Democratize the White Coat by Honoring Black, Indigenous, and People of Color in Science
This article is part of the magazine, "The Future of Science In America: The Election Issue," co-published by LeapsMag, the Aspen Institute Science & Society Program, and GOOD.
Journalists, educators, and curators have responded to Black Lives Matter by highlighting the history and achievements of Black Americans in a variety of fields, including science. The movement has also sparked important demands to address longstanding scientific inequities such as lack of access to quality healthcare and the disproportionate impact of climate change and environmental pollution on neighborhoods of Black, Indigenous, and people of color (BIPOC). Making such improvements requires bringing BIPOC into science and into positions of leadership in laboratories, graduate schools, medical practices, and clinical trials. The moment is right to challenge scientific gatekeepers to respond to Black Lives Matter by widening the pathways that determine who becomes a scientist, a researcher, or a clinician.
The scientific workforce has long lacked diversity, which in turn discourages Black people from pursuing such careers. Causes include a dearth of mentors and role models, preconceived notions that science is exclusive to white males, and subpar STEM education. Across race, gender, class, ability, and all other dimensions that inform how an individual navigates the world, from the familial to the global level, seeing role models who resemble you impacts what you strive for and believe possible. As Marian Wright Edelman stated, "You can't be what you can't see"—a truth with ever-increasing resonance since the U.S. is projected to be minority-white by 2045.
Black Americans have paved the way for the nation to lead in science and technology, despite marginalization and exclusion from textbooks. Physicist Dr. Shirley Ann Jackson invented the technology behind Caller I.D. and Call Waiting. Otis Boykin's patents made televisions and radios what they are today. Thanks to the 2017 movie Hidden Figures, millions of Americans know about Katherine Johnson, the NASA mathematician whose calculations were essential to the successful trajectory of the Apollo 11 mission.
However, highlighting past role models who were Black achievers is not enough and paints too static a picture—especially when examples of transformative work by contemporary BIPOC scientists serving BIPOC communities abound. Cognitive neuroscientist Dr. Jonathan Jackson founded the Community Access, Recruitment, & Engagement (CARE) Research Center with the goal to break down barriers so that people of color participate in clinical trials. Geneticist Dr. Nanibaa' Garrison's research creates ethical frameworks to overcome genomic injustices so Indigenous populations can benefit from genetic research. Computer scientists Joy Buolamwini and Dr. Timnit Gebru's research drew attention to reinforced racial bias in artificial intelligence, leading Microsoft, Amazon, and IBM this summer to halt use of their facial recognition software.
"Integration does not mean equality if the space being integrated isn't exuberantly down for the cause."
In order to honor concretely the ubiquitous public statements and commitments to justice and equity that flooded everyone's inboxes in early June, we must include traditionally underrepresented voices in all phases of science and its applications. For guidance, we would benefit from listening to activists leading, for example, climate marches and protests over toxic water. Indeed, science is at the core of the issues for which young BIPOC are mobilizing. We need to sit down with these individuals to gain their input on how the narratives, practices, and opportunities in science should change. As Zeena Abdulkarim, a youth climate change organizer working with Zero Hour, explains: "Minority communities are exposed to what the privileged and people in power are not; therefore these communities know the right steps to take in the change we need for the kickstart of true social and environmental justice."
Two other Black youth, for example, used the platform of the laboratory while in high school to mobilize for change. Elle Lanair Lett, now specializing in epidemiology as an M.D.-Ph.D. student in Philadelphia, was prompted by family prevalence of diabetes to research the genetics of pancreatic cells. Dr. Otana Jakpor, now an ophthalmology resident in Michigan, was motivated by the pollution in her hometown of Riverside, California, to research the pulmonary effects of indoor air purifiers, with findings that influenced California ozone regulations. Both became finalists in a national science fair, propelling them on paths toward science careers. These young scientists demonstrate how people's communities and lived experiences can shape trajectories of science research, which, in turn, determines which visions for society are materialized and popularized.
We can also gain insight from another childhood science fair veteran, self-proclaimed "Black STEMinist" Augusta Uwamanzu-Nna, who graduated from college in May and works as a bioengineer. In her view, "we need to shift the burden away from Black people and onto individuals who have contributed to our current reality—fundamentally requiring understanding, open-mindedness, a lack of bias, cultural competency, anti-racism, anti-homophobia, and many, many other things."
Celebrating BIPOC's accomplishments in science and cultivating new leadership today are strong first steps to make science a guiding force for all. Ms. Uwamanzu-Nna keenly reminds us, "Integration does not mean equality if the space being integrated isn't exuberantly down for the cause." Indeed, educational institutions, scientific companies, and medical centers must acknowledge and embrace their role in democratizing science in order for society to realize racial and scientific justice.
[Editor's Note: To read other articles in this special magazine issue, visit the beautifully designed e-reader version.]
Catching colds may help protect kids from Covid
A common cold virus causes the immune system to produce T cells that also provide protection against SARS-CoV-2, according to new research. The study, published last month in PNAS, shows that this effect is most pronounced in young children. The finding may help explain why most young people who have been exposed to the cold-causing coronavirus have not developed serious cases of COVID-19.
One curiosity stood out in the early days of the COVID-19 pandemic – why were so few kids getting sick. Generally young children and the elderly are the most vulnerable to disease outbreaks, particularly viral infections, either because their immune systems are not fully developed or they are starting to fail.
But solid information on the new infection was so scarce that many public health officials acted on the precautionary principle, assumed a worst-case scenario, and applied the broadest, most restrictive policies to all people to try to contain the coronavirus SARS-CoV-2.
One early thought was that lockdowns worked and kids (ages 6 months to 17 years) simply were not being exposed to the virus. So it was a shock when data started to come in showing that well over half of them carried antibodies to the virus, indicating exposure without getting sick. That trend grew over time and the latest tracking data from the CDC shows that 96.3 percent of kids in the U.S. now carry those antibodies.
Antibodies are relatively quick and easy to measure, but some scientists are exploring whether the reactions of T cells could serve as a more useful measure of immune protection.
But that couldn't be the whole story because antibody protection fades, sometimes as early as a month after exposure and usually within a year. Additionally, SARS-CoV-2 has been spewing out waves of different variants that were more resistant to antibodies generated by their predecessors. The resistance was so significant that over time the FDA withdrew its emergency use authorization for a handful of monoclonal antibodies with earlier approval to treat the infection because they no longer worked.
Antibodies got most of the attention early on because they are part of the first line response of the immune system. Antibodies can bind to viruses and neutralize them, preventing infection. They are relatively quick and easy to measure and even manufacture, but as SARS-CoV-2 showed us, often viruses can quickly evolve to become more resistant to them. Some scientists are exploring whether the reactions of T cells could serve as a more useful measure of immune protection.
Kids, colds and T cells
T cells are part of the immune system that deals with cells once they have become infected. But working with T cells is much more difficult, takes longer, and is more expensive than working with antibodies. So studies often lags behind on this part of the immune system.
A group of researchers led by Annika Karlsson at the Karolinska Institute in Sweden focuses on T cells targeting virus-infected cells and, unsurprisingly, saw that they can play a role in SARS-CoV-2 infection. Other labs have shown that vaccination and natural exposure to the virus generates different patterns of T cell responses.
The Swedes also looked at another member of the coronavirus family, OC43, which circulates widely and is one of several causes of the common cold. The molecular structure of OC43 is similar to its more deadly cousin SARS-CoV-2. Sometimes a T cell response to one virus can produce a cross-reactive response to a similar protein structure in another virus, meaning that T cells will identify and respond to the two viruses in much the same way. Karlsson looked to see if T cells for OC43 from a wide age range of patients were cross-reactive to SARS-CoV-2.
And that is what they found, as reported in the PNAS study last month; there was cross-reactive activity, but it depended on a person’s age. A subset of a certain type of T cells, called mCD4+,, that recognized various protein parts of the cold-causing virus, OC43, expressed on the surface of an infected cell – also recognized those same protein parts from SARS-CoV-2. The T cell response was lower than that generated by natural exposure to SARS-CoV-2, but it was functional and thus could help limit the severity of COVID-19.
“One of the most politicized aspects of our pandemic response was not accepting that children are so much less at risk for severe disease with COVID-19,” because usually young children are among the most vulnerable to pathogens, says Monica Gandhi, professor of medicine at the University of California San Francisco.
“The cross-reactivity peaked at age six when more than half the people tested have a cross-reactive immune response,” says Karlsson, though their sample is too small to say if this finding applies more broadly across the population. The vast majority of children as young as two years had OC43-specific mCD4+ T cell responses. In adulthood, the functionality of both the OC43-specific and the cross-reactive T cells wane significantly, especially with advanced age.
“Considering that the mortality rate in children is the lowest from ages five to nine, and higher in younger children, our results imply that cross-reactive mCD4+ T cells may have a role in the control of SARS-CoV-2 infection in children,” the authors wrote in their paper.
“One of the most politicized aspects of our pandemic response was not accepting that children are so much less at risk for severe disease with COVID-19,” because usually young children are among the most vulnerable to pathogens, says Monica Gandhi, professor of medicine at the University of California San Francisco and author of the book, Endemic: A Post-Pandemic Playbook, to be released by the Mayo Clinic Press this summer. The immune response of kids to SARS-CoV-2 stood our expectations on their head. “We just haven't seen this before, so knowing the mechanism of protection is really important.”
Why the T cell immune response can fade with age is largely unknown. With some viruses such as measles, a single vaccination or infection generates life-long protection. But respiratory tract infections, like SARS-CoV-2, cause a localized infection - specific to certain organs - and that response tends to be shorter lived than systemic infections that affect the entire body. Karlsson suspects the elderly might be exposed to these localized types of viruses less often. Also, frequent continued exposure to a virus that results in reactivation of the memory T cell pool might eventually result in “a kind of immunosenescence or immune exhaustion that is associated with aging,” Karlsson says. https://leaps.org/scientists-just-started-testing-a-new-class-of-drugs-to-slow-and-even-reverse-aging/particle-3 This fading protection is why older people need to be repeatedly vaccinated against SARS-CoV-2.
Policy implications
Following the numbers on COVID-19 infections and severity over the last three years have shown us that healthy young people without risk factors are not likely to develop serious disease. This latest study points to a mechanism that helps explain why. But the inertia of existing policies remains. How should we adjust policy recommendations based on what we know today?
The World Health Organization (WHO) updated their COVID-19 vaccination guidance on March 28. It calls for a focus on vaccinating and boosting those at risk for developing serious disease. The guidance basically shrugged its shoulders when it came to healthy children and young adults receiving vaccinations and boosters against COVID-19. It said the priority should be to administer the “traditional essential vaccines for children,” such as those that protect against measles, rubella, and mumps.
“As an immunologist and a mother, I think that catching a cold or two when you are a kid and otherwise healthy is not that bad for you. Children have a much lower risk of becoming severely ill with SARS-CoV-2,” says Karlsson. She has followed public health guidance in Sweden, which means that her young children have not been vaccinated, but being older, she has received the vaccine and boosters. Gandhi and her children have been vaccinated, but they do not plan on additional boosters.
The WHO got it right in “concentrating on what matters,” which is getting traditional childhood immunizations back on track after their dramatic decline over the last three years, says Gandhi. Nor is there a need for masking in schools, according to a study from the Catalonia region of Spain. It found “no difference in masking and spread in schools,” particularly since tracking data indicate that nearly all young people have been exposed to SARS-CoV-2.
Both researchers lament that public discussion has overemphasized the quickly fading antibody part of the immune response to SARS-CoV-2 compared with the more durable T cell component. They say developing an efficient measure of T cell response for doctors to use in the clinic would help to monitor immunity in people at risk for severe cases of COVID-19 compared with the current method of toting up potential risk factors.
The Friday Five covers five stories in research that you may have missed this week. There are plenty of controversies and troubling ethical issues in science – and we get into many of them in our online magazine – but this news roundup focuses on new scientific theories and progress to give you a therapeutic dose of inspiration headed into the weekend.
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Here are the stories covered this week:
- The eyes are the windows to the soul - and biological aging?
- What bean genes mean for health and the planet
- This breathing practice could lower levels of tau proteins
- AI beats humans at assessing heart health
- Should you get a nature prescription?