains , however improbable , must be the truth.
” Such simple but incorrect narratives abound in science folklore and textbooks .
Richard Feynman in his book QED , right after @ @ @ @ @ @ @ quantum electrodynamics came about , said , `` What I have just outlined is what I call a “ physicist ’ s history of physics , ” which is never correct .
What I am telling you is a sort of conventionalized myth-story that the physicists tell to their students , and those students tell to their students , and is not necessarily related to the actual historical development which I do not really know ! ''
But if you propagate a “ myth-story ” enough times and it gets passed on from @ @ @ @ @ @ @ into a fact , and falsification is one such myth-story .
It is time we abandoned it .

J.B.S. Haldane, one of the founders of modern evolutionary biology theory, was reportedly asked what it would take for him to lose faith in the theory of evolution and is said to have replied, “Fossil rabbits in the Precambrian.” Since the so-called “Cambrian explosion” of 500 million years ago marks the earliest appearance in the fossil record of complex animals, finding mammal fossils that predate them would falsify the theory.
But would it really?
The Haldane story, though apocryphal, is one of many in the scientific folklore that suggest that falsification is the defining characteristic of science. As expressed by astrophysicist Mario Livio in his book Brilliant Blunders: "[E]ver since the seminal work of philosopher of science Karl Popper, for a scientific theory to be worthy of its name, it has to be falsifiable by experiments or observations. This requirement has become the foundation of the ‘scientific method.’”
But the field known as science studies (comprising the history, philosophy and sociology of science) has shown that falsification cannot work even in principle. This is because an experimental result is not a simple fact obtained directly from nature. Identifying and dating Haldane's bone involves using many other theories from diverse fields, including physics, chemistry and geology. Similarly, a theoretical prediction is never the product of a single theory but also requires using many other theories. When a “theoretical” prediction disagrees with “experimental” data, what this tells us is that that there is a disagreement between two sets of theories, so we cannot say that any particular theory is falsified.
Fortunately, falsification—or any other philosophy of science—is not necessary for the actual practice of science. The physicist Paul Dirac was right when he said, "Philosophy will never lead to important discoveries. It is just a way of talking about discoveries which have already been made.” Actual scientific history reveals that scientists break all the rules all the time, including falsification. As philosopher of science Thomas Kuhn noted, Newton's laws were retained despite the fact that they were contradicted for decades by the motions of the perihelion of Mercury and the perigee of the moon. It is the single-minded focus on finding what works that gives science its strength, not any philosophy. Albert Einstein said that scientists are not, and should not be, driven by any single perspective but should be willing to go wherever experiment dictates and adopt whatever works.
Unfortunately, some scientists have disparaged the entire field of science studies, claiming that it was undermining public confidence in science by denying that scientific theories were objectively true. This is a mistake since science studies play vital roles in two areas. The first is that it gives scientists a much richer understanding of their discipline. As Einstein said: "So many people today—and even professional scientists—seem to me like somebody who has seen thousands of trees but has never seen a forest. A knowledge of the historic and philosophical background gives that kind of independence from prejudices of his generation from which most scientists are suffering. This independence created by philosophical insight is—in my opinion—the mark of distinction between a mere artisan or specialist and a real seeker after truth." The actual story of how science evolves results in inspiring more confidence in science, not less.
The second is that this knowledge equips people to better argue against antiscience forces that use the same strategy over and over again, whether it is about the dangers of tobacco, climate change, vaccinations or evolution. Their goal is to exploit the slivers of doubt and discrepant results that always exist in science in order to challenge the consensus views of scientific experts. They fund and report their own results that go counter to the scientific consensus in this or that narrow area and then argue that they have falsified the consensus. In their book Merchants of Doubt, historians Naomi Oreskes and Erik M. Conway say that for these groups “[t]he goal was to fight science with science—or at least with the gaps and uncertainties in existing science, and with scientific research that could be used to deflect attention from the main event.”
Science studies provide supporters of science with better arguments to combat these critics, by showing that the strength of scientific conclusions arises because credible experts use comprehensive bodies of evidence to arrive at consensus judgments about whether a theory should be retained or rejected in favor of a new one. These consensus judgments are what have enabled the astounding levels of success that have revolutionized our lives for the better. It is the preponderance of evidence that is relevant in making such judgments, not one or even a few results.
So, when anti-vaxxers or anti-evolutionists or climate change deniers point to this or that result to argue that they have falsified the scientific consensus, they are making a meaningless statement. What they need to do is produce a preponderance of evidence in support of their case, and they have not done so.
Falsification is appealing because it tells a simple and optimistic story of scientific progress, that by steadily eliminating false theories we can eventually arrive at true ones. As Sherlock Holmes put it, “When you have eliminated the impossible, whatever remains, however improbable, must be the truth.” Such simple but incorrect narratives abound in science folklore and textbooks. Richard Feynman in his book QED, right after “explaining” how the theory of quantum electrodynamics came about, said, "What I have just outlined is what I call a “physicist’s history of physics,” which is never correct. What I am telling you is a sort of conventionalized myth-story that the physicists tell to their students, and those students tell to their students, and is not necessarily related to the actual historical development which I do not really know!"
But if you propagate a “myth-story” enough times and it gets passed on from generation to generation, it can congeal into a fact, and falsification is one such myth-story.
It is time we abandoned it.


scientificamerican--2020-09-07--Algorithm Aids Search for Those Lost at Sea

When a craft sinks or goes missing at sea , search-and-rescue teams often rely on computer models to determine where to scour for survivors .
Currently used models incorporate data from satellites and offshore sensors to predict a drifting object 's path , producing maps of the areas where it is most likely to be found .
If the initial search is unsuccessful , the models incorporate that information to update their predictions .
Now a team of researchers has developed a new algorithm to anticipate the location of drifting objects during the first three hours of a search .
@ @ @ @ @ @ @ missing person , the tool identifies zones in the water called transient attracting profiles ( TRAPs ) , where currents and waves conspire to pull in nearby objects .
In the early hours of future search-and-rescue operations , factoring in these previously hidden “ attractors ” could prove crucial in saving lives .
The movement of ocean water can be represented mathematically as a velocity field , which in this case describes the speed and direction of water at each point on the surface .
The new algorithm , described in May in @ @ @ @ @ @ @ and forecast models of this field to find zones with the strongest pull .
Though invisible in the water , each TRAP can be drawn on a map as a curve of about 100 to 1,000 meters long .
As surface conditions change , TRAPs move slowly enough to drag objects along with them—similar to how a magnet moving under a table can pull an iron item along the tabletop .
Study lead author Mattia Serra of Harvard University and his colleagues field-tested the method by throwing GPS-tagged manikins in the turbulent waters @ @ @ @ @ @ @ Massachusetts .
Each manikin followed a different trajectory , but “ they all clustered on the same TRAP , ” just as the algorithm predicted , Serra says .
These initial tests were carried out close to shore , but the same mathematics predicts the presence of TRAPs in the open ocean .
Lawrence Stone , chief scientist at the scientific consulting company Metron and chief designer of the U.S. Coast Guard 's standard search-and-rescue protocol , welcomes these “ absolutely fascinating , impressive results.
” The study “ fits right in with @ @ @ @ @ @ @ to do , and it 's good scientific research that holds up , ” says Stone , who was not involved in the new study .
“ Let 's put it in.
” Stone emphasizes that the TRAPs tool would supplement , not replace , existing models .
A spokesperson confirms that the Coast Guard is working to incorporate TRAP curves into its prediction maps .
As research continues , Serra and his colleagues hope to factor in the effects of wind and buoyancy , thus increasing the predictions ' accuracy .

When a craft sinks or goes missing at sea, search-and-rescue teams often rely on computer models to determine where to scour for survivors. Currently used models incorporate data from satellites and offshore sensors to predict a drifting object's path, producing maps of the areas where it is most likely to be found. If the initial search is unsuccessful, the models incorporate that information to update their predictions.
Now a team of researchers has developed a new algorithm to anticipate the location of drifting objects during the first three hours of a search. Instead of modeling the trajectory of a missing person, the tool identifies zones in the water called transient attracting profiles (TRAPs), where currents and waves conspire to pull in nearby objects. In the early hours of future search-and-rescue operations, factoring in these previously hidden “attractors” could prove crucial in saving lives.
The movement of ocean water can be represented mathematically as a velocity field, which in this case describes the speed and direction of water at each point on the surface. The new algorithm, described in May in Nature Communications, uses ocean wave data and forecast models of this field to find zones with the strongest pull. Though invisible in the water, each TRAP can be drawn on a map as a curve of about 100 to 1,000 meters long. As surface conditions change, TRAPs move slowly enough to drag objects along with them—similar to how a magnet moving under a table can pull an iron item along the tabletop.
Study lead author Mattia Serra of Harvard University and his colleagues field-tested the method by throwing GPS-tagged manikins in the turbulent waters just south of Martha's Vineyard in Massachusetts. Each manikin followed a different trajectory, but “they all clustered on the same TRAP,” just as the algorithm predicted, Serra says. These initial tests were carried out close to shore, but the same mathematics predicts the presence of TRAPs in the open ocean.
Lawrence Stone, chief scientist at the scientific consulting company Metron and chief designer of the U.S. Coast Guard's standard search-and-rescue protocol, welcomes these “absolutely fascinating, impressive results.” The study “fits right in with the sort of thing that we like to do, and it's good scientific research that holds up,” says Stone, who was not involved in the new study. “Let's put it in.”
Stone emphasizes that the TRAPs tool would supplement, not replace, existing models. A spokesperson confirms that the Coast Guard is working to incorporate TRAP curves into its prediction maps. As research continues, Serra and his colleagues hope to factor in the effects of wind and buoyancy, thus increasing the predictions' accuracy.


scientificamerican--2020-09-08--Our Health Depends on Our Homes and Work Spaces

When COVID-19 hit the U.S. , most of us became homebodies .
Journalist Emily Anthes was thus propitious in the timing of her new book , The Great Indoors : The Surprising Science of How Buildings Shape Our Behavior , Health , and Happiness ( Scientific American/Farrar , Straus and Giroux ) .
You may distract yourself from cabin fever by learning about the cabin .
Actually , the work covers a wide variety of indoor situations .
One chapter looks at architectural design that encourages exercise .
For example , apartment building planners stumbled on this shocking strategy : @ @ @ @ @ @ @ more , make the stairwells wider and well lit .
You know , nicer to use .
Another entry analyzes ways to contend with flooding , namely , throw in the towel : build homes with “ buoyancy blocks ” that absorb H O .
The blocks then—get this—expand and lift the house .
Just be careful walking out the front door .
Other parts of the book deal with prisons , hospitals , offices , smart homes , housing for neurodiverse people , and even living spaces in space .
For instance @ @ @ @ @ @ @ Space Station has a greenhouse for testing off-planet agronomy .
Gardening in orbit seems to be a mood enhancer and could lead to asteroid belt borscht .
All fascinating stuff , but it was the material in the chapter “ The Indoor Jungle ” about dwellings , the walls of which we 've been staring at for months , that really grabbed me by the throat .
Or maybe the armpit .
A study found that homes with more women than men had a lot of Lactobacillus bacteria , “ a major component @ @ @ @ @ @ @ study revealed that where men were in the majority , homes had bacteria that thrive in the gut , on the skin and in armpits .
I just felt a great disturbance in the force , as if thousands of readers suddenly cried out in terror and ran to open up a window .
Living indoors inevitably means sharing our habitats with such human-associated microbial communities .
Anthes mentions a 2016 study in the Amazon basin that sampled homes in communities ranging from a remote village to Manaus , with a population of @ @ @ @ @ @ @ thatched huts of the village contained mostly bacteria found on and in soil , water and insects .
Bacteria in the city residences were mostly those found on , and in , us .
In a footnote , Anthes also notes that wild animals , notorious for their lack of constructed walls and ceilings , leave barely a trace of themselves in their homes , microscopically speaking .
She quotes North Carolina State University ecologist Rob Dunn , who took part in the surveys already mentioned and who also studied what you would @ @ @ @ @ @ @ d'ooh ooh ah ah : “ Chimp nests are all environmental microbes .
You ca n't tell a chimp has ever been there.
” Well , not by the bacteria , anyway .
Anthes rounds up a lot of research demonstrating that the right home microbe mix can promote health .
For example , kids who grow up on farms or with dogs have some protection against asthma , probably because the animals ' microbes train the young immune systems .
Homes without such microbes leave us less prepared for the challenges that @ @ @ @ @ @ @ our warm , moist bodies .
Big bacterial differences exist even among farming communities .
A 2016 New England Journal of Medicine study found that the Hutterites , who use modern agricultural methods , have more than four times the childhood asthma rates of the Amish , who still plow with horses .
Amish kids have more infection-fighting white blood cells than do young Hutterites , whereas the latter group outpaced the former in cells involved with allergic reactions .
The root cause can be found all over the root cellar : the @ @ @ @ @ @ @ molecules than did the Hutterites ' .
Anthes includes a prescription for a healthful home microbiome : “ Keep things dry .
Forgo cleansers , textiles , and materials that contain added antimicrobials .
Open a window .
Get a dog .
( Or , if you can swing it , a cow . )
” That 's no bum steer .

When COVID-19 hit the U.S., most of us became homebodies. Journalist Emily Anthes was thus propitious in the timing of her new book, The Great Indoors: The Surprising Science of How Buildings Shape Our Behavior, Health, and Happiness (Scientific American/Farrar, Straus and Giroux). You may distract yourself from cabin fever by learning about the cabin.
Actually, the work covers a wide variety of indoor situations. One chapter looks at architectural design that encourages exercise. For example, apartment building planners stumbled on this shocking strategy: to get people to use the stairs more, make the stairwells wider and well lit. You know, nicer to use.
Another entry analyzes ways to contend with flooding, namely, throw in the towel: build homes with “buoyancy blocks” that absorb H 2 O. The blocks then—get this—expand and lift the house. Just be careful walking out the front door.
Other parts of the book deal with prisons, hospitals, offices, smart homes, housing for neurodiverse people, and even living spaces in space. For instance, the Russian part of the International Space Station has a greenhouse for testing off-planet agronomy. Gardening in orbit seems to be a mood enhancer and could lead to asteroid belt borscht.
All fascinating stuff, but it was the material in the chapter “The Indoor Jungle” about dwellings, the walls of which we've been staring at for months, that really grabbed me by the throat. Or maybe the armpit. A study found that homes with more women than men had a lot of Lactobacillus bacteria, “a major component of the vaginal microbiome.” The same study revealed that where men were in the majority, homes had bacteria that thrive in the gut, on the skin and in armpits. I just felt a great disturbance in the force, as if thousands of readers suddenly cried out in terror and ran to open up a window.
Living indoors inevitably means sharing our habitats with such human-associated microbial communities. Anthes mentions a 2016 study in the Amazon basin that sampled homes in communities ranging from a remote village to Manaus, with a population of more than two million. The open-air thatched huts of the village contained mostly bacteria found on and in soil, water and insects. Bacteria in the city residences were mostly those found on, and in, us.
In a footnote, Anthes also notes that wild animals, notorious for their lack of constructed walls and ceilings, leave barely a trace of themselves in their homes, microscopically speaking. She quotes North Carolina State University ecologist Rob Dunn, who took part in the surveys already mentioned and who also studied what you would expect to be a particularly ripe objet d'ooh ooh ah ah: “Chimp nests are all environmental microbes. You can't tell a chimp has ever been there.” Well, not by the bacteria, anyway.
Anthes rounds up a lot of research demonstrating that the right home microbe mix can promote health. For example, kids who grow up on farms or with dogs have some protection against asthma, probably because the animals' microbes train the young immune systems. Homes without such microbes leave us less prepared for the challenges that arise when a tiny troublemaker does find our warm, moist bodies.
Big bacterial differences exist even among farming communities. A 2016 New England Journal of Medicine study found that the Hutterites, who use modern agricultural methods, have more than four times the childhood asthma rates of the Amish, who still plow with horses. Amish kids have more infection-fighting white blood cells than do young Hutterites, whereas the latter group outpaced the former in cells involved with allergic reactions. The root cause can be found all over the root cellar: the dust in Amish homes contained more bacterial molecules than did the Hutterites'.
Anthes includes a prescription for a healthful home microbiome: “Keep things dry. Forgo cleansers, textiles, and materials that contain added antimicrobials. Open a window. Get a dog. (Or, if you can swing it, a cow.)” That's no bum steer.


scientificamerican--2020-09-08--We Must Reduce the Trauma of Medical Diagnoses

At some point in your life , you will likely experience the anxiety of sitting in a hospital room , waiting for a serious medical diagnosis .
Even those lucky enough to avoid that situation will likely accompany a loved one—a parent , grandparent or child—who is receiving the news .
You might remember the stiffness of the chair , the pattern of the hospital gown or the doctor ’ s folded hands .
Whatever the diagnosis—cancer , Alzheimer ’ s disease , diabetes or even COVID-19—the event is not one you will easily forget .
Powerful emotional experiences such @ @ @ @ @ @ @ memories : recollections that are highly salient and appear as vivid as a snapshot .
Most of us who lived through the assassination of President John F. Kennedy or 9/11 are confident we can pinpoint precisely where we were when we found out about the event .
These memories are not perfect—they are distorted like any other recollection .
Yet when they recount the experience , people describe it as if it happened yesterday .
And these memories influence our personal identity , social bonds , decision-making and behaviors over time .
After @ @ @ @ @ @ @ example , those who witnessed acts of heroism and remembered them in detail were more likely to engage in helping behaviors such as donating blood or supporting Boston-related charities , even months after the attack .
In a recent study we demonstrated that for some individuals , a medical diagnosis event does create a flashbulb memory that endures for years after the fact .
But our findings also showed that the intensity of these memories and the emotions associated with them depend on the doctor ’ s delivery , which either softens the @ @ @ @ @ @ @ professionals would be wise to carefully consider how they convey such news .
For our study , we surveyed more than 300 mothers , recruited through support groups on social media , who had received a diagnosis of Down syndrome for their child .
The mothers ranged in age from 21 to 79 years and had been given the diagnosis between 52 years and one month ago .
In the survey , they wrote a narrative describing in detail how they were informed their child had Down syndrome—incorporating as many specifics as they @ @ @ @ @ @ @ weather , time and other features .
These narratives were coded and rated using the Flashbulb Memory Checklist ( FBMC ) for specificity .
The mothers also responded to a series of statements from the Autobiographical Memory Questionnaire ( AMQ ) to indicate the perceived intensity , vividness , rehearsal , confidence and valence of their diagnosis memory .
Finally , they answered a series of questions about their interactions with medical staff at the time of the diagnosis to determine how these conversations affected their recollection of the event .
The majority @ @ @ @ @ @ @ after learning of their child ’ s Down syndrome .
In fact , our participants described their diagnosis memory as more vivid , intense and visceral than the ratings subjects had given to their recollection of 9/11 in another flashbulb memory study .
The flashbulb nature of these medical-diagnosis memories lingered for many years .
Although we did not examine the way individual memories changed over time , as a longitudinal study would , we were able to compare recollections from decades earlier to those from a few months ago .
Diagnosis memories @ @ @ @ @ @ @ than recent ones , and they were just as likely to have a flashbulb effect .
Time seemed to soften the intensity of the memories , but even decades-old diagnoses were still rated as more emotional , vivid , and salient than everyday recollections .
The support that the participating mothers received from medical staff also determined the emotional tenor of their memory and its persistence over time .
Respondents who described positive interactions with the staff—such as a balanced delivery and additional resources and information for support—were less likely to report negative @ @ @ @ @ @ @ a decrease in the memory ’ s intensity over time .
More often , however , the mothers reported negative experiences with medical staff , including a lack of compassion , pressure to terminate their pregnancy , and pessimistic expectations about outcomes for their child and family .
Many received limited or no additional resources or support systems .
For those individuals , memories of the diagnosis continued to be associated with negative emotions , and the time that had elapsed had not helped lessen the impact .
Mothers who had not received @ @ @ @ @ @ @ in specific , often haunting detail , even after 20 years .
One of the essential ethical standards of the Hippocratic oath is to do no harm .
Our findings suggest that in adhering to this tenet , health professionals should focus not only on the medical procedures and treatments provided to people but also on the way patients are informed about their health and what the future might hold .

At some point in your life, you will likely experience the anxiety of sitting in a hospital room, waiting for a serious medical diagnosis. Even those lucky enough to avoid that situation will likely accompany a loved one—a parent, grandparent or child—who is receiving the news. You might remember the stiffness of the chair, the pattern of the hospital gown or the doctor’s folded hands. Whatever the diagnosis—cancer, Alzheimer’s disease, diabetes or even COVID-19—the event is not one you will easily forget.
Powerful emotional experiences such as this one can develop into flashbulb memories: recollections that are highly salient and appear as vivid as a snapshot. Most of us who lived through the assassination of President John F. Kennedy or 9/11 are confident we can pinpoint precisely where we were when we found out about the event. These memories are not perfect—they are distorted like any other recollection. Yet when they recount the experience, people describe it as if it happened yesterday. And these memories influence our personal identity, social bonds, decision-making and behaviors over time. After the 2013 Boston Marathon bombing, for example, those who witnessed acts of heroism and remembered them in detail were more likely to engage in helping behaviors such as donating blood or supporting Boston-related charities, even months after the attack.
In a recent study we demonstrated that for some individuals, a medical diagnosis event does create a flashbulb memory that endures for years after the fact. But our findings also showed that the intensity of these memories and the emotions associated with them depend on the doctor’s delivery, which either softens the impact or prolongs the pain. Medical professionals would be wise to carefully consider how they convey such news.
For our study, we surveyed more than 300 mothers, recruited through support groups on social media, who had received a diagnosis of Down syndrome for their child. The mothers ranged in age from 21 to 79 years and had been given the diagnosis between 52 years and one month ago. In the survey, they wrote a narrative describing in detail how they were informed their child had Down syndrome—incorporating as many specifics as they could about the day, location, weather, time and other features. These narratives were coded and rated using the Flashbulb Memory Checklist (FBMC) for specificity. The mothers also responded to a series of statements from the Autobiographical Memory Questionnaire (AMQ) to indicate the perceived intensity, vividness, rehearsal, confidence and valence of their diagnosis memory. Finally, they answered a series of questions about their interactions with medical staff at the time of the diagnosis to determine how these conversations affected their recollection of the event.
The majority of respondents—nearly 80 percent—experienced a flashbulb memory after learning of their child’s Down syndrome. In fact, our participants described their diagnosis memory as more vivid, intense and visceral than the ratings subjects had given to their recollection of 9/11 in another flashbulb memory study.
The flashbulb nature of these medical-diagnosis memories lingered for many years. Although we did not examine the way individual memories changed over time, as a longitudinal study would, we were able to compare recollections from decades earlier to those from a few months ago. Diagnosis memories from long ago were no less detailed than recent ones, and they were just as likely to have a flashbulb effect. Time seemed to soften the intensity of the memories, but even decades-old diagnoses were still rated as more emotional, vivid, and salient than everyday recollections.
The support that the participating mothers received from medical staff also determined the emotional tenor of their memory and its persistence over time. Respondents who described positive interactions with the staff—such as a balanced delivery and additional resources and information for support—were less likely to report negative feelings when recounting the experience and saw a decrease in the memory’s intensity over time.
More often, however, the mothers reported negative experiences with medical staff, including a lack of compassion, pressure to terminate their pregnancy, and pessimistic expectations about outcomes for their child and family. Many received limited or no additional resources or support systems. For those individuals, memories of the diagnosis continued to be associated with negative emotions, and the time that had elapsed had not helped lessen the impact. Mothers who had not received positive feedback could recall their diagnosis experience in specific, often haunting detail, even after 20 years.
One of the essential ethical standards of the Hippocratic oath is to do no harm. Our findings suggest that in adhering to this tenet, health professionals should focus not only on the medical procedures and treatments provided to people but also on the way patients are informed about their health and what the future might hold.


scientificamerican--2020-09-08--COVID19's Disparate Impacts Are Not a Story about Race

George Floyd could not breathe .
Like one hundred thousand other Americans , he gasped horribly for air before his world went dark .
Unlike them , his agony was not born from a lung-ravaging virus .
He was strangled .
He was murdered in public , with the weight of anti-Black hatred kneeling terribly—almost boastfully—down on his neck .
Weeks before , and miles away , a comparison of public parks in New York shows the tale of two cities .
In some , uniformed officers protect groups of friends basking in the sunlight by handing out masks and @ @ @ @ @ @ @ With eyebrows narrowed , they brutally arrest grieving folks of color for disobedience .
In Sacramento , a 14-year-old child is pinned to asphalt and beaten in the face .
In Manhattan , a Black man is ground into asphalt for violating the six-feet social distancing order .
An officer slaps him , kneels terribly down on his neck .
In the Emergency Department , a patient ’ s father halts me with a fanned palm a foot from my chest—prevents me from examining his child even though I ’ ve introduced myself @ @ @ @ @ @ @ ve “ been home recently.
” My ability to take care of a gasping boy is questioned on account of my Taiwanese ethnicity .
A week later , a triage nurse asks a new patient why he has come to the hospital .
He responds , simply , that he had recently been “ coughed on by [ an ] Asian.
” In this pandemic , data are taking a back seat to racial prejudice .
The irrational racist surveillance that leads to the brutalization of Black Americans in their neighborhoods is spilling @ @ @ @ @ @ @ Fueled by a president who continues to blame a faceless China for the pandemic ’ s miseries , citizens and caregivers of color face fear and disdain .
Simultaneously , re-emerging myths of genetic racial differences scrutinize bodies of color as sources of disease , all while obscuring the deadly climate of injustice that hastens breathlessness .
America ’ s racism is rampant , and it ’ s shaping the response to this pandemic to the detriment of us all .
Travel bans missed the mark .
Travelers from Europe—not Asia—brought the first @ @ @ @ @ @ @ countries across five continents .
Voyages from Italy were responsible for bringing COVID-19 to 46 nations , while travel from China is responsible for just 27 index cases .
Yet , while the United States issued a travel ban on China at the end of January , it took another month and a half to limit European travel .
During that time , an estimated two million people flew from Europe to the land of the free .
As with the greater globe , a majority of US index cases came coughing , @ @ @ @ @ @ @ followed these lines of export the way it sticks to Asia and other “ aliens.
” Conservative legislators call for deportations and stronger defenses at the Southern border , while the “ normal reaction ” of anti-Asian hatred skyrockets .
Public political displays urging citizens to eat at empty China Town restaurants do little to stem the Sinophobia , but no such exhibition has been necessary to demonstrate the safety of spaghetti and meatballs .
The widespread media narrative is similarly skewed .
German Chancellor Angela Merkel ’ s pedigree as a scientist @ @ @ @ @ @ @ was celebrated as an explanation for the prowess of her pandemic response .
But the reported success of Germany—a country of 83 million people , $ 3.9 trillion GDP , and over 9,300 COVID19 deaths—does not seem so successful when compared to Vietnam , a country of 96 million people and $ 245 billion GDP , with zero COVID19 deaths even in May .
Though East Asia had fewer deaths in total than Europe had every day throughout the early months of the pandemic , a New York Times list of “ true @ @ @ @ @ @ @ in Medium , “ exactly one sentence on Asia and the rest on white leaders that mostly did worse than Iran ” ( a country that , according to the New York Times , “ Completely and Utterly Botched Its Response to Coronavirus.
” ) The same New York Times article praised the heroics of Italian leaders—who bore responsibility for a death toll 115 times that of South Korea ’ s count of 310 COVID deaths—and focused on Western leadership without mentioning the relative summer success of countries in Africa , or the @ @ @ @ @ @ @ of this writing .
We are supposed to use data to mitigate bias—to be objective—but we are picking and choosing what information we digest to fit our own narratives about who is to blame , where sickness comes from .
These statistics that we look to in order to be empirical , are actually imperial .
On the frontlines , I order a chest x ray to investigate a man ’ s shortness of breath .
He clutches my protective yellow gown and asks , anxiously , if I think a package delivered @ @ @ @ @ @ @ the culprit .
Later , he mentions that a close family friend recently traveled in Europe .
He does not connect this information to COVID19—offers it only in passing to tell me where to buy good chocolates .
Later , a woman screams in my direction that she wants to f—ing destroy China .
The increasingly overt racism against Asian-Americans—who today are broadly seen as “ Chinese ” —is a rehash of the historic entanglement of pandemic xenophobia with disease , genes , race , and risk .
Immigrants are caricaturized as innately-disposed @ @ @ @ @ @ @ texts , like Dr. Arthur Stout ’ s 1862 publication on “ Chinese Immigration and the Physiologic Causes of the Decay of the Nation , ” add legitimacy to this racist folktale which contends that foreigners , in addition to their biologic lowliness , also possess behavioral inferiority as evidenced by lack of sanitation and strange foods .
This fable is being told anew ; this February , the governor of Veneto , Italy—which grieves over 2,000 COVID-19 deaths amongst a population of 4.9 million—argued that Italy would fare better than Wuhan , @ @ @ @ @ @ @ to hygiene , washing hands…whereas we have all seen the Chinese eating mice alive.
” President Trump—in direct violation of WHO guidelines for naming new pandemics—continues to reference COVID19 as the Wuhan or Chinese Virus , even using the phrase “ kung flu ” at a campaign rally in Tulsa , Oklahoma , this June .
The idea that the color of someone ’ s skin determines their capacity for intelligence , health , and morality , is the same idea that leads some people to feel the innate entitlement—the birthright—to assault Black @ @ @ @ @ @ @ ’ re just jogging through the neighborhood .
Already in this pandemic , the same false ideas about biologic susceptibility have entered public discussion to skew national conversation .
On February 29 , Trump mega-fan Bill Mitchell tweeted to 550,000 followers : “ I read that Asian lungs have more receptors and are therefore more susceptible to this kind of virus .
Is this true or urban myth ?
” In June , during a legislative briefing on COVID19 , Democratic Representative Bill Foster noted that there may be a “ genetic component @ @ @ @ @ @ @ pandemic , and suggested the need for altering policy responses and “ genetic engineering ” to accommodate for potential differences in racial biology .
Taken in its worst form , these suggestions are redolent of Nazi-era scientific racism .
But these ideas , in fact , came from a non-peer reviewed 2020 study—already referenced in the Journal of the American Medical Association—which postulated that increased expression of specific lung cell receptors might explain why COVID19 is “ concentrated in the Asian area.
” American citizens who share George Floyd ’ s skin color @ @ @ @ @ @ @ numbers .
Data show that Black Americans face excess COVID death as a result of disparate access to testing , high levels of underlying health conditions , greater occupational exposure , and lower rates of medical insurance coverage .
Black bodies have been wounded and strained by decades of discriminatory housing policies , mass incarceration , malnutrition , and trauma .
Their lungs cough disproportionately with asthma because they ’ ve been forced to live near disease-producing highways and toxic landfills ; because they ’ ve been maliciously targeted by predatory business strategies @ @ @ @ @ @ @ industry .
These are the injustices that make them unable to breathe .
And yet , Trump ’ s Surgeon General Jerome Adams ordered communities of color to “ step up ” and avoid drugs and alcohol during the pandemic , as if the individual behavior of Black people is to blame .
Ohio state senator and emergency medicine physician Steve Huffman wondered aloud during a hearing , if “ African Americans or the colored population ” face disparate coronavirus deaths because they “ do not wash their hands as well as other @ @ @ @ @ @ @ medical journals such as Health Affairs and the British Medical Journal continue to hypothesize that the disproportionate severity of COVID19 in African American communities may be as result of yet unfound genetic factors .
Like the work of Dr. Stout , these theories—backed by the weight of physician and legislative authority—guide endeavors to focus on internal deficiencies within bodies of color , instead of intervening on the stark inequities of social treatment that leave them gasping for air .
We can not allow fables of inherent racial difference to sanction the disproportionate burden @ @ @ @ @ @ @ as if the excess death of 13,000 Black people came from the consent of their genomes .
Still , the biology and behavior of people are color are being made into scapegoats for systemic suffering .
So while COVID-19 is not a story about race , it is a story about racism .
One that judges bodies of color as preordained sources of disease and menace—dangerous even down to their DNA .
It is the same gaze that indicted George Floyd as a worthy target of violence even as he was handcuffed , @ @ @ @ @ @ @ was not genetically predisposed to breathlessness .
He , like thousands of other Black patients , died because the color of his skin made him susceptible to inequity .
Today , no one suspects that Italy was terrorized by COVID19 because Italian genes incline the population to respiratory illness .
Researchers understand that low COVID mortality rates in New Zealand are not explained by beneficial polymorphisms .
We reach for fantasies of physiologic dissent only when it supports our existing biases .
We see how ideas of danger and biologic difference map easily @ @ @ @ @ @ @ by its perceived whiteness , normalcy , and health—does not seem like a site of sickness or genetic variation .
This isn ’ t scientific .
This is a manifestation of the racist enterprise that registers certain groups as more diseased , more threatening , more worthy of policing .
It leads to irrational travel restrictions , public brutality .
The degree to which these reactionary impulses can influence decision-making—even in the face of logical , factual information—is indication of how strong these implicit biases are , how muscular this inequity is .
@ @ @ @ @ @ @ and West were a terrible mistake that shows how the massive gap between our biased narratives and our reality generates enormous anguish .
Systemic racism—and the hubris and blindness it bears—has hampered our ability to formulate cogent decisions at prodigious cost .
COVID-19 trekked , unchecked , on the backs of the assumed benign : the rich , the white , the wealthy .
But that ’ s not whom it hurt .
The people who suffered the most are the most vulnerable : the essential workers , the elders who can ’ @ @ @ @ @ @ @ children without internet or clean water .
It ’ s the men and women who can not shelter in place because they have no refuge to crouch in .
The locked-up folks who don ’ t have six feet to give , the transplanted asylum-seekers who can not escape despair or disease .
They are the ones who pay .
They even the ledger , dripping in red .
The power that permitted the murder of George Floyd has inflicted a lethal shortness of breath on thousands of other citizens who share his @ @ @ @ @ @ @ the country , abetted by a racist gaze that arbitrates bodies of color as cesspools of disease and danger .
This prejudiced contemplation has distorted our attention to focus on Asia , on DNA , despite clear testimony that indicts major , pre-existing health inequities for the undue burden of pandemic suffering in communities of color .
This bigotry endangers the people who are thought to look dangerous , while waving through threats that do not fit the preordained description of a hazard—the European traveler , the international businessman , the uniformed cop @ @ @ @ @ @ @ U.S. counties are experiencing COVID death rates six times higher than everyone else , it is impossible not to remember Eric Garner , choking , gasping .
It is impossible not to remember Ahmaud Arbery , whose sunny jog should not have robbed him of his breath .
It is impossible not to remember how George Floyd struggled against a knee to tell the world he could not breathe .
How he died , months before his forty-seventh rotation around the sun .

George Floyd could not breathe. Like other Americans now numbering in the hundreds of thousands, he gasped horribly for air before his world went dark. Unlike them, his agony was not born from a lung-ravaging virus. He was strangled. He was killed in public, with the weight of anti-Black hatred kneeling terribly—almost boastfully—down on his neck.
Weeks before, and miles away, a comparison of public parks in New York shows the tale of two cities. In some, uniformed officers protect groups of friends basking in the sunlight by handing out masks and water. Elsewhere, they patrol. With eyebrows narrowed, they brutally arrest grieving folks of color for disobedience. Near Sacramento, a 14-year-old child is pinned to asphalt and beaten in the face. In Manhattan, a Black man is ground into asphalt for violating the six-feet social distancing order. An officer slaps him, kneels terribly down on his neck.
In the Emergency Department, a patient’s father halts me with a fanned palm a foot from my chest—prevents me from examining his child even though I’ve introduced myself as the doctor—and inquires if I’ve “been home recently.” My ability to take care of a gasping boy is questioned on account of my Taiwanese ethnicity. A week later, a triage nurse asks a new patient why he has come to the hospital. He responds, simply, that he had recently been “coughed on by [an] Asian.”
In this pandemic, data are taking a back seat to racial prejudice. The irrational racist surveillance that leads to the brutalization of Black Americans in their neighborhoods is spilling into public health and medical care. Fueled by a president who continues to blame a faceless China for the pandemic’s miseries, citizens and caregivers of color face fear and disdain. Simultaneously, re-emerging myths of genetic racial differences scrutinize bodies of color as sources of disease, all while obscuring the deadly climate of injustice that hastens breathlessness. America’s racism is rampant, and it’s shaping the response to this pandemic to the detriment of us all.
Travel bans missed the mark. Travelers from Europe—not Asia—brought the first cases of COVID-19 to at least 93 countries across five continents. Voyages from Italy were responsible for bringing COVID-19 to 46 nations, while travel from China is responsible for just 27 index cases. Yet, while the United States issued a travel ban on China at the end of January, it took another month and a half to limit European travel. During that time, an estimated two million people flew from Europe to the land of the free.
As with the greater globe, a majority of U.S. index cases came coughing, from Europe. But stigma has not followed these lines of export the way it sticks to Asia and other “aliens.” Conservative legislators call for deportations and stronger defenses at the Southern border, while the “normal reaction” of anti-Asian hatred skyrockets. Public political displays urging citizens to eat at empty Chinatown restaurants do little to stem the Sinophobia, but no such exhibition has been necessary to demonstrate the safety of spaghetti and meatballs.
The widespread media narrative is similarly skewed. German Chancellor Angela Merkel’s pedigree as a scientist with an advanced degree in quantum chemistry was celebrated as an explanation for the prowess of her pandemic response. But the reported success of Germany—a country of 83 million people, $3.9 trillion GDP, and over 9,300 COVID-19 deaths—does not seem so successful when compared to Vietnam, a country of 96 million people and $245 billion GDP, with zero COVID-19 deaths even in May. Though East Asia had fewer deaths in total than Europe had every day throughout the early months of the pandemic, a New York Times list of “true leaders” spent, said an essay in Medium, “exactly one sentence on Asia and the rest on white leaders that mostly did worse than Iran” (a country that, according to the New York Times, “Completely and Utterly Botched Its Response to Coronavirus”).
The same New York Times article praised the heroics of Italian leaders—who bore responsibility for a death toll 115 times that of South Korea’s count of 310 COVID-19 deaths—and focused on Western leadership without mentioning the relative summer success of countries in Africa, or the pandemic death count in Taiwan—just seven as of this writing.
We are supposed to use data to mitigate bias—to be objective—but we are picking and choosing what information we digest to fit our own narratives about who is to blame, where sickness comes from. These statistics that we look to in order to be empirical, are actually imperial.
On the front lines, I order a chest x ray to investigate a man’s shortness of breath. He clutches my protective yellow gown and asks, anxiously, if I think a package delivered from China three weeks ago could be the culprit. Later, he mentions that a close family friend recently traveled in Europe. He does not connect this information to COVID-19—offers it only in passing to tell me where to buy good chocolates. Later, a woman screams in my direction that she wants to f—ing destroy China.
The increasingly overt racism against Asian Americans—who today are broadly seen as “Chinese”—is a rehash of the historic entanglement of pandemic xenophobia with disease, genes, race, and risk. Immigrants are caricaturized as innately disposed and dangerous sources of disease. Medical texts, like Arthur Stout’s 1862 publication on “Chinese Immigration and the Physiologic Causes of the Decay of the Nation,” add legitimacy to this racist folktale, which contends that foreigners, in addition to their biologic lowliness, also possess behavioral inferiority as evidenced by lack of sanitation and strange foods.
This fable is being told anew; this February, the governor of Veneto, Italy—which grieves over 2,000 COVID-19 deaths amongst a population of 4.9 million—argued that Italy would fare better than Wuhan, since Italians have “culturally strong attention to hygiene, washing hands ... whereas we have all seen the Chinese eating mice alive.” President Trump—in direct violation of WHO guidelines for naming new pandemics—continues to reference COVID-19 as the Wuhan or Chinese Virus, even using the phrase “kung flu” at a campaign rally in Tulsa, Okla., this June.
The idea that the color of someone’s skin determines their capacity for intelligence, health, and morality, is the same idea that leads some people to feel the innate entitlement—the birthright—to assault Black bodies deemed suspicious, even if they’re just jogging through the neighborhood. Already in this pandemic, the same false ideas about biologic susceptibility have entered public discussion to skew national conversation.
On February 29, Trump mega-fan Bill Mitchell tweeted to 550,000 followers: “I read that Asian lungs have more receptors and are therefore more susceptible to this kind of virus. Is this true or urban myth?” In June, during a legislative briefing on COVID-19, Democratic Representative Bill Foster noted that there may be a “genetic component” to racial disparities seen during the pandemic.
These ideas came, in part, from a non-peer reviewed 2020 study—already referenced in the Journal of the American Medical Association—which postulated that increased expression of specific lung cell receptors might explain why COVID-19 is “concentrated in the Asian area.”
American citizens who share George Floyd’s skin color are perishing from COVID-19 at shockingly inordinate numbers. Data show that Black Americans face excess COVID-19 death as a result of disparate access to testing, high levels of underlying health conditions, greater occupational exposure, and lower rates of medical insurance coverage. Black bodies have been wounded and strained by decades of discriminatory housing policies, mass incarceration, malnutrition, and trauma. Their lungs cough disproportionately with asthma because they’ve been forced to live near disease-producing highways and toxic landfills; because they’ve been maliciously targeted by predatory business strategies to drive profits up for the tobacco industry. These are the injustices that make them unable to breathe.
And yet, Trump’s Surgeon General Jerome Adams ordered communities of color to “step up” and avoid drugs and alcohol during the pandemic, as if the individual behavior of Black people is to blame. Ohio state senator and emergency medicine physician Steve Huffman wondered aloud during a hearing, if “African Americans or the colored population” face disparate coronavirus deaths because they “do not wash their hands as well as other groups.”
Simultaneously, publications in prestigious medical journals such as Health Affairs and the British Medical Journal continue to hypothesize that the disproportionate severity of COVID-19 in African American communities may be as result of yet unfound genetic factors. Like the work of Stout, these theories—backed by the weight of physician and legislative authority—guide endeavors to focus on internal deficiencies within bodies of color, instead of intervening on the stark inequities of social treatment that leave them gasping for air.
We cannot allow fables of inherent racial difference to sanction the disproportionate burden of COVID-19 on people of color, as if the excess death of 13,000 Black people came from the consent of their genomes. Still, the biology and behavior of people are color are being made into scapegoats for systemic suffering.
So while COVID-19 is not a story about race, it is a story about racism. One that judges bodies of color as preordained sources of disease and menace—dangerous even down to their DNA. It is the same gaze that indicted George Floyd as a worthy target of violence even as he was handcuffed, helpless, unable to breathe.
Floyd was not genetically predisposed to breathlessness. He, like thousands of other Black patients, died because the color of his skin made him susceptible to inequity.
Today, no one suspects that Italy was terrorized by COVID-19 because Italian genes incline the population to respiratory illness. Researchers understand that low COVID-19 mortality rates in New Zealand are not explained by beneficial polymorphisms.
We reach for fantasies of physiologic dissent only when it supports our existing biases. We see how ideas of danger and biologic difference map easily and automatically onto Asia, while Europe—buffered by its perceived whiteness, normalcy, and health—does not seem like a site of sickness or genetic variation.
This isn’t scientific. This is a manifestation of the racist enterprise that registers certain groups as more diseased, more threatening, more worthy of policing. It leads to irrational travel restrictions, public brutality. The degree to which these reactionary impulses can influence decision-making—even in the face of logical, factual information—is indication of how strong these implicit biases are, how muscular this inequity is.
The disparate travel bans on the East and West were a terrible mistake that shows how the massive gap between our biased narratives and our reality generates enormous anguish. Systemic racism—and the hubris and blindness it bears—has hampered our ability to formulate cogent decisions at prodigious cost.
COVID-19 trekked, unchecked, on the backs of the assumed benign: the rich, the white, the wealthy. But that’s not whom it hurt. The people who suffered the most are the most vulnerable: the essential workers, the elders who can’t afford the hospital bill, the children without internet or clean water. It’s the men and women who cannot shelter in place because they have no refuge to crouch in. The locked-up folks who don’t have six feet to give, the transplanted asylum-seekers who cannot escape despair or disease. They are the ones who pay. They even the ledger, dripping in red.
The power that permitted the murder of George Floyd has inflicted a lethal shortness of breath on thousands of other citizens who share his skin tone. COVID-19 has burned through the country, abetted by a racist gaze that arbitrates bodies of color as cesspools of disease and danger. This prejudiced contemplation has distorted our attention to focus on Asia, on DNA, despite clear testimony that indicts major, preexisting health inequities for the undue burden of pandemic suffering in communities of color. This bigotry endangers the people who are thought to look dangerous, while waving through threats that do not fit the preordained description of a hazard—the European traveler, the international businessman, the uniformed cop.
At a time when predominantly Black U.S. counties are experiencing COVID-19 death rates six times higher than everyone else, it is impossible not to remember Eric Garner, choking, gasping. It is impossible not to remember Ahmaud Arbery, whose sunny jog should not have robbed him of his breath. It is impossible not to remember how George Floyd struggled against a knee to tell the world he could not breathe. How he died, months before his 47th revolution around the sun.
Editor’s Note (9/11/20): This article has been edited after posting to correct the description of Representative Bill Foster’s comments.