Publisher Health

Long-term exposure to air pollution is associated with a higher risk of developing COVID-19 among those people who get infected, shows a study led by the Barcelona Institute of Global Health (ISGlobal), a centre supported by the “la Caixa” Foundation, and co-led by the GCAT| Genomes for Life-Germans Trias i Pujol Research Institute (IGTP), Badalona. The study, published in Environment Health Perspectives, provides further evidence on the health benefits of reducing air pollution.
A series of studies suggest that regions with higher pre-pandemic levels of air pollution had a higher incidence of COVID-19 cases and deaths. However, the reasons for this associations are not yet clear; air pollution could favor airborne transmission of the virus, or it could increase an individual’s susceptibility to infection or disease. “The problem is that previous studies were based on reported cases, which had been diagnosed, but missed all the asymptomatic or undiagnosed cases,” says Manolis Kogevinas, ISGlobal researcher and first author of the study.
The research team decided to combine the technology developed by Carlota Dobaño’s team to measure a series of virus-specific antibodies in a cohort of adults living in Catalonia (the COVICAT cohort), with information on the long-term exposure of such individuals to air pollutants (NO2, PM2.5, black carbon and ozone).
“This is the first study to perform mass screening of SARS-CoV-2 specific antibodies in an adult cohort to examine the association between their residential exposure to air pollution before the pandemic, SARS-CoV-2 infection, and disease,” says Cathryn Tonne, cosenior author of the study together with Dobaño.
Higher viral burden and/or symptom severity
The study included 9,605 participants among which there were 481 confirmed cases (5%). In addition, blood samples from over 4,000 participants were taken to determine the presence and quantity of IgM, IgA and IgG antibodies to five viral antigens. Of these, 18% had virus-specific antibodies, but no association was found between infection and exposure to air pollutants. However, among those who were seropositive (i.e. got infected), an association was found between higher exposure to NO2 and PM2.5 and higher levels of IgG specific for the five viral antigens (an indication of higher viral burden and/or symptom severity).
For the total study population (the 9,605 participants), an association was found between higher exposure to NO2 and PM2.5 and disease (symptoms), particularly for severe cases that ended in the hospital or in intensive care. The association with PM2.5 was stronger for men over 60 years of age and people living in socioeconomically deprived areas.
Strongest evidence globally
“Our study provides the strongest evidence globally on the association of ambient air pollution and COVID-19,” says Kogevinas. “These results are in line with the association between air pollution and hospitalization described for other respiratory diseases such as influenza or pneumonia.” Air pollution could also contribute by favouring the development of cardiovascular, respiratory or other chronic conditions, which in turn increase the risk of severe COVID-19.
“The combination of individual genetic risks that we have previously identified in COVICAT individuals and this new data on environmental impact caused by air pollution exposure will contribute to understanding the complex interplay and mechanisms underlying the severity of COVID-19,” says Rafael de Cid, from the IGTP.
The authors conclude that the results provide additional support for the public health benefits of reducing air pollution levels, and highlight the influence of environmental factors on infectious diseases.
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Chemotherapy successfully treats many forms of cancer, but the side effects can wreak havoc on the rest of the body. Delivering drugs directly to cancer cells could help reduce these unpleasant symptoms. Now, in a proof-of-concept study, researchers reporting in ACS Nano made fish-shaped microrobots that are guided with magnets to cancer cells, where a pH change triggers them to open their mouths and release their chemotherapy cargo.
Scientists have previously made microscale (smaller than 100 µm) robots that can manipulate tiny objects, but most can’t change their shapes to perform complex tasks, such as releasing drugs. Some groups have made 4D-printed objects (3D-printed devices that change shape in response to certain stimuli), but they typically perform only simple actions, and their motion can’t be controlled remotely. In a step toward biomedical applications for these devices, Jiawen Li, Li Zhang, Dong Wu and colleagues wanted to develop shape-morphing microrobots that could be guided by magnets to specific sites to deliver treatments. Because tumors exist in acidic microenvironments, the team decided to make the microrobots change shape in response to lowered pH.
So the researchers 4D printed microrobots in the shape of a crab, butterfly or fish using a pH-responsive hydrogel. By adjusting the printing density at certain areas of the shape, such as the edges of the crab’s claws or the butterfly’s wings, the team encoded pH-responsive shape morphing. Then, they made the microrobots magnetic by placing them in a suspension of iron oxide nanoparticles.
The researchers demonstrated various capabilities of the microrobots in several tests. For example, a fish-shaped microrobot had an adjustable “mouth” that opened and closed. The team showed that they could steer the fish through simulated blood vessels to reach cancer cells at a specific region of a petri dish. When they lowered the pH of the surrounding solution, the fish opened its mouth to release a chemotherapy drug, which killed nearby cells. Although this study is a promising proof of concept, the microrobots need to be made even smaller to navigate actual blood vessels, and a suitable imaging method needs to be identified to track their movements in the body, the researchers say.
The authors acknowledge funding from the National Natural Science Foundation of China, the National Key R&D Program of China, Major Scientific and Technological Projects in Anhui Province, the Fundamental Research Funds for the Central Universities, the Youth Innovation Promotion Association of the Chinese Academy of Sciences, the Hong Kong Research Grants Council, CAS-Croucher Funding Scheme for Joint Laboratories, the Hong Kong Special Administrative Region of the People’s Republic of China Innovation and Technology Commission and the Multi-scale Medical Robotics Center.
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Researchers at Karolinska Institutet, Umeå University, and the University of Bonn have identified a new group of molecules that have an antibacterial effect against many antibiotic-resistant bacteria. Since the properties of the molecules can easily be altered chemically, the hope is to develop new, effective antibiotics with few side effects. The findings have been published in the scientific journal PNAS.
The increasing resistance to antibiotics in the world is alarming while few new types of antibiotics have been developed in the past 50 years. There is therefore a great need to find new antibacterial substances.
The majority of antibiotics in clinical use work by inhibiting the bacteria’s ability to form a protective cell wall, causing the bacteria to crack (cell lysis). Besides the well-known penicillin, that inhibit enzymes building up the wall, newer antibiotics such as daptomycin or the recently discovered teixobactin bind to a special molecule, lipid II. Lipid II is needed by all bacteria to build up the cell wall. Antibiotics that bind to this cell wall building block are usually very large and complex molecules and therefore more difficult to improve with chemical methods. These molecules are in addition mostly inactive against a group of problematic bacteria, which are surrounded by an additional layer, the outer membrane, that hinders penetration of these antibacterials.
“Lipid II is a very attractive target for new antibiotics. We have identified the first small antibacterial compounds that work by binding to this lipid molecule, and in our study, we found no resistant bacterial mutants, which is very promising,” says Birgitta Henriques Normark, professor at the Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, and one of the article’s three corresponding authors.
In this study, researchers at Karolinska Institutet and Umeå University in Sweden have tested a large number of chemical compounds for their ability to lyse pneumococci, bacteria that are the most common cause of community-acquired pneumonia. The initial tests were carried out in collaboration with the Chemical Biology Consortium Sweden (CBCS), a national research infrastructure at SciLifeLab. After a careful follow-up of active compounds from this screening, the researchers, in collaboration with the University of Bonn in Germany, found that a group of molecules called THCz inhibits the formation of the cell wall of the bacterium by binding to lipid II. The molecules could also prevent the formation of the sugar capsule that pneumococci need to escape the immune system and to cause disease.
“The advantage of small molecules like these is that they are more easy to change chemically. We hope to be able to change THCz so that the antibacterial effect increases and any negative effects on human cells decrease,” says Fredrik Almqvist, professor at the Department of Chemistry at Umeå University and one of the corresponding authors.
In laboratory experiments, THCz have an antibacterial effect against many antibiotic-resistant bacteria, such as methicillin-resistant staphylococci (MRSA), vancomycin-resistant enterococci (VRE), and penicillin-resistant pneumococci (PNSP). An antibacterial effect was also found against gonococci, which causes gonorrhoea, and mycobacteria, bacteria that can cause severe diseases such as tuberculosis in humans. The researchers were unable to identify any bacteria that developed resistance to THCz in a laboratory environment.
“We will now also initiate attempts to change the THCzmolecule, allowing it to penetrate the outer cell membrane found in some, especially intractable, multi-resistant bacteria,” says Tanja Schneider, professor at the Institute of Pharmaceutical Microbiology at the University of Bonn and one of the corresponding authors.
The research was carried out in close collaboration with Karolinska University Hospital and the University Hospital in Bonn. The study was funded by the Swedish Foundation for Strategic Research, the Swedish Research Council, the Knut and Alice Wallenberg Foundation, Region Stockholm, the Göran Gustafsson Foundation, the German Research Foundation (DFG; TRR261) and the German Center for Infection Research (DZIF). There are no reported conflicts of interest.
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Northwestern University researchers have invented a new high-resolution camera that can see the unseen — including around corners and through scattering media, such as skin, fog or potentially even the human skull.
Called synthetic wavelength holography, the new method works by indirectly scattering coherent light onto hidden objects, which then scatters again and travels back to a camera. From there, an algorithm reconstructs the scattered light signal to reveal the hidden objects. Due to its high temporal resolution, the method also has potential to image fast-moving objects, such as the beating heart through the chest or speeding cars around a street corner.
The study will be published on Nov. 17 in the journal Nature Communications.
The relatively new research field of imaging objects behind occlusions or scattering media is called non-line-of-sight (NLoS) imaging. Compared to related NLoS imaging technologies, the Northwestern method can rapidly capture full-field images of large areas with submillimeter precision. With this level of resolution, the computational camera could potentially image through the skin to see even the tiniest capillaries at work.
While the method has obvious potential for noninvasive medical imaging, early-warning navigation systems for automobiles and industrial inspection in tightly confined spaces, the researchers believe potential applications are endless.
“Our technology will usher in a new wave of imaging capabilities,” said Northwestern’s Florian Willomitzer, first author of the study. “Our current sensor prototypes use visible or infrared light, but the principle is universal and could be extended to other wavelengths. For example, the same method could be applied to radio waves for space exploration or underwater acoustic imaging. It can be applied to many areas, and we have only scratched the surface.”
Willomitzer is a research assistant professor of electrical and computer engineering at Northwestern’s McCormick School of Engineering. Northwestern co-authors include Oliver Cossairt, associate professor of computer science and electrical and computer engineering, and former Ph.D. student Fengqiang Li. The Northwestern researchers collaborated closely with Prasanna Rangarajan, Muralidhar Balaji and Marc Christensen, all researchers at Southern Methodist University.

Arterial stiffness is a novel risk factor to be targeted for preventing and treating hypertension and obesity from a young age, a new study published in Hypertension suggests.
Researchers from the University of Eastern Finland, the University of Exeter, and the University of Bristol carried out the study using data from one of the world’s most extensive ongoing prospective birth cohort studies — the Avon Longitudinal Study of Parents and Children (ALSPAC).
Globally, hypertension and obesity are major preventable risk factors for atherosclerotic cardiovascular diseases and death. However, several efforts to decrease the incidence and prevalence of hypertension and obesity have yielded minimal effects. Hence, understanding the natural development and pathogenesis of hypertension and obesity is important to decreasing these risks. In the newly published study, the researchers examined whether atherosclerotic traits such as arterial stiffness temporally precede the development of hypertension and obesity. This is the first time over 3800 adolescents, aged 17 years were followed up for seven years. The researchers employed several statistical approaches to untangle potential causal associations.
The researchers found that higher arterial stiffness during adolescence increased the risk of systolic hypertension by 20 percent and diastolic hypertension by two-fold, seven years later. Moreover, participants were categorised into four equal groups according to their level of arterial stiffness. Adolescents whose arterial stiffness levels were in the highest quartile both at 17 years of age and 24 years of age had a systolic blood pressure increase of 4 mmHg, and their diastolic blood pressure increased by 3 mmHg during the seven-year observation period. Of note, mild elevations in systolic and diastolic blood pressure were also observed in adolescents with mildly increased arterial stiffness but within normal limits. However, the change in blood pressure in the “mild” group was half that of the change in the “high” group. These results were similar in both males and females, despite controlling for important risk factors such as smoking, physical activity, lipid and glucose, body fat, heart rate, family history of cardiovascular diseases, etc.
Previous studies have focused on the adverse effect of obesity on the heart and blood vessels. However, the present study found that higher arterial stiffness at age 17 years increased the risk of abdominal obesity and whole body obesity by 20 percent at age 24 years. The findings reveal a possible two-way direction between unhealthy arteries and obesity, although the evidence was stronger for obesity leading to unhealthy arteries, and not vice versa.
A recent American Heart Association scientific statement notes that “lifestyle modification, including diet, reduced sedentariness, and increased physical activity, is usually recommended for patients with obesity; however, the long-term success of these strategies for reducing adiposity, maintaining weight loss, and reducing blood pressure has been limited.” It has also been established that a 5 mmHg rise in blood pressure over five years increases the risk of death in the adult population by 16 percent.
“Therefore, our novel findings are significant clinically and for population health, in that future hypertension and obesity prevention and treatment strategies may now consider reducing arterial stiffness, particularly from adolescence,” says Andrew Agbaje, a physician and clinical epidemiologist at the University of Eastern Finland.
This research was supported in part by research grants from Jenny and Antti Wihuri Foundation, the Finnish Cultural Foundation Central Fund, the Finnish Cultural Foundation North Savo Regional Fund, and the Doctoral Programme of Clinical Research, Faculty of Health Sciences, University of Eastern Finland. The UK Medical Research Council, Wellcome Trust, and the University of Bristol provided core support for theALSPAC study. 
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Exercise increases the body’s own cannabis-like substances, which in turn helps reduce inflammation and could potentially help treat certain conditions such as arthritis, cancer and heart disease.
In a new study, published in Gut Microbes, experts from the University of Nottingham found that exercise intervention in people with arthritis, did not just reduce their pain, but it also lowered the levels of inflammatory substances (called cytokines). It also increased levels of cannabis-like substances produced by their own bodies, called endocannabinoids. Interestingly, the way exercise resulted in these changes was by altering the gut microbes.
Exercise is known to decrease chronic inflammation, which in turn causes many diseases including cancer, arthritis and heart disease, but little is known as to how it reduces inflammation.
A group of scientists, led by Professor Ana Valdes from the School of Medicine at the University, tested 78 people with arthritis. Thirty-eight of them carried out 15 minutes of muscle strengthening exercises every day for six weeks, and 40 did nothing.
At the end of the study, participants who did the exercise intervention had not only reduced their pain, but they also had more microbes in their guts of the kind that produce anti-inflammatory substances, lower levels of cytokines and higher levels of endocannabinoids.
The increase in endocannabinoids was strongly linked to changes in the gut microbes and anti-inflammatory substances produced by gut microbes called SCFAS. In fact, at least one third of the anti-inflammatory effects of the gut microbiome was due to the increase in endocannabinoids.
Doctor Amrita Vijay, a Research Fellow in the School of Medicine and first author of the paper, said: “Our study clearly shows that exercise increases the body’s own cannabis-type substances. Which can have a positive impact on many conditions.
“As interest in cannabidiol oil and other supplements increases, it is important to know that simple lifestyle interventions like exercise can modulate endocannabinoids.”
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Current medications aren’t particularly effective against fungi. The situation is becoming more challenging because these organisms are developing resistance to antimicrobial treatments, just as bacteria are. Now, researchers report in ACS Infectious Diseases that they have identified compounds that tackle these infections in a new way — by interfering with fungal enzymes required for fatty acid synthesis — potentially opening the door to better therapies.
Superficial infections by Candida or other types of fungi can cause irritating but relatively minor conditions such as oral thrush and athlete’s foot, but invasive infections can result in debilitating and deadly diseases such as cryptococcal meningitis and some hospital-acquired infections. More people are getting these infections because of the growing use of invasive surgery, implanted catheters and immunosuppressive therapy. And some patients, such as those with severe COVID-19 or HIV, are especially susceptible to fungal infections. In addition, treatments can be toxic and often don’t work, in part because of increasing resistance. Current targets for these compounds include molecules necessary for making fungal cell walls. As an alternative, Glen. E. Palmer and colleagues began looking for potential therapies that could work through a different mechanism and thereby avoid the drawbacks of these drugs.
The researchers zeroed in on fungal fatty acid (FA) synthase and desaturase enzymes, which are essential for the growth and virulence of human fungal pathogens. It’s been difficult to devise a rapid chemical assay to find inhibitors for these enzymes, since it’s hard to isolate the enzymes. So the team instead combined genetic engineering with a whole-cell assay to screen thousands of small molecules. Although none of the tested compounds blocked FA synthase activity in Candida albicans cell cultures, 16 inhibited FA desaturase activity. A core acyl hydrazide structure was found to be key to the activity of several of these molecules, which were effective even against drug-resistant strains of several infectious species of fungi, while showing little to no toxicity to mammalian cells. The researchers note that these compounds are promising leads for further development as antifungal agents.
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More than 46,000 cancers in America each year, or about 3 percent of cases, could be prevented by meeting physical activity guidelines.More than 46,000 cancer cases in the United States might be prevented each year if almost all of us walked for about 45 minutes a day, according to an eye-opening new study of inactivity, exercise and malignancies. The study, which analyzed cancer incidence and the physical activity habits of nearly 600,000 American men and women in every state and the District of Columbia, found that about 3 percent of common cancers in the United States are strongly linked to inactivity. Something as simple as getting up and moving, the findings suggest, might help tens of thousands of us avoid developing cancer in the coming years.Already we have plenty of evidence that exercise affects cancer risk. In past experiments, physical activity has changed the immune system in ways that amplify the body’s ability to fight tumor growth. Exercise can, for example, ramp up the activity of certain immune cells known to target cancer cells. Exercise has also been associated with longer survival in people with certain forms of cancer, possibly by boosting levels of inflammatory substances that inhibit cancer cell growth. A 2016 review in JAMA Internal Medicine concluded that our risks for at least 13 types of cancer, including breast, bladder, blood and rectal cancers, drop substantially if we are physically active, and a separate 2019 report calculated that those reductions could be as high as 69 percent. At the same time, many studies show that being inactive raises our risks for various cancers. But scientists know surprisingly little about how those risks translate into actual cases or, more concretely, how many people each year are likely to develop cancers closely linked to moving too little.So, for the new study, which was published in October in Medicine & Science in Sports & Exercise, researchers with the American Cancer Society and Emory University in Atlanta used a sophisticated type of statistical analysis called P.A.F. to measure the links between cancer and inactivity. P.A.F. stands for population-attributable fraction and is a mathematical way for scientists to estimate how many occurrences of a disease — or drug responses or other biological reactions — within a larger population seem to be the result of a particular behavior or other factor. It can tell us, in essence, how many annual cases of, say, colon cancer — out of all the known instances of the disease each year — can reasonably be laid at the feet of smoking or alcohol or fatty foods or over-sitting.To start calculating the P.A.F. of cancer resulting from inactivity, the American Cancer Society scientists first pulled anonymized data from the U.S. Cancer Statistics database about cases, nationally and by state, for all Americans 20 and older between 2013 and 2016. The team focused both on total cancer cases and on seven types of cancer that in past studies had been closely tied in part to activity (or inactivity), which are stomach, kidney, esophageal, colon, bladder, breast and endometrial tumors.Next they checked on how much American adults claim to move, based on more than half a million replies to two large federal surveys. Both ask people in what ways and how often they exercise. The researchers drew responses from adults in every state and grouped them, based on whether or not people met the American Cancer Society recommendations for physical activity. Those guidelines call for, ideally, 300 minutes, or five hours, of moderate exercise, like a brisk walk, every week to reduce cancer risk. Finally, the researchers adjusted these statistics for body mass and other factors, gathered additional data about cancer risks and plugged all of the numbers into an equation, which then spit out the P.A.F. for cancers linked to inactivity. That number turned out to be 46,356, or about 3 percent of all cancers annually (excluding non-melanoma skin cancers). When they then looked at individual types of cancer, stomach cancer was most tied to inactivity, with about 17 percent of all cases annually attributable to not moving, versus 4 percent of bladder cancers. Likewise, the numbers varied by state, rising to nearly 4 percent of cancers in many Southern states, where residents tend to report getting relatively little exercise, but about 2 percent in much of the Mountain West, which has relatively active populations.The good news, however, is that these numbers are malleable. We have the ability to lower them. Exercise could “potentially prevent many cancers in the United States,” said Adair K. Minihan, an associate scientist at the American Cancer Society, who led the new study. If everyone in America who can exercise started walking for an hour on weekdays, she said, theoretically the 46,356 cases tied to inactivity should disappear.Of course, cancer is a bogglingly complex disease that has many overlapping, entwined causes, with inactivity playing just a small potential role. Furthermore, statistical risks never drop to zero. Many of the most active people can and do develop cancer, Ms. Minihan pointed out.This study, she emphasized, is not meant “to shame people for not exercising,” or suggest someone’s tumor is his or her fault for skipping the gym sometimes. “There are so many obstacles” to exercise, she said, and so many factors that go into who ultimately develops cancer. But the results do intimate that if each of us could find a way to fit in 45 minutes a day or so of simple exercise, like walking, we might reshape our odds of developing many types of malignancies.

Nearly 10 million children in lower-income countries like Nigeria and Pakistan have never been vaccinated, leaving them vulnerable to deadly diseases like polio, measles and pneumonia. Two-thirds of these “zero-dose” kids live below the international poverty line, their families subsisting on less than $2.35 a day in poor villages, in urban slums, in conflict zones.
Over the last 20 years, international organizations spearheaded by GAVI, The Vaccine Alliance -in partnership with national governments, the World Health Organization and UNICEF — have ensured that significantly more children in poor countries in Africa and elsewhere get routine vaccinations: 81 per cent today versus 59 per cent in 2000.
And that has had a major impact — a 70 per cent drop in child mortality from vaccine-preventable diseases over two decades. As an anchor donor to the Gavi Alliance, Canada has played a major part in this success.
But what about the root causes of non-vaccination of the young: is the problem one of poverty alone, of the failure of domestic governments and their public-health departments to reach the most vulnerable communities, or simply of an inability to overcome deep-rooted social disadvantages? A new Canada-India study of tens of thousands of zero-dose children in India suggests that the causes of low-vaccination rates in lower-income countries is all of those and more.
Published today in the Lancet Global Health and led by Université de Montréal public-health professor Mira Johri with colleagues S.V. Subramanian at Harvard University and Sunil Rajpal at FLAME University in Pune, the study analyses a quarter century of national survey data to better understand how social, economic and geographical inequalities in India shaped the chances of children remaining unvaccinated between 1992 and 2016.
The researchers analysed data over four survey rounds from close to 73,000 babies between 12 and 23 months, the standard age when immunization data are assessed. They found that India had made tremendous progress in reaching children with routine immunisation: the proportion of zero dose-children in India declined threefold in a quarter-century: from 33 per cent in 1992 to 10 per cent in 2016.

Back and forth transmission of SARS-CoV-2 between people and other mammals increases the risk of new variants and threatens efforts to control COVID-19. A new study, published today in Proceedings of the Royal Society B, used a novel modelling approach to predict the zoonotic capacity of 5,400 mammal species, extending predictive capacity by an order of magnitude. Of the high risk species flagged, many live near people and in COVID-19 hotspots.
A major bottleneck to predicting high-risk mammal species is limited data on ACE2, the cell receptor that SARS-CoV-2 binds to in animals. ACE2 allows SARS-CoV-2 to enter host cells, and is found in all major vertebrate groups. It is likely that all vertebrates have ACE2 receptors, but sequences were only available for 326 species.
To overcome this obstacle, the team developed a machine learning model that combined data on the biological traits of 5,400 mammal species with available data on ACE2. The goal: to identify mammal species with high ‘zoonotic capacity’ — the ability to become infected with SARS-CoV-2 and transmit it to other animals and people. The method they developed could help extend predictive capacity for disease systems beyond COVID-19.
Co-lead author Ilya Fischhoff, a postdoctoral associate at Cary Institute of Ecosystem Studies, comments, “SARS-CoV-2, the virus that causes COVID-19, originated in an animal before making the jump to people. Now, people have caused spillback infections in a variety of mammals, including those kept in farms, zoos, and even our homes. Knowing which mammals are capable of re-infecting us is vital to preventing spillback infections and dangerous new variants.”
When a virus passes from people to animals and back to people it is called secondary spillover. This phenomenon can accelerate new variants establishing in humans that are more virulent and less responsive to vaccines. Secondary spillover of SARS-CoV-2 has already been reported among farmed mink in Denmark and the Netherlands, where it has led to at least one new SARS-CoV-2 variant.
Senior author and Cary Institute disease ecologist, Barbara Han, says, “Secondary spillover allows SARS-CoV-2 established in new hosts to transmit potentially more infectious strains to people. Identifying mammal species that are efficient at transmitting SARS-CoV-2 is an important step in guiding surveillance and preventing the virus from continually circulating between people and other animals, making disease control even more costly and difficult.”
Binding to ACE2 receptors is not always enough to facilitate SARS-CoV-2 viral replication, shedding, and onward transmission. The team trained their models on a conservative binding strength threshold informed by published ACE2 amino acid sequences of vertebrates, analyzed using a software tool called HADDOCK (High Ambiguity Driven protein-protein DOCKing). This software scored each species on predicted binding strength; stronger binding likely promotes successful infection and viral shedding.