scientificamerican--2020-09-25--Coronavirus News Roundup: September 19-September 25

The items below are highlights from the free newsletter , “ Smart , useful , science stuff about COVID-19.
” To receive newsletter issues daily in your inbox , sign up here .
Please consider a monthly contribution to support this newsletter .
For some SARS-CoV-2 vaccine makers , a vaccine `` could meet the companies ' benchmarks for success if it lowered the risk of mild COVID-19 , but was never shown to reduce moderate or severe '' COVID-19 , nor the risk of hospitalization , intensive care admission or death , according to an essay published 9/22/20 in @ @ @ @ @ @ @ pertains to vaccines being developed by Moderna , by Pfizer , and by AstraZeneca , the essay states .
The benchmarks should be higher , the authors contend .
Evidence should instead show that a vaccine reduces the risk of moderate or severe cases , write Dr. Peter Doshi of the University of Maryland School of Pharmacy and Dr. Eric Topol at Scripps Research .
The essay states that reducing the risk of mild COVID-19 does not guarantee a similar reduction for moderate or severe cases .
In both the Moderna vaccine experiments @ @ @ @ @ @ @ people report feeling “ side effects that are similar to the symptoms of mild COVID-19 , ” the essay states .
London could be the site of the first experiments in which quarantined volunteers would be deliberately exposed to SARS-CoV-2 after being inoculated with a candidate vaccine to protect against the new coronavirus , according to various reports .
Such experiments are called human challenge trials .
The London experiments are expected to start in January , Reuters reported 9/23/20 , picking up an initial report by The Financial Times ( paywalled ) @ @ @ @ @ @ @ have volunteered with the group 1Day Sooner for coronavirus challenge trials , the Reuters story states .
Tanya Lewis at Scientific American has reported a feature story on some of the more than 100 U.S. universities and colleges that have contracted rapid , frequent SARS-CoV-2 testing for their campus to a program offered by the Broad Institute of the Massachusetts Institute of Technology and Harvard University ( 9/23/20 ) .
Institutions ’ reports on the program so far are positive , and such an approach to testing “ could be a model for @ @ @ @ @ @ @ Lewis writes .
The program enables testing once or twice a week throughout the semester for students , faculty and staff , the story states .
The story includes comments from users of the Broad program , including representatives from Tufts University , Bowdoin College , and University of Massachusetts Amherst , where the basketball arena reportedly has been converted into a SARS-CoV-2 testing center .
Plans for early access to highly anticipated SARS-CoV-2 vaccines are “ taking shape , ” reports Nidhi Subbaraman at Nature ( 9/17/20 ) .
Organizations that have @ @ @ @ @ @ @ include an advisory group at the World Health Organization and a panel convened by the U.S. National Academies of Sciences , Engineering , and Medicine ( NASEM ) , the story states .
The NASEM panel gives top priority for vaccination to health-care workers and first responders , and then to “ medically vulnerable groups , ” such as people with preexisting conditions such as heart disease or diabetes as well as “ older people living in crowded conditions , ” Subbaraman reports .
The NASEM panel 's third priority group includes high-risk-of-exposure @ @ @ @ @ @ @ public transit and schools , as well as people living in homeless shelters and prisons , the story states .
Fourth priority goes to young adults , children and essential workers “ at increased risk of exposure , ” and the fifth priority is everyone remaining .
NASEM is set to release a final plan in October , the story states .
In a feature story for The Scientist , Katarina Zimmer explores the latest theories for why some people develop severe COVID-19 and others do not ( 9/16/20 ) .
More details @ @ @ @ @ @ @ immune system “ goes haywire ” in some people infected with the virus .
One study she mentions found that the blood of patients with severe COVID-19 showed an initial diminished response of interferons , which she defines as `` cytokines [ small signaling compounds/proteins ] that , in general , act to curtail viral replication.
” And that can lead to damage that leads to inflammation , the story states .
“ The higher the damage , the more the immune system is trying to get rid of the damage , ” @ @ @ @ @ @ @ Institute at Mount Sinai .
“ So it gets activated and at some point…it goes completely crazy.
” That leads to the phenomenon called a cytokine storm — the immune system over-reaction .
The piece also details new insights into function problems and creation problems in various immune cells ( e.g .
myeloid cells , T cells , and antibodies ) .
Near the end of the piece , the same researcher is attributed as saying that the myeloid defects could be at the root of the runaway cytokine responses .
But an @ @ @ @ @ @ @ that it ’ s hard to tease apart the chicken and the egg .
Parts of the U.S. “ may be witnessing the first days of an autumn surge , ” according a daily coronavirus data page updated 9/24/20 at National Geographic .
Lower on the page , graphs indicate that SARS-CoV-2 case-counts have increased in the past week in Utah , Wisconsin , South Dakota , Montana , and Texas ; and decreases appear to have taken place in the same period in Delaware , Louisiana , Indiana , Georgia , and @ @ @ @ @ @ @ appears so far not to be spreading inside U.S. schools , report Laura Meckler and Valerie Strauss at The Washington Post ( 9/23/20 ) .
Thousands of teachers and students have been reported as infected , the story suggests , but these “ rates of infection are far below what is found in the surrounding communities , ” the reporters write .
The evidence hints that re-opening schools “ may not be as risky as many have feared , ” the story states .
The story notes that testing and reporting for SARS-CoV-2 @ @ @ @ @ @ @ U.S. , so it ’ s hard to say if this is an accurate picture of in-school transmission .
The story also quotes epidemiologist Michael Osterholm of the Center for Infectious Disease Research and Policy at the University of Minnesota as saying : “ Everyone had a fear there would be explosive outbreaks of transmission in the schools .
In colleges , there have been .
We have to say that , to date , we have not seen those in the younger kids.
” Several indoor-air quality researchers and other scientists have @ @ @ @ @ @ @ , “ FAQs on protecting yourself from COVID-19 aerosol transmission , ” designed to inform the general public ( 9/15/20 ) .
The information represents “ our best understanding at this time and should always be similar or more stringent than information provided by [ the U.S. Centers for Disease Control ] , [ World Health Organization ] , and most regional & local health authorities.
” The document ’ s authors include Linsey Marr of Virginia Tech ; Shelly Miller and Jose-Luis Jimenez both of University of Colorado , Boulder ; Kimberly @ @ @ @ @ @ @ Diego ; Charles Haas at Drexel University ; and Richard Corsi of Portland State University .
I haven ’ t read the whole document , but a primary point regarding reducing SARS-CoV-2 transmission is that “ you should pay at least as much attention to the air you breathe as you do to sanitizing surfaces and your hands.
” This 9/22/20 Bloomberg piece by opinion columnists Max Nisen and Elaine He features an easy-to-read graphic that illustrates the risks to long-term health posed by infection with SARS-CoV-2 .
The data came from a @ @ @ @ @ @ @ who reported to an Indiana University Medical School researcher nearly 100 different long-term health problems .
“ Researchers have yet to ascertain what share of people infected with COVID-19 suffer from long-term symptoms .
But the potential for harm is vast , ” based on the number of people infected with SARS-CoV-2 , the story states .
There ’ s also a powerful graphic lower on the page showing a data scientist 's estimate of the actual number of U.S. infections through November compared with the confirmed figures .
You might enjoy , @ @ @ @ @ @ @ dining begins , ” by Jeremy Hooper for McSweeney ’ s ( 9/23/20 ) .

The items below are highlights from the free newsletter, “Smart, useful, science stuff about COVID-19.” To receive newsletter issues daily in your inbox, sign up here. Please consider a monthly contribution to support this newsletter.
For some SARS-CoV-2 vaccine makers, a vaccine "could meet the companies' benchmarks for success if it lowered the risk of mild COVID-19, but was never shown to reduce moderate or severe" COVID-19, nor the risk of hospitalization, intensive care admission or death, according to an essay published 9/22/20 in The New York Times. This statement pertains to vaccines being developed by Moderna, by Pfizer, and by AstraZeneca, the essay states. The benchmarks should be higher, the authors contend. Evidence should instead show that a vaccine reduces the risk of moderate or severe cases, write Dr. Peter Doshi of the University of Maryland School of Pharmacy and Dr. Eric Topol at Scripps Research. The essay states that reducing the risk of mild COVID-19 does not guarantee a similar reduction for moderate or severe cases. In both the Moderna vaccine experiments and the Pfizer vaccine experiments, some people report feeling “side effects that are similar to the symptoms of mild COVID-19,” the essay states.
London could be the site of the first experiments in which quarantined volunteers would be deliberately exposed to SARS-CoV-2 after being inoculated with a candidate vaccine to protect against the new coronavirus, according to various reports. Such experiments are called human challenge trials. The London experiments are expected to start in January, Reuters reported 9/23/20, picking up an initial report by The Financial Times (paywalled). So far, about 2,000 participants have volunteered with the group 1Day Sooner for coronavirus challenge trials, the Reuters story states.
Tanya Lewis at Scientific American has reported a feature story on some of the more than 100 U.S. universities and colleges that have contracted rapid, frequent SARS-CoV-2 testing for their campus to a program offered by the Broad Institute of the Massachusetts Institute of Technology and Harvard University (9/23/20). Institutions’ reports on the program so far are positive, and such an approach to testing “could be a model for reopening colleges and institutions nationwide,” Lewis writes. The program enables testing once or twice a week throughout the semester for students, faculty and staff, the story states. The story includes comments from users of the Broad program, including representatives from Tufts University, Bowdoin College, and University of Massachusetts Amherst, where the basketball arena reportedly has been converted into a SARS-CoV-2 testing center.
Plans for early access to highly anticipated SARS-CoV-2 vaccines are “taking shape,” reports Nidhi Subbaraman at Nature (9/17/20). Organizations that have issued preliminary plans or guidance so far include an advisory group at the World Health Organization and a panel convened by the U.S. National Academies of Sciences, Engineering, and Medicine (NASEM), the story states. The NASEM panel gives top priority for vaccination to health-care workers and first responders, and then to “medically vulnerable groups,” such as people with preexisting conditions such as heart disease or diabetes as well as “older people living in crowded conditions,” Subbaraman reports. The NASEM panel's third priority group includes high-risk-of-exposure essential workers such as those working in public transit and schools, as well as people living in homeless shelters and prisons, the story states. Fourth priority goes to young adults, children and essential workers “at increased risk of exposure,” and the fifth priority is everyone remaining. NASEM is set to release a final plan in October, the story states.
In a feature story for The Scientist, Katarina Zimmer explores the latest theories for why some people develop severe COVID-19 and others do not (9/16/20). More details are coming into focus on why the immune system “goes haywire” in some people infected with the virus. One study she mentions found that the blood of patients with severe COVID-19 showed an initial diminished response of interferons, which she defines as "cytokines [small signaling compounds/proteins] that, in general, act to curtail viral replication.” And that can lead to damage that leads to inflammation, the story states. “The higher the damage, the more the immune system is trying to get rid of the damage,” says the director of the Precision Medicine Institute at Mount Sinai. “So it gets activated and at some point…it goes completely crazy.” That leads to the phenomenon called a cytokine storm — the immune system over-reaction. The piece also details new insights into function problems and creation problems in various immune cells (e.g. myeloid cells, T cells, and antibodies). Near the end of the piece, the same researcher is attributed as saying that the myeloid defects could be at the root of the runaway cytokine responses. But an immunologist at Emory University is quoted saying that it’s hard to tease apart the chicken and the egg.
Parts of the U.S. “may be witnessing the first days of an autumn surge,” according a daily coronavirus data page updated 9/24/20 at National Geographic. Lower on the page, graphs indicate that SARS-CoV-2 case-counts have increased in the past week in Utah, Wisconsin, South Dakota, Montana, and Texas; and decreases appear to have taken place in the same period in Delaware, Louisiana, Indiana, Georgia, and Kentucky.
Early evidence suggests that SARS-CoV-2 appears so far not to be spreading inside U.S. schools, report Laura Meckler and Valerie Strauss at The Washington Post (9/23/20). Thousands of teachers and students have been reported as infected, the story suggests, but these “rates of infection are far below what is found in the surrounding communities,” the reporters write. The evidence hints that re-opening schools “may not be as risky as many have feared,” the story states. The story notes that testing and reporting for SARS-CoV-2 is weak in many parts of the U.S., so it’s hard to say if this is an accurate picture of in-school transmission. The story also quotes epidemiologist Michael Osterholm of the Center for Infectious Disease Research and Policy at the University of Minnesota as saying: “Everyone had a fear there would be explosive outbreaks of transmission in the schools. In colleges, there have been. We have to say that, to date, we have not seen those in the younger kids.”
Several indoor-air quality researchers and other scientists have collaborated on a highly accessible 53-page google-document, “FAQs on protecting yourself from COVID-19 aerosol transmission,” designed to inform the general public (9/15/20). The information represents “our best understanding at this time and should always be similar or more stringent than information provided by [the U.S. Centers for Disease Control], [World Health Organization], and most regional & local health authorities.” The document’s authors include Linsey Marr of Virginia Tech; Shelly Miller and Jose-Luis Jimenez both of University of Colorado, Boulder; Kimberly Prather at University of California, San Diego; Charles Haas at Drexel University; and Richard Corsi of Portland State University. I haven’t read the whole document, but a primary point regarding reducing SARS-CoV-2 transmission is that “you should pay at least as much attention to the air you breathe as you do to sanitizing surfaces and your hands.”
This 9/22/20 Bloomberg piece by opinion columnists Max Nisen and Elaine He features an easy-to-read graphic that illustrates the risks to long-term health posed by infection with SARS-CoV-2. The data came from a survey of more than 1,500 COVID-19 survivors who reported to an Indiana University Medical School researcher nearly 100 different long-term health problems. “Researchers have yet to ascertain what share of people infected with COVID-19 suffer from long-term symptoms. But the potential for harm is vast,” based on the number of people infected with SARS-CoV-2, the story states. There’s also a powerful graphic lower on the page showing a data scientist's estimate of the actual number of U.S. infections through November compared with the confirmed figures.
You might enjoy, “Where the sidewalk ends, outdoor dining begins,” by Jeremy Hooper for McSweeney’s (9/23/20).


scientificamerican--2020-09-29--The Most Confused of the Scientific Branches

Quantum researchers seem to have more theories than they know what to do with .
Of the handful of options , take , for example , the many-worlds view , which posits that when a quantum observation is made , reality splits into parallel universes , each representing all potential outcomes .
Or there is the relatively new QBism camp , members of which argue that quantum mechanics is subjective to the individuals making predictions about how they will measure an experiment .
On top of these conflicting theories , any new experimental data invariably support one possible explanation and @ @ @ @ @ @ @ this confounding research situation ?
Where some see an impasse , others see opportunity .
At the very end of this issue ’ s cover story , Michele Reilly , co-founder of a quantum computing company based in New York City , tells our reporter that such confusion opens the door for novel experiments , of both the theoretical variety and the physical ( see “ This Twist on Schrödinger ’ s Cat Paradox Has Major Implications for Quantum Theory ” ) .
If that ’ s not a pure emblem of the @ @ @ @ @ @ @ t know what is .
Elsewhere in this issue , Anil Ananthaswamy examines the latest estimates of alien life in the universe—estimates that ride on 18th-century statistics ( see “ How Many Aliens Are in the Milky Way ?
Astronomers Turn to Statistics for Answers ” ) .
And Alexandra Witze gives a dazzling overview of NASA ’ s latest rover project : Perseverance ( see “ NASA Has Launched the Most Ambitious Mars Rover Ever Built : Here ’ s What Happens Next ” ) .
If any field needed the gumption @ @ @ @ @ @ @ , it ’ s space and physics .
Enjoy !

Quantum researchers seem to have more theories than they know what to do with. Of the handful of options, take, for example, the many-worlds view, which posits that when a quantum observation is made, reality splits into parallel universes, each representing all potential outcomes. Or there is the relatively new QBism camp, members of which argue that quantum mechanics is subjective to the individuals making predictions about how they will measure an experiment. On top of these conflicting theories, any new experimental data invariably support one possible explanation and contradict another. What to make of this confounding research situation? Where some see an impasse, others see opportunity. At the very end of this issue’s cover story, Michele Reilly, co-founder of a quantum computing company based in New York City, tells our reporter that such confusion opens the door for novel experiments, of both the theoretical variety and the physical (see “This Twist on Schrödinger’s Cat Paradox Has Major Implications for Quantum Theory”). If that’s not a pure emblem of the scientific method, then I don’t know what is.
Elsewhere in this issue, Anil Ananthaswamy examines the latest estimates of alien life in the universe—estimates that ride on 18th-century statistics (see “How Many Aliens Are in the Milky Way? Astronomers Turn to Statistics for Answers”). And Alexandra Witze gives a dazzling overview of NASA’s latest rover project: Perseverance (see “NASA Has Launched the Most Ambitious Mars Rover Ever Built: Here’s What Happens Next”). If any field needed the gumption to keep going for the long haul, it’s space and physics. Enjoy!


scientificamerican--2020-09-29--Lessons from AIDS for the COVID-19 Pandemic

“ We are now engaged in another deadly episode in the historic battle of man versus microbe .
These battles have shaped the course of human evolution and of history .
We have seen the face of our adversary , in this case a tiny virus.
” I spoke these words in testimony before a U.S. Senate subcommittee on September 26 , 1985 .
I was talking about HIV , but I could say the same thing today about the coronavirus we are facing .
Like all viruses , coronaviruses are expert code crackers .
SARS-CoV-2 has certainly cracked ours @ @ @ @ @ @ @ intelligent biological machine continuously running DNA experiments to adapt to the ecological niche it inhabits .
This virus has caused a pandemic in large part because it acted on three of our most human vulnerabilities : our biological defenses , our clustering patterns of social behavior and our simmering political divides .
How will the confrontation unfold in the next years and decades ?
What will be the human toll in deaths , ongoing disease , injuries and other impairments ?
How effective will new vaccines and treatments be in containing or even @ @ @ @ @ @ @ say .
But several lessons from the long battle with HIV , the human immunodeficiency virus that causes AIDS , suggest what may lie ahead .
HIV/AIDS is one of the worst scourges humans have encountered .
As a code cracker , HIV is an expert .
By the end of 2019 the global death toll from this virus was roughly 33 million people .
In all , 76 million people have been infected , and scientists estimate another 1.7 million people acquire the virus every year .
Yet we must appreciate what @ @ @ @ @ @ @ the nearly 38 million people currently living with HIV/AIDS , 25 million are receiving full antiretroviral treatments that prevent disease and suppress the virus so well they are unlikely to pass it along .
I would wager that another 25 million or more infections never happened , primarily in sub-Saharan Africa , because these treatments became available in most countries .
From fighting this epic war against AIDS , doctors , virologists , epidemiologists and public health experts have learned crucial lessons that we can apply to the battle we are currently waging @ @ @ @ @ @ @ vaccines are never a guarantee but that treatments can be our most important weapon .
We discovered that human behavior plays a vital role in any disease-fighting effort and that we can not overlook human nature .
We have also seen how critical it is to build on knowledge and tools gained fighting earlier outbreaks—a strategy only possible if we continue funding research in between pandemics .
Early observations of how HIV behaves in our bodies showed the road to a vaccine would be long and challenging .
As the outbreak unfolded , @ @ @ @ @ @ @ cells ( the white blood cells that wage war against invaders ) in those infected .
The high levels of both showed that patients were mounting incredibly active immune responses , more forceful than anything we had seen for any other disease .
But even working at its highest capacity , the body 's immune system was never strong enough to clear out the virus completely .
Unlike the hit-and-run polio virus , which evokes long-term immunity after an infection , HIV is a “ catch it and keep it ” virus—if you @ @ @ @ @ @ @ your body until it destroys the immune system , leaving you undefended against even mild infections .
Moreover , HIV continually evolves—a shrewd opponent seeking ways to elude our immune responses .
Although this does not mean a vaccine is impossible , it certainly meant developing one , especially when the virus hit in the 1980s , would not be easy .
“ Unfortunately , no one can predict with certainty that an AIDS vaccine can ever be made , ” I testified in 1988 to the Presidential Commission on the HIV Epidemic @ @ @ @ @ @ @ it is impossible to make such a vaccine , only that we are not certain of success.
” More than 30 years later there still is no effective vaccine to prevent HIV infection .
From what we have seen of SARS-CoV-2 , it interacts with our immune system in complex ways , resembling polio in some of its behavior and HIV in others .
We know from nearly 60 years of observing coronaviruses that a body 's immune system can clear them .
That seems to be generally the case for SARS-CoV-2 as @ @ @ @ @ @ @ just like HIV , also have their tricks .
Infection from one of them never seems to confer immunity to reinfection or symptoms by the same strain of virus—that is why the same cold viruses return each season .
These coronaviruses are not a hit-and-run virus like polio or a catch-it-and-keep-it virus like HIV .
I call them “ get it and forget it ” viruses—once cleared , your body tends to forget it ever fought this foe .
Early studies with SARS-CoV-2 suggest it might behave much like its cousins , raising @ @ @ @ @ @ @ a SARS-CoV-2 vaccine may be filled with obstacles .
Whereas some people with COVID-19 make neutralizing antibodies that can clear the virus , not everybody does .
Whether a vaccine will stimulate such antibodies in everyone is still unknown .
Moreover , we do not know how long those antibodies can protect someone from infection .
It may be two or three years before we will have the data to tell us and any confidence in the outcome .
Another challenge is how this virus enters the body : through the nasal mucosal @ @ @ @ @ @ @ development has shown an ability to prevent infection through the nose .
In nonhuman primates , some vaccines can prevent the disease from spreading efficiently to the lungs .
But those studies do not tell us much about how the same drug will work in humans ; the disease in our species is very different from what it is in monkeys , which do not become noticeably ill. We learned with HIV that attempts to prevent virus entry altogether do not work well—not for HIV and not for many other viruses , including @ @ @ @ @ @ @ more like fire alarms : rather than preventing fires from breaking out , they call the immune system for help once a fire has ignited .
The hopes of the world rest on a COVID-19 vaccine .
It seems likely that scientists will announce a “ success ” sometime this year , but success is not as simple as it sounds .
As I write , officials in Russia have reported approving a COVID-19 vaccine .
Will it work ?
Will it be safe ?
Will it be long lasting ?
No one @ @ @ @ @ @ @ to these questions for any forthcoming vaccine soon , perhaps not for at least several years .
We have made remarkable improvements in our molecular biology tools since the 1980s , yet the slowest part of drug development remains human testing .
That said , the infrastructure created for HIV/AIDS research is accelerating the testing process now .
Thirty thousand volunteers around the world participate in networks built by the National Institutes of Health for studies of new HIV vaccine candidates , and these networks are being tapped for initial testing of COVID-19 @ @ @ @ @ @ @ a patient who is likely to die , they are willing to risk that a drug might sicken the patient but still save their life .
But doctors are less willing to do that to prevent disease ; the chances of causing greater harm to the patient are too high .
This is why for decades the quest for a vaccine to prevent HIV infection has lagged so far behind development of therapeutic drugs for HIV .
These drugs now stand as an incredible success story .
The first set of HIV drugs @ @ @ @ @ @ @ chain terminator drugs .
They inserted an additional “ chain terminating ” nucleotide as the virus copied its viral RNA into DNA , preventing the HIV chain of DNA from elongating .
By the 1990s we had gotten better at using combinations of drugs to control HIV infections soon after patients were exposed .
The first drug , AZT , found immediate application for health care workers who accidentally had a needlestick injury that infected them with contaminated blood .
It was also used to reduce mother-to-child transmission .
For example , prenatal @ @ @ @ @ @ @ time reduced the number of babies born infected by as much as two thirds .
Today combination chemotherapy reduces mother-to-child transmission to undetectable levels .
The next set of drugs was protease inhibitors , one of which I helped to develop .
The first was introduced in 1995 and was combined with other drugs in treating patients .
These drugs inhibited the viral protease enzyme responsible for longer precursor proteins in the short active components of the virus .
But there is a fundamental problem with these drugs , as well as those @ @ @ @ @ @ @ to create virus DNA .
Our bodies also use proteases for normal functioning , and we need polymerases to replicate our own nucleic acids .
The same drugs that inhibit the viral proteins also inhibit our own cells .
The difference between a concentration in which the drug inhibits the virus target and a concentration in which it hurts the human proteins is called the therapeutic index .
The therapeutic index gives you the window in which the drug will be effective against the virus without causing undue side effects .
That window @ @ @ @ @ @ @ protease inhibitors .
The gold standard for AIDS treatment now is called antiretroviral therapy—essentially patients take a cocktail of at least three different drugs that attack the HIV virus in different ways .
The strategy is based on earlier success we had in fighting cancer .
In the late 1970s I established a laboratory at Harvard University 's Dana-Farber Cancer Institute to develop new drugs to treat cancer patients .
Cancers developed resistance over time to single drugs , but combinations of drugs were effective in slowing , stopping or killing the cancers @ @ @ @ @ @ @ combination chemotherapy to HIV .
By the early 1990s the first combination AIDS treatments were saving the lives of people infected with HIV .
Today an infection is far from the death sentence it used to be—patients can now live almost unaffected by HIV , with a relatively minimal impact on life expectancy .
We already know resistance to single drugs will bedevil COVID-19 treatments .
We have seen resistance to single , anti-SARS-CoV-2 drugs develop rapidly in early lab studies .
Just as with AIDS and cancer , we need a combination @ @ @ @ @ @ @ The goal of the biotechnology and pharmaceutical industries now is to develop an array of highly potent and specific drugs , each of which targets a different function of the virus .
Decades of research on HIV has shown the way and gives us confidence in our eventual success .
In trying to understand and counter the AIDS epidemic , physician and virologist Robert Redfield ( who is now head of the Centers for Disease Control and Prevention ) and I became good friends in the early 1980s .
We quickly learned that @ @ @ @ @ @ @ to recognize HIV as a threat to their populations , militaries were an exception .
Nearly all countries considered AIDS a serious danger to troops and military readiness and a potentially huge drain on future military funds .
Their view was , “ Let 's not blind ourselves and pretend soldiers are saints .
They are not .
They are humans.
” Redfield , then at Walter Reed Army Medical Center , helped to design and manage a program to test the entire U.S. uniformed forces for HIV infection ( although the consequences @ @ @ @ @ @ @ recruits who tested positive were barred from service ) .
At the time there were no effective drugs ; the disease killed more than 90 percent of those infected .
When married couples were tested and one partner was infected and one not , doctors advised them in the strongest possible terms to use condoms .
I was stunned to learn that fewer than a third complied with the advice .
“ If people do n't respond to the lethal danger of unprotected sex with their husband or wife , we are in @ @ @ @ @ @ @ Over the next five years more than three quarters of the uninfected partners contracted HIV .
I have always used this experience as a guide to pit hope against reality .
Human sexuality—the drive for sex and physical connection—is deeply embedded in our nature .
I knew in the 1980s it was very unlikely people would change their sexual behavior in a major way .
In the 19th century everyone knew how syphilis was contracted and that it was serious disease .
Yet syphilis still infected at least 10 to 15 percent of @ @ @ @ @ @ @ 20th century .
It was not that people were ignorant of how to catch it ; it is that they did not change their lifestyle accordingly .
There is likewise a sexual dynamic to COVID-19 that often goes unmentioned .
It is part of what is driving people out of their homes and into bars and parties .
Anyone with a craving for a beer can quench their thirst in the safety of their own home , but gratification comes less easily for other desires , especially when one is young , single @ @ @ @ @ @ @ strategies should not ignore this fact .
The same lessons we learned in the midst of the HIV epidemic to help young people change their behaviors apply today to COVID-19 : know your risk , know your partners and take necessary precautions .
Many young people operate under the false assumption that even if they become infected , they will not become severely ill. Not only is this belief untrue , but even people with asymptomatic infections can suffer serious , lasting damage .
But the more people understand the risk—younger people especially—the @ @ @ @ @ @ @ necessary to protect themselves and others .
We saw this happen with AIDS .
When I ask world experts what they know about the detailed molecular biology of SARS-CoV-2 or , for that matter , any other coronavirus , they do not have the kind of answers they should .
Why ?
Because governments and industry pulled the plug on coronavirus research funding in 2006 after the first SARS ( severe acute respiratory syndrome ) pandemic faded away and again in the years immediately following the MERS ( Middle East respiratory syndrome , @ @ @ @ @ @ @ when it seemed to be controllable .
Funding agencies everywhere , not just in the U.S. but in China , Japan , Singapore , Hong Kong and the Middle East—countries affected by SARS and MERS—underestimated the threat of coronaviruses .
Despite clear , persistent , highly vocal warnings from many of those who battled SARS and MERS up close , funding dried up .
The development of promising anti-SARS and MERS drugs , which might have been active against SARS-CoV-2 as well , was left unfinished for lack of money .
With 776,000 @ @ @ @ @ @ @ of mid-August , we have every motive to accelerate funding .
The U.S. quickly opened the funding spigots last spring for research to hasten discoveries of vaccines and drugs .
But will it be enough ?
We learned from the HIV crisis that it was important to have research pipelines already established .
Cancer research in the 1950s , 1960s and 1970s built a foundation for HIV/AIDS studies .
The government responded to public concerns , sharply increasing federal funding of cancer research during those decades .
These efforts culminated in Congress 's @ @ @ @ @ @ @ Cancer Act in 1971 .
This $ 1.6-billion commitment for cancer research , equal to $ 10 billion in today 's money , built the science we needed to identify and understand HIV in the 1980s , although of course no one knew that payoff was coming .
In the 1980s the Reagan administration did not want to talk about AIDS or commit much public funding to HIV research .
The first time President Ronald Reagan gave a major speech on AIDS was in 1987 .
In his first administration , funding for @ @ @ @ @ @ @ were willing to stake their careers on deciphering the molecular biology .
Yet once the news broke that actor Rock Hudson was seriously ill with AIDS , Ted Stevens , the Senate Republican Whip , joined with Democratic Senator Ted Kennedy , actor Elizabeth Taylor , me and a few others in campaigning effectively to add $ 320 million in the fiscal 1986 budget for AIDS research .
Barry Goldwater , Jesse Helms and John Warner , Republican leaders in the Senate , supported us .
The money flowed , and outstanding scientists @ @ @ @ @ @ @ this first congressionally funded AIDS research program with Anthony Fauci , the doctor now leading our nation 's fight against COVID-19 .
( And if there is one person in the world who has made the greatest contribution to the prevention and treatment of AIDS , that person is Fauci . )
One difference between the 1980s and now is that Republican members of Congress were more willing to stand up to the president and White House staff when they failed to take the necessary steps to fight a global disease .
For @ @ @ @ @ @ @ job to protect the U.S. Army and other arms of the military and Secret Service as much as possible from HIV infection .
He helped to move $ 55 million within the defense budget , designating it for screening recruits for HIV/AIDS .
Our tool set for virus and pharmaceutical research has improved enormously in the past 36 years since HIV was discovered .
This is one reason I am confident we will have effective antiviral drugs for treating COVID-19 infections by next year , if not sooner .
What used to take @ @ @ @ @ @ @ 1980s and 1990s in many cases now can be done in five or 10 months .
We can rapidly identify and synthesize chemicals to predict which drugs will be effective .
We can do cryoelectron microscopy to probe virus structures and simulate molecule-by-molecule interactions in a matter of weeks—something that used to take years .
The lesson is to never let down our guard when it comes to funding antivirus research .
We would have no hope of beating COVID-19 if it were not for the molecular biology gains we made during earlier @ @ @ @ @ @ @ time around will help us out during the next pandemic , but we must keep the money coming .
In November 2019 I spent several days in Wuhan , China , chairing a meeting of the U.S.-China Health Summit .
Our group 's major concern , looming amid the U.S.-China trade war , was the threat of restrictions on sharing research discoveries .
Otherwise , it was a delightful time in a beautiful city .
Weeks later , back home in New York City , I could not shake a lingering cold virus @ @ @ @ @ @ @ trip .
( I later tested negative for COVID-19 antibodies , but that result is not definitive . )
The head of my foundation in China called me one day with awful news .
Three of his grandparents had died from some strange virus .
“ Everyone who gets this is really sick , ” my colleague , in his mid-30s , said .
“ Everything is closed down .
I ca n't even go to my grandparents ' funerals.
” A few weeks later I received a vivid firsthand account of how @ @ @ @ @ @ @ another colleague who had just emerged from 14 days of isolation in a quarantine hotel .
He explained that when one person in the back of his flight from Frankfurt , Germany , to Shanghai tested positive for the coronavirus , contact tracers called my friend days later and ordered him into isolation .
His only human contact then was with hazmat-clad inspectors who came daily to disinfect his room and drop off meals .
We are just beginning to glimpse what the long-term toll of COVID-19 might be .
This is a @ @ @ @ @ @ @ have a clearer idea until after a few years , but we know it will be very high .
We have barely scratched the surface of coronavirus molecular biology .
What story will our children and grandchildren recount about our successes as scientists and as a society , and our failures , to contain this pandemic—the worst we have faced in 100 years ?
Science leaps into the darkness , the very edge of human knowledge .
That is where we begin , as if deep in a cave , chipping away at @ @ @ @ @ @ @ do not know what you will find on the other side .
Some people chip away for a lifetime , only to accumulate a pile of flakes .
We may be in for a protracted pandemic , or we may get lucky with effective treatments and vaccines soon .
But we have been here before , facing an unknown viral enemy , and we can lean on lessons we have learned .
This is not the first and will not be the last global epidemic .

“We are now engaged in another deadly episode in the historic battle of man versus microbe. These battles have shaped the course of human evolution and of history. We have seen the face of our adversary, in this case a tiny virus.” I spoke these words in testimony before a U.S. Senate subcommittee on September 26, 1985. I was talking about HIV, but I could say the same thing today about the coronavirus we are facing.
Like all viruses, coronaviruses are expert code crackers. SARS-CoV-2 has certainly cracked ours. Think of this virus as an intelligent biological machine continuously running DNA experiments to adapt to the ecological niche it inhabits. This virus has caused a pandemic in large part because it acted on three of our most human vulnerabilities: our biological defenses, our clustering patterns of social behavior and our simmering political divides.
How will the confrontation unfold in the next years and decades? What will be the human toll in deaths, ongoing disease, injuries and other impairments? How effective will new vaccines and treatments be in containing or even eradicating the virus?
No one can say. But several lessons from the long battle with HIV, the human immunodeficiency virus that causes AIDS, suggest what may lie ahead. HIV/AIDS is one of the worst scourges humans have encountered. As a code cracker, HIV is an expert. By the end of 2019 the global death toll from this virus was roughly 33 million people. In all, 76 million people have been infected, and scientists estimate another 1.7 million people acquire the virus every year.
Yet we must appreciate what our scientific defenses have accomplished. Of the nearly 38 million people currently living with HIV/AIDS, 25 million are receiving full antiretroviral treatments that prevent disease and suppress the virus so well they are unlikely to pass it along. I would wager that another 25 million or more infections never happened, primarily in sub-Saharan Africa, because these treatments became available in most countries.
From fighting this epic war against AIDS, doctors, virologists, epidemiologists and public health experts have learned crucial lessons that we can apply to the battle we are currently waging. For instance, we saw that vaccines are never a guarantee but that treatments can be our most important weapon. We discovered that human behavior plays a vital role in any disease-fighting effort and that we cannot overlook human nature. We have also seen how critical it is to build on knowledge and tools gained fighting earlier outbreaks—a strategy only possible if we continue funding research in between pandemics.
Vaccine Challenges
Early observations of how HIV behaves in our bodies showed the road to a vaccine would be long and challenging. As the outbreak unfolded, we began tracking antibody levels and T cells (the white blood cells that wage war against invaders) in those infected. The high levels of both showed that patients were mounting incredibly active immune responses, more forceful than anything we had seen for any other disease. But even working at its highest capacity, the body's immune system was never strong enough to clear out the virus completely.
Unlike the hit-and-run polio virus, which evokes long-term immunity after an infection, HIV is a “catch it and keep it” virus—if you are infected, the pathogen stays in your body until it destroys the immune system, leaving you undefended against even mild infections. Moreover, HIV continually evolves—a shrewd opponent seeking ways to elude our immune responses. Although this does not mean a vaccine is impossible, it certainly meant developing one, especially when the virus hit in the 1980s, would not be easy. “Unfortunately, no one can predict with certainty that an AIDS vaccine can ever be made,” I testified in 1988 to the Presidential Commission on the HIV Epidemic. “That is not to say it is impossible to make such a vaccine, only that we are not certain of success.” More than 30 years later there still is no effective vaccine to prevent HIV infection.
From what we have seen of SARS-CoV-2, it interacts with our immune system in complex ways, resembling polio in some of its behavior and HIV in others. We know from nearly 60 years of observing coronaviruses that a body's immune system can clear them. That seems to be generally the case for SARS-CoV-2 as well. But the cold-causing coronaviruses, just like HIV, also have their tricks. Infection from one of them never seems to confer immunity to reinfection or symptoms by the same strain of virus—that is why the same cold viruses return each season. These coronaviruses are not a hit-and-run virus like polio or a catch-it-and-keep-it virus like HIV. I call them “get it and forget it” viruses—once cleared, your body tends to forget it ever fought this foe. Early studies with SARS-CoV-2 suggest it might behave much like its cousins, raising transient immune protection.
The path to a SARS-CoV-2 vaccine may be filled with obstacles. Whereas some people with COVID-19 make neutralizing antibodies that can clear the virus, not everybody does. Whether a vaccine will stimulate such antibodies in everyone is still unknown. Moreover, we do not know how long those antibodies can protect someone from infection. It may be two or three years before we will have the data to tell us and any confidence in the outcome.
Another challenge is how this virus enters the body: through the nasal mucosal membranes. No COVID-19 vaccine currently in development has shown an ability to prevent infection through the nose. In nonhuman primates, some vaccines can prevent the disease from spreading efficiently to the lungs. But those studies do not tell us much about how the same drug will work in humans; the disease in our species is very different from what it is in monkeys, which do not become noticeably ill.
We learned with HIV that attempts to prevent virus entry altogether do not work well—not for HIV and not for many other viruses, including influenza and even polio. Vaccines act more like fire alarms: rather than preventing fires from breaking out, they call the immune system for help once a fire has ignited.
The hopes of the world rest on a COVID-19 vaccine. It seems likely that scientists will announce a “success” sometime this year, but success is not as simple as it sounds. As I write, officials in Russia have reported approving a COVID-19 vaccine. Will it work? Will it be safe? Will it be long lasting? No one will be able to provide convincing answers to these questions for any forthcoming vaccine soon, perhaps not for at least several years.
We have made remarkable improvements in our molecular biology tools since the 1980s, yet the slowest part of drug development remains human testing. That said, the infrastructure created for HIV/AIDS research is accelerating the testing process now. Thirty thousand volunteers around the world participate in networks built by the National Institutes of Health for studies of new HIV vaccine candidates, and these networks are being tapped for initial testing of COVID-19 vaccines, too.
When doctors treat a patient who is likely to die, they are willing to risk that a drug might sicken the patient but still save their life. But doctors are less willing to do that to prevent disease; the chances of causing greater harm to the patient are too high. This is why for decades the quest for a vaccine to prevent HIV infection has lagged so far behind development of therapeutic drugs for HIV.
Focus on Treatments
These drugs now stand as an incredible success story.
The first set of HIV drugs were nucleic acid inhibitors, known as chain terminator drugs. They inserted an additional “chain terminating” nucleotide as the virus copied its viral RNA into DNA, preventing the HIV chain of DNA from elongating.
By the 1990s we had gotten better at using combinations of drugs to control HIV infections soon after patients were exposed. The first drug, AZT, found immediate application for health care workers who accidentally had a needlestick injury that infected them with contaminated blood. It was also used to reduce mother-to-child transmission. For example, prenatal treatments for mothers with AIDS at that time reduced the number of babies born infected by as much as two thirds. Today combination chemotherapy reduces mother-to-child transmission to undetectable levels.
The next set of drugs was protease inhibitors, one of which I helped to develop. The first was introduced in 1995 and was combined with other drugs in treating patients. These drugs inhibited the viral protease enzyme responsible for longer precursor proteins in the short active components of the virus. But there is a fundamental problem with these drugs, as well as those that inhibit viral polymerases, which help to create virus DNA. Our bodies also use proteases for normal functioning, and we need polymerases to replicate our own nucleic acids. The same drugs that inhibit the viral proteins also inhibit our own cells. The difference between a concentration in which the drug inhibits the virus target and a concentration in which it hurts the human proteins is called the therapeutic index. The therapeutic index gives you the window in which the drug will be effective against the virus without causing undue side effects. That window is rather narrow for all polymerase and protease inhibitors.
The gold standard for AIDS treatment now is called antiretroviral therapy—essentially patients take a cocktail of at least three different drugs that attack the HIV virus in different ways. The strategy is based on earlier success we had in fighting cancer. In the late 1970s I established a laboratory at Harvard University's Dana-Farber Cancer Institute to develop new drugs to treat cancer patients. Cancers developed resistance over time to single drugs, but combinations of drugs were effective in slowing, stopping or killing the cancers. We took that same lesson of combination chemotherapy to HIV. By the early 1990s the first combination AIDS treatments were saving the lives of people infected with HIV. Today an infection is far from the death sentence it used to be—patients can now live almost unaffected by HIV, with a relatively minimal impact on life expectancy.
We already know resistance to single drugs will bedevil COVID-19 treatments. We have seen resistance to single, anti-SARS-CoV-2 drugs develop rapidly in early lab studies. Just as with AIDS and cancer, we need a combination of medicines to treat this disease. The goal of the biotechnology and pharmaceutical industries now is to develop an array of highly potent and specific drugs, each of which targets a different function of the virus. Decades of research on HIV has shown the way and gives us confidence in our eventual success.
AIDS memorial quilt, made up of 48,000 panels, commemorates those who have died of AIDS-related causes. Credit: Karen Bleiber Getty Images
Human Behavior
In trying to understand and counter the AIDS epidemic, physician and virologist Robert Redfield (who is now head of the Centers for Disease Control and Prevention) and I became good friends in the early 1980s. We quickly learned that while many politicians across the globe refused to recognize HIV as a threat to their populations, militaries were an exception. Nearly all countries considered AIDS a serious danger to troops and military readiness and a potentially huge drain on future military funds. Their view was, “Let's not blind ourselves and pretend soldiers are saints. They are not. They are humans.” Redfield, then at Walter Reed Army Medical Center, helped to design and manage a program to test the entire U.S. uniformed forces for HIV infection (although the consequences of this test were controversial, and recruits who tested positive were barred from service).
At the time there were no effective drugs; the disease killed more than 90 percent of those infected. When married couples were tested and one partner was infected and one not, doctors advised them in the strongest possible terms to use condoms. I was stunned to learn that fewer than a third complied with the advice. “If people don't respond to the lethal danger of unprotected sex with their husband or wife, we are in real trouble,” I thought. Over the next five years more than three quarters of the uninfected partners contracted HIV.
I have always used this experience as a guide to pit hope against reality. Human sexuality—the drive for sex and physical connection—is deeply embedded in our nature. I knew in the 1980s it was very unlikely people would change their sexual behavior in a major way. In the 19th century everyone knew how syphilis was contracted and that it was serious disease. Yet syphilis still infected at least 10 to 15 percent of American citizens at the beginning of the 20th century. It was not that people were ignorant of how to catch it; it is that they did not change their lifestyle accordingly.
There is likewise a sexual dynamic to COVID-19 that often goes unmentioned. It is part of what is driving people out of their homes and into bars and parties. Anyone with a craving for a beer can quench their thirst in the safety of their own home, but gratification comes less easily for other desires, especially when one is young, single and living alone. Our public health strategies should not ignore this fact.
The same lessons we learned in the midst of the HIV epidemic to help young people change their behaviors apply today to COVID-19: know your risk, know your partners and take necessary precautions. Many young people operate under the false assumption that even if they become infected, they will not become severely ill. Not only is this belief untrue, but even people with asymptomatic infections can suffer serious, lasting damage. But the more people understand the risk—younger people especially—the greater likelihood they will take the steps necessary to protect themselves and others. We saw this happen with AIDS.
Funding
When I ask world experts what they know about the detailed molecular biology of SARS-CoV-2 or, for that matter, any other coronavirus, they do not have the kind of answers they should. Why? Because governments and industry pulled the plug on coronavirus research funding in 2006 after the first SARS (severe acute respiratory syndrome) pandemic faded away and again in the years immediately following the MERS (Middle East respiratory syndrome, also caused by a coronavirus) outbreak when it seemed to be controllable. Funding agencies everywhere, not just in the U.S. but in China, Japan, Singapore, Hong Kong and the Middle East—countries affected by SARS and MERS—underestimated the threat of coronaviruses. Despite clear, persistent, highly vocal warnings from many of those who battled SARS and MERS up close, funding dried up. The development of promising anti-SARS and MERS drugs, which might have been active against SARS-CoV-2 as well, was left unfinished for lack of money.
With 776,000 dead and 22 million infected globally as of mid-August, we have every motive to accelerate funding. The U.S. quickly opened the funding spigots last spring for research to hasten discoveries of vaccines and drugs. But will it be enough?
We learned from the HIV crisis that it was important to have research pipelines already established. Cancer research in the 1950s, 1960s and 1970s built a foundation for HIV/AIDS studies. The government responded to public concerns, sharply increasing federal funding of cancer research during those decades. These efforts culminated in Congress's approval of President Richard Nixon's National Cancer Act in 1971. This $1.6-billion commitment for cancer research, equal to $10 billion in today's money, built the science we needed to identify and understand HIV in the 1980s, although of course no one knew that payoff was coming.
In the 1980s the Reagan administration did not want to talk about AIDS or commit much public funding to HIV research. The first time President Ronald Reagan gave a major speech on AIDS was in 1987. In his first administration, funding for HIV research was scarce; few scientists were willing to stake their careers on deciphering the molecular biology. Yet once the news broke that actor Rock Hudson was seriously ill with AIDS, Ted Stevens, the Senate Republican Whip, joined with Democratic Senator Ted Kennedy, actor Elizabeth Taylor, me and a few others in campaigning effectively to add $320 million in the fiscal 1986 budget for AIDS research. Barry Goldwater, Jesse Helms and John Warner, Republican leaders in the Senate, supported us. The money flowed, and outstanding scientists signed on. I helped to design this first congressionally funded AIDS research program with Anthony Fauci, the doctor now leading our nation's fight against COVID-19. (And if there is one person in the world who has made the greatest contribution to the prevention and treatment of AIDS, that person is Fauci.)
One difference between the 1980s and now is that Republican members of Congress were more willing to stand up to the president and White House staff when they failed to take the necessary steps to fight a global disease. For example, Stevens decided it was his job to protect the U.S. Army and other arms of the military and Secret Service as much as possible from HIV infection. He helped to move $55 million within the defense budget, designating it for screening recruits for HIV/AIDS.
Our tool set for virus and pharmaceutical research has improved enormously in the past 36 years since HIV was discovered. This is one reason I am confident we will have effective antiviral drugs for treating COVID-19 infections by next year, if not sooner. What used to take us five or 10 years in the 1980s and 1990s in many cases now can be done in five or 10 months. We can rapidly identify and synthesize chemicals to predict which drugs will be effective. We can do cryoelectron microscopy to probe virus structures and simulate molecule-by-molecule interactions in a matter of weeks—something that used to take years. The lesson is to never let down our guard when it comes to funding antivirus research. We would have no hope of beating COVID-19 if it were not for the molecular biology gains we made during earlier virus battles. What we learn this time around will help us out during the next pandemic, but we must keep the money coming.
A Leap into Darkness
In November 2019 I spent several days in Wuhan, China, chairing a meeting of the U.S.-China Health Summit. Our group's major concern, looming amid the U.S.-China trade war, was the threat of restrictions on sharing research discoveries. Otherwise, it was a delightful time in a beautiful city.
Weeks later, back home in New York City, I could not shake a lingering cold virus infection I picked up on the Wuhan trip. (I later tested negative for COVID-19 antibodies, but that result is not definitive.) The head of my foundation in China called me one day with awful news. Three of his grandparents had died from some strange virus. “Everyone who gets this is really sick,” my colleague, in his mid-30s, said. “Everything is closed down. I can't even go to my grandparents' funerals.”
A few weeks later I received a vivid firsthand account of how aggressively China was confronting the outbreak from another colleague who had just emerged from 14 days of isolation in a quarantine hotel. He explained that when one person in the back of his flight from Frankfurt, Germany, to Shanghai tested positive for the coronavirus, contact tracers called my friend days later and ordered him into isolation. His only human contact then was with hazmat-clad inspectors who came daily to disinfect his room and drop off meals.
We are just beginning to glimpse what the long-term toll of COVID-19 might be. This is a new virus, so we will not have a clearer idea until after a few years, but we know it will be very high. We have barely scratched the surface of coronavirus molecular biology. What story will our children and grandchildren recount about our successes as scientists and as a society, and our failures, to contain this pandemic—the worst we have faced in 100 years?
Science leaps into the darkness, the very edge of human knowledge. That is where we begin, as if deep in a cave, chipping away at a wall of hard stone. You do not know what you will find on the other side. Some people chip away for a lifetime, only to accumulate a pile of flakes. We may be in for a protracted pandemic, or we may get lucky with effective treatments and vaccines soon. But we have been here before, facing an unknown viral enemy, and we can lean on lessons we have learned. This is not the first and will not be the last global epidemic.


scientificamerican--2020-09-29--How to Narrow Achievement Gaps for Underrepresented Students

General chemistry has a terrible reputation on most college campuses .
It ’ s seen as a killer—a place where dreams of careers in science , technology , engineering and mathematics ( STEM ) go to die .
Now the data have spoken , and their message is clear : the bad rep is justified .
And the numbers are especially bleak for students who are underrepresented in STEM .
Women , underrepresented minority racial and ethnic groups , individuals from low-socioeconomic-status households and students who will be the first person in their family with a four-year degree are all @ @ @ @ @ @ @ some cases , they experience achievement gaps of more than half a grade point .
But gloom doesn ’ t have to equate to doom .
The data my research group analyzed also say that if underrepresented students pass general chemistry with even an “ okay ” grade—in most cases , a C+ at minimum—they persist in the general chemistry sequence , and thus stay in STEM training tracks , at much higher rates than overrepresented individuals who get the same grades .
When compared with their peers , the underrepresented “ hyperpersist.
@ @ @ @ @ @ @ to how we teach can lift more underrepresented students into that hyperpersistent zone .
Recent work by my group used data from 41 studies and almost 54,000 students to show that across the STEM disciplines—and while controlling for exam difficulty—college courses that used “ active learning ” reduced the achievement gaps observed in lecture-oriented courses .
Wider adoption of research-based teaching holds the potential for a virtuous cycle : Performance gaps will close , more underrepresented students will get grades that inspire them to hyperpersist , and more underrepresented students will complete STEM @ @ @ @ @ @ @ engineering firms will benefit from the problem-solving ability , resilience and cultural proficiency of a diverse workforce .
A stubborn barrier to economic mobility will begin to crumble .
To get from here to there , we first need to recognize two key obstacles that hold underrepresented students back .
One affects the heart ; the other affects the head .
The fact of underrepresentation can lead to alienation : “ I don ’ t belong here.
” Even capable students are unlikely to thrive after receiving that message .
For women and @ @ @ @ @ @ @ the problem is compounded by stereotype threat .
First described by psychologists Claude Steele and and Joshua Aronson in 1995 , stereotype threat is the cognitive burden of dealing with a stigma that is attached to your gender , race or ethnicity .
Women in linear algebra courses , for example , spend a lot of time and energy dealing with male classmates who think that their female peers can ’ t do math .
That time and energy can ’ t be used to solve linear algebra problems , which leads to @ @ @ @ @ @ @ our analysis of general and organic chemistry grades found evidence of underperformance .
When we controlled for college entrance examination scores and high school grade point averages—allowing us to compare outcomes for students with identical indices of academic preparation and ability—we found that underrepresented individuals were still experiencing significant gaps in their final grades .
This result means that something about these courses caused underrepresented students to perform at less than their capability—a pattern that ’ s been observed for women across STEM courses .
Fortunately , research has revealed a range of @ @ @ @ @ @ @ writing assignments that affirm self-worth in the face of stereotype threat have helped reduce achievement gaps in STEM classrooms .
And short but highly structured exercises that promote a sense of belonging can improve outcomes for underrepresented minority groups in college .
Inclusive teaching can do so as well .
The technique starts with grading systems that are mastery-based and noncompetitive and continues with micro affirmations from the instructor that reinforce a key idea : all students can rise to the demands of this rigorous course and succeed .
And what about achievement @ @ @ @ @ @ @ poor preparation arising from educational and economic disadvantage , which represented the larger portion of those we documented ?
If college instructors don ’ t do anything about them , it means that birth is destiny when it comes to STEM careers .
This is where active learning comes in .
Active learning classrooms are noisy , energetic places where students work together to wrestle with challenging problems .
Instead of serving strictly as a source of information and authority , the instructor acts like a good athletic coach or music teacher , @ @ @ @ @ @ @ students to progress and providing timely feedback .
Students in active learning classrooms team up to collaborate with their peers , just as STEM careers demand .
Our results have shown that people from low-income backgrounds get an extra benefit from this intense exposure to deliberate practice , which their prior education has lacked .
So we know there ’ s a way to narrow achievement gaps .
But is there a will ?
Creating learning environments where underrepresented students can thrive—and where equity and inclusion are realities and not platitudes—will have to @ @ @ @ @ @ @ course and program by program .
The time to start is now .

General chemistry has a terrible reputation on most college campuses. It’s seen as a killer—a place where dreams of careers in science, technology, engineering and mathematics (STEM) go to die.
Now the data have spoken, and their message is clear: the bad rep is justified. And the numbers are especially bleak for students who are underrepresented in STEM. Women, underrepresented minority racial and ethnic groups, individuals from low-socioeconomic-status households and students who will be the first person in their family with a four-year degree are all getting pounded in general chemistry. In some cases, they experience achievement gaps of more than half a grade point.
But gloom doesn’t have to equate to doom. The data my research group analyzed also say that if underrepresented students pass general chemistry with even an “okay” grade—in most cases, a C+ at minimum—they persist in the general chemistry sequence, and thus stay in STEM training tracks, at much higher rates than overrepresented individuals who get the same grades. When compared with their peers, the underrepresented “hyperpersist.” They show grit. And changes to how we teach can lift more underrepresented students into that hyperpersistent zone.
Recent work by my group used data from 41 studies and almost 54,000 students to show that across the STEM disciplines—and while controlling for exam difficulty—college courses that used “active learning” reduced the achievement gaps observed in lecture-oriented courses.
Wider adoption of research-based teaching holds the potential for a virtuous cycle: Performance gaps will close, more underrepresented students will get grades that inspire them to hyperpersist, and more underrepresented students will complete STEM degrees. Clinics, research labs and engineering firms will benefit from the problem-solving ability, resilience and cultural proficiency of a diverse workforce. A stubborn barrier to economic mobility will begin to crumble.
To get from here to there, we first need to recognize two key obstacles that hold underrepresented students back. One affects the heart; the other affects the head.
The fact of underrepresentation can lead to alienation: “I don’t belong here.” Even capable students are unlikely to thrive after receiving that message. For women and underrepresented minority racial and ethnic groups, the problem is compounded by stereotype threat. First described by psychologists Claude Steele and and Joshua Aronson in 1995, stereotype threat is the cognitive burden of dealing with a stigma that is attached to your gender, race or ethnicity. Women in linear algebra courses, for example, spend a lot of time and energy dealing with male classmates who think that their female peers can’t do math. That time and energy can’t be used to solve linear algebra problems, which leads to underperformance.
Consistent with this view, our analysis of general and organic chemistry grades found evidence of underperformance. When we controlled for college entrance examination scores and high school grade point averages—allowing us to compare outcomes for students with identical indices of academic preparation and ability—we found that underrepresented individuals were still experiencing significant gaps in their final grades. This result means that something about these courses caused underrepresented students to perform at less than their capability—a pattern that’s been observed for women across STEM courses.
Fortunately, research has revealed a range of effective countermeasures. Interventions based on short writing assignments that affirm self-worth in the face of stereotype threat have helped reduce achievement gaps in STEM classrooms. And short but highly structured exercises that promote a sense of belonging can improve outcomes for underrepresented minority groups in college. Inclusive teaching can do so as well. The technique starts with grading systems that are mastery-based and noncompetitive and continues with micro affirmations from the instructor that reinforce a key idea: all students can rise to the demands of this rigorous course and succeed.
And what about achievement gaps that appear to be caused by poor preparation arising from educational and economic disadvantage, which represented the larger portion of those we documented? If college instructors don’t do anything about them, it means that birth is destiny when it comes to STEM careers. This is where active learning comes in.
Active learning classrooms are noisy, energetic places where students work together to wrestle with challenging problems. Instead of serving strictly as a source of information and authority, the instructor acts like a good athletic coach or music teacher, setting goals in a sequence that pushes students to progress and providing timely feedback. Students in active learning classrooms team up to collaborate with their peers, just as STEM careers demand. Our results have shown that people from low-income backgrounds get an extra benefit from this intense exposure to deliberate practice, which their prior education has lacked.
So we know there’s a way to narrow achievement gaps. But is there a will? Creating learning environments where underrepresented students can thrive—and where equity and inclusion are realities and not platitudes—will have to happen instructor by instructor, course by course and program by program. The time to start is now.


scientificamerican--2020-09-29--Nature's Splendor Exceeds Our Imagination

The sincerest expression of love is to learn the characteristics of the object of our affection as they are , without reservations or prejudice .
By this definition , the pursuit of scientific knowledge is the ultimate act of loving nature in its full splendor .
Scientific inquiry can only enhance the awe we feel when witnessing reality in all of its quantitative detail .
The beauty of nature comes for free .
The fact that all phenomena in the physical world obey a small set of strict laws is remarkable , given how difficult it is to enforce societal @ @ @ @ @ @ @ often imagine how disorganized the universe could have been if it resembled my daughters ’ rooms each morning .
We tend to feel hubris when we contemplate cutting-edge technological accomplishments , such as self-driving cars .
But in fact , a more balanced perspective requires humility , not hubris .
Following a recent injury , my body healed from its bruises faster than it took my optometrist to get me a new pair of glasses .
Our most advanced technologies are yet to produce a self-healing car that repairs itself after accidents like @ @ @ @ @ @ @ just beautiful ; it exceeds the limits of our imagination .
Relatively recent examples in astronomy include the unexpected discoveries of dark matter and dark energy whose nature are still mysterious ; the ubiquity of “ hot Jupiters ” that hug their suns in tight orbits , in contrast to the Jupiter in our own planetary system ; or the strange properties of ` Oumuamua , the first interstellar object discovered in the solar system .
This experience is generic to all research fields , making science a learning experience in which we @ @ @ @ @ @ @ observing reality .
The scientific process is a dialogue with nature where we propose theoretical ideas and listen to nature ’ s response through our experiments , rather than a monologue in which we focus on mathematical beauty and simply assume its relevance to reality .
Figuring out the subtleties of nature is more challenging than proving theorems in mathematics , because the latter activity involves only the human .
But there is only one physical reality out there , out of an infinite number of possibilities that could have existed .
The @ @ @ @ @ @ @ up to us : reality is predetermined by nature .
While pursuing research , we could miss important discoveries if we expect the future course of science to resemble its past history .
When you are not ready to find exceptional things , you will never discover them .
The 1995 discovery of the first “ hot Jupiter , ” 51 Pergasi b , by Michel Mayor and Didier Queloz , for which they won the 2019 Nobel Prize in Physics , confirmed a theoretical proposal by Otto Struve from 1952 .
The @ @ @ @ @ @ @ of the mainstream to allocate telescope time for a hot Jupiter search based on the argument that it would violate what we “ know ” about the solar system .
A similar sort of delay predated the 1992 discovery of the first Kuiper belt object in the outer solar system by David Jewitt and Jane Luu .
These examples illustrate how scientists rely on conventional wisdom to decide what ’ s true rather than having the humility to subject their assumptions to experimental tests .
Before Galileo Galilei , it was the conventional @ @ @ @ @ @ @ light objects under the influence of gravity .
But he dared to conduct an experimental test that proved this notion wrong , and established the “ equivalence principle , ” which in turn became a foundation for Albert Einstein ’ s theory of general relativity .
In reaction to his contesting another false prejudice—that the sun orbits the Earth—Galileo was kept in house arrest for nine years until his death in 1642 .
But this did not make the sun revolve around the Earth nine times ; it only delayed the natural progression @ @ @ @ @ @ @ new ideas based on the conviction that they are “ unreasonable ” is not the only repeating pattern since the days of Galileo .
There is also the tendency , after data are taken , to ignore anomalies—to downplay the unexplained and declare “ business as usual ” even in the face of contradicting evidence .
Giant arcs of light around the cores of clusters of galaxies appeared in images that were published in the Astrophysical Journal , but were ignored until the topic of gravitational lensing became fashionable in the 1980s .
@ @ @ @ @ @ @ such arcs in 1937 , more than four decades earlier .
Scientists are not immune to wishful thinking , and a reality check on their convictions is mandatory .
This is a particularly important lesson to keep in mind when considering the risk from in-person events before an experimentally tested vaccine for COVID-19 is widely available .
Scientific rigor should not be compromised , especially in life-and-death situations .
In a recent exchange with a philosopher who suggested that there is “ no loss ” inherent in our natural death because we do @ @ @ @ @ @ @ that from the perspective of astronomy , death involves losing the ability to follow the universe as it evolves .
The experience of death therefore feels like being in a concert hall , with the usher escorting you out while the orchestra is still playing the symphony .
It is a fundamentally lesser experience to listen just to a part of the symphony , whose full meaning and beauty is apparent from the whole .
Cutting our stay short represents a loss .
He conceded .
The human being as a spectator of @ @ @ @ @ @ @ other times tragic , but most of the time insignificant relative to everything else taking place out there .
Humanity ’ s lack of imagination should be forgiven as a temporary handicap that scientists are attempting to repair .
Education takes time even when the students love the class .

The sincerest expression of love is to learn the characteristics of the object of our affection as they are, without reservations or prejudice. By this definition, the pursuit of scientific knowledge is the ultimate act of loving nature in its full splendor. Scientific inquiry can only enhance the awe we feel when witnessing reality in all of its quantitative detail.
The beauty of nature comes for free. The fact that all phenomena in the physical world obey a small set of strict laws is remarkable, given how difficult it is to enforce societal laws in the human world. I often imagine how disorganized the universe could have been if it resembled my daughters’ rooms each morning.
We tend to feel hubris when we contemplate cutting-edge technological accomplishments, such as self-driving cars. But in fact, a more balanced perspective requires humility, not hubris. Following a recent injury, my body healed from its bruises faster than it took my optometrist to get me a new pair of glasses. Our most advanced technologies are yet to produce a self-healing car that repairs itself after accidents like the human body.
Nature is not just beautiful; it exceeds the limits of our imagination. Relatively recent examples in astronomy include the unexpected discoveries of dark matter and dark energy whose nature are still mysterious; the ubiquity of “hot Jupiters” that hug their suns in tight orbits, in contrast to the Jupiter in our own planetary system; or the strange properties of `Oumuamua, the first interstellar object discovered in the solar system. This experience is generic to all research fields, making science a learning experience in which we expand our ability to imagine simply by observing reality.
The scientific process is a dialogue with nature where we propose theoretical ideas and listen to nature’s response through our experiments, rather than a monologue in which we focus on mathematical beauty and simply assume its relevance to reality. Figuring out the subtleties of nature is more challenging than proving theorems in mathematics, because the latter activity involves only the human. But there is only one physical reality out there, out of an infinite number of possibilities that could have existed. The outcome of our scientific inquiry is not up to us: reality is predetermined by nature.
While pursuing research, we could miss important discoveries if we expect the future course of science to resemble its past history. When you are not ready to find exceptional things, you will never discover them. The 1995 discovery of the first “hot Jupiter,” 51 Pergasi b, by Michel Mayor and Didier Queloz, for which they won the 2019 Nobel Prize in Physics, confirmed a theoretical proposal by Otto Struve from 1952. The four-decade delay was caused by the refusal of the mainstream to allocate telescope time for a hot Jupiter search based on the argument that it would violate what we “know” about the solar system. A similar sort of delay predated the 1992 discovery of the first Kuiper belt object in the outer solar system by David Jewitt and Jane Luu.
These examples illustrate how scientists rely on conventional wisdom to decide what’s true rather than having the humility to subject their assumptions to experimental tests. Before Galileo Galilei, it was the conventional wisdom that heavy objects fall faster than light objects under the influence of gravity. But he dared to conduct an experimental test that proved this notion wrong, and established the “equivalence principle,” which in turn became a foundation for Albert Einstein’s theory of general relativity. In reaction to his contesting another false prejudice—that the sun orbits the Earth—Galileo was kept in house arrest for nine years until his death in 1642. But this did not make the sun revolve around the Earth nine times; it only delayed the natural progression of scientific knowledge.
Reluctance to test new ideas based on the conviction that they are “unreasonable” is not the only repeating pattern since the days of Galileo. There is also the tendency, after data are taken, to ignore anomalies—to downplay the unexplained and declare “business as usual” even in the face of contradicting evidence. Giant arcs of light around the cores of clusters of galaxies appeared in images that were published in the Astrophysical Journal, but were ignored until the topic of gravitational lensing became fashionable in the 1980s. In this case, Fritz Zwicky predicted such arcs in 1937, more than four decades earlier.
Scientists are not immune to wishful thinking, and a reality check on their convictions is mandatory. This is a particularly important lesson to keep in mind when considering the risk from in-person events before an experimentally tested vaccine for COVID-19 is widely available. Scientific rigor should not be compromised, especially in life-and-death situations.
In a recent exchange with a philosopher who suggested that there is “no loss” inherent in our natural death because we do not own our future, I responded that from the perspective of astronomy, death involves losing the ability to follow the universe as it evolves. The experience of death therefore feels like being in a concert hall, with the usher escorting you out while the orchestra is still playing the symphony. It is a fundamentally lesser experience to listen just to a part of the symphony, whose full meaning and beauty is apparent from the whole. Cutting our stay short represents a loss. He conceded.
The human being as a spectator of nature appears on occasion comical, at other times tragic, but most of the time insignificant relative to everything else taking place out there. Humanity’s lack of imagination should be forgiven as a temporary handicap that scientists are attempting to repair. Education takes time even when the students love the class.


scientificamerican--2020-09-29--Structure and Chemistry Dictate How Cicada Wings Repel Water and Kill Bacteria

Nature often inspires engineering .
Cicada wings , for example , have long tantalized researchers with their water-repellent and antimicrobial properties , which would be useful to replicate in manufactured products .
But previous studies involved totally removing the wings ' surface chemicals , sometimes damaging the wings and giving an incomplete picture of how those chemicals work together with the wings ' structure .
New research investigates substances coating cicada wings layer by layer , revealing a complex interplay between topography and chemistry .
Researchers analyzed two cicada species that each have a highly ordered pattern of tiny , @ @ @ @ @ @ @ .
Previous work suggested nanopillars contribute to the insects ' ability to shed water and help kill microbes .
To avoid wing damage , the team tested a method called microwave-assisted extraction that had not been used on intact insect wings before , says Jessica Román-Kustas , an analytical chemist at Sandia National Laboratories .
Román-Kustas is lead author on the new study , which appeared in May in Advanced Materials Interfaces .
The method involved heating and cooling wings immersed in chloroform and methanol , analyzing layers of chemicals as they came @ @ @ @ @ @ @ days of sitting at the microwave with a timer and a computer , ” she says .
In both cicada species , the researchers found that the nanopillars ' chemical makeup is important for maintaining structural integrity .
“ When you remove the outer [ chemical ] layers from the nanopillar , the pillars become shorter and bend toward each other , ” says Marianne Alleyne , a biologist at the University of Illinois at Urbana-Champaign and a senior author on the study .
In the annual cicada Neotibicen pruinosus , this wilting @ @ @ @ @ @ @ wings less water-repellent at first ( although they recovered some of that ability as more chemicals were removed ) .
Bacteria-killing activity actually increased as the first layers were removed but then decreased again as more compounds were stripped .
The team found that the cicada Magicicada cassinii , which emerges every 17 years and has shorter nanopillars , has surface chemicals that by themselves seem to have bactericidal properties—suggesting these cicadas rely more on their chemical components than structure to kill microbes .
“ It is clear … that different layers serve @ @ @ @ @ @ @ , a physical chemist at West Virginia University , who was not involved in the study , “ and the ability to probe only specific layers is very important [ to obtain ] a much better understanding of the overall physical properties ' dependence on chemical makeup.
” Understanding how chemicals do ( or do not ) affect structure may help scientists engineer better products .
“ By having this fundamental knowledge about how structure and chemistry relate to each other , ” Alleyne says , “ we can design new materials more @ @ @ @ @ @ @ and chemistry … based on what we have observed in nature .
”

Nature often inspires engineering. Cicada wings, for example, have long tantalized researchers with their water-repellent and antimicrobial properties, which would be useful to replicate in manufactured products. But previous studies involved totally removing the wings' surface chemicals, sometimes damaging the wings and giving an incomplete picture of how those chemicals work together with the wings' structure. New research investigates substances coating cicada wings layer by layer, revealing a complex interplay between topography and chemistry.
Researchers analyzed two cicada species that each have a highly ordered pattern of tiny, conelike structures called nanopillars on their wings. Previous work suggested nanopillars contribute to the insects' ability to shed water and help kill microbes.
To avoid wing damage, the team tested a method called microwave-assisted extraction that had not been used on intact insect wings before, says Jessica Román-Kustas, an analytical chemist at Sandia National Laboratories. Román-Kustas is lead author on the new study, which appeared in May in Advanced Materials Interfaces. The method involved heating and cooling wings immersed in chloroform and methanol, analyzing layers of chemicals as they came off. “It [was] days of sitting at the microwave with a timer and a computer,” she says.
In both cicada species, the researchers found that the nanopillars' chemical makeup is important for maintaining structural integrity. “When you remove the outer [chemical] layers from the nanopillar, the pillars become shorter and bend toward each other,” says Marianne Alleyne, a biologist at the University of Illinois at Urbana-Champaign and a senior author on the study.
In the annual cicada Neotibicen pruinosus, this wilting effect was more extreme and made the wings less water-repellent at first (although they recovered some of that ability as more chemicals were removed). Bacteria-killing activity actually increased as the first layers were removed but then decreased again as more compounds were stripped. The team found that the cicada Magicicada cassinii, which emerges every 17 years and has shorter nanopillars, has surface chemicals that by themselves seem to have bactericidal properties—suggesting these cicadas rely more on their chemical components than structure to kill microbes.
“It is clear … that different layers serve different purposes,” says Terry Gullion, a physical chemist at West Virginia University, who was not involved in the study, “and the ability to probe only specific layers is very important [to obtain] a much better understanding of the overall physical properties' dependence on chemical makeup.”
Understanding how chemicals do (or do not) affect structure may help scientists engineer better products. “By having this fundamental knowledge about how structure and chemistry relate to each other,” Alleyne says, “we can design new materials more rationally, making choices about the structure and chemistry … based on what we have observed in nature.”