It's intuitive and scientifically shown that wearing a face covering can help reduce the spread of the novel coronavirus that causes COVID-19. But not all masks are created equal, according to new University of Arizona-led research.
Amanda Wilson, an environmental health sciences doctoral candidate in the Department of Community, Environment and Policy in the Mel and Enid Zuckerman College of Public Health, is lead author on a recent study published in the Journal of Hospital Infection that assessed the ability of a variety of nontraditional mask materials to protect a person from infection after 30 seconds and after 20 minutes of exposure in a highly contaminated environment.
When the researchers compared wearing masks to wearing no protection during 20-minute and 30-second exposures to the virus, they found that infection risks were reduced by 24-94% or by 44-99% depending on the mask and exposure duration. Risk reduction decreased as exposure duration increased, they found.
"N99 masks, which are even more efficient at filtering airborne particles than N95 masks, are obviously one of the best options for blocking the virus, as they can reduce average risk by 94-99% for 20-minute and 30-second exposures, but they can be hard to come by, and there are ethical considerations such as leaving those available for medical professionals," Wilson said.
The next best options, according to the research, are N95 and surgical masks and, perhaps surprisingly, vacuum cleaner filters, which can be inserted into filter pockets in cloth masks. The vacuum filters reduced infection risk by 83% for a 30-second exposure and 58% for a 20-minute exposure. Of the other nontraditional materials evaluated by the researchers, tea towels, cotton-blend fabrics and antimicrobial pillowcases were the next best for protection.
Scarves, which reduced infection risk by 44% after 30 seconds and 24% after 20 minutes, and similarly effective cotton t-shirts are only slightly better than wearing no mask at all, they found.
"We knew that masks work, but we wanted to know how well and compare different materials' effects on health outcomes," said Wilson, who specializes in quantitative microbial risk assessment.
Wilson and her team collected data from various studies of mask efficacy and created a computer model to simulate infection risk, taking various factors into consideration.
"One big component of risk is how long you're exposed. We compared risk of infection at both 30 seconds and 20 minutes in a highly contaminated environment," she said.
Other conditions that impact risk of infection are the number of people around you and their distance from you, she said.
The size of virus-transporting droplets from sneezes, coughs or even speech is also a very important factor. Larger, heavier droplets carrying the virus drop out of the air faster than smaller, lighter ones. That's one reason distance helps reduce exposure.
"Aerosol size can also be affected by humidity," Wilson said. "If the air is drier, then aerosols become smaller faster. If humidity is higher, then aerosols will stay larger for a longer period of time, dropping out faster. That might sound good at first, but then those aerosols fall on surfaces, and that object becomes another potential exposure route."
The study also showed that the more time a person spends in an environment where the virus is present, the less effective a mask becomes.
"That doesn't mean take your mask off after 20 minutes," Wilson said, "but it does mean that a mask can't reduce your risk to zero. Don't go to a bar for four hours and think you're risk free because you're wearing a mask. Stay home as much as possible, wash your hands often, wear a mask when you're out and don't touch your face."
Masks protect the wearer and others in a number of different ways. Wilson said there are two "intuitive ways" that masks filter larger aerosols: mechanical interception and inertial impaction.
"The denser the fibers of a material, the better it is at filtering. That's why higher thread counts lead to higher efficacy. There's just more to block the virus," she said. "But some masks (such as those made from silk) also have electrostatic properties, which can attract smaller particles and keep them from passing through the mask as well."
The model developed by Wilson and her colleagues included parameters such as inhalation rate -- the volume of air inhaled over time -- and virus concentration in the air.
"We took a lot of research data, put it into a mathematical model and related those data points to each other," Wilson said. "For example, if we know people's inhalation rates vary by this much and know this much virus is in the air and these materials offer this much efficiency in terms of filtration, what does that mean for infection risk? We provide a range, in part, because everyone is different, such as in how much air we breathe over time."
Wilson also said it's important for a mask to have a good seal that pinches at nose, and she noted that people shouldn't wear a mask beneath the nose or tuck it under the chin when not in use.
"Proper use of masks is so important," Wilson said. "Also, we were focusing on masks protecting the wearer, but they're most important to protect others around you if you're infected. If you put less virus out into the air, you're creating a less contaminated environment around you. As our model shows, the amount of infectious virus you're exposed to has a big impact on your infection risk and the potential for others' masks to protect them as well."
Amanda M. Wilson, Sarah E. Abney, Marco-Felipe King, Mark H. Weir, Martín López-García, Jonathan D. Sexton, Stephanie J. Dancer, Jessica Proctor, Catherine J. Noakes, Kelly A. Reynolds. COVID-19 and non-traditional mask use: How do various materials compare in reducing the infection risk for mask wearers?Journal of Hospital Infection, 2020; DOI: 10.1016/j.jhin.2020.05.036
A Newcastle University study involving thousands of families is helping prospective parents work out whether they are likely to have sons or daughters.
The work by Corry Gellatly, a research scientist at the university, has shown that men inherit a tendency to have more sons or more daughters from their parents. This means that a man with many brothers is more likely to have sons, while a man with many sisters is more likely to have daughters.
The research involved a study of 927 family trees containing information on 556,387 people from North America and Europe going back to 1600.
"The family tree study showed that whether you’re likely to have a boy or a girl is inherited. We now know that men are more likely to have sons if they have more brothers but are more likely to have daughters if they have more sisters. However, in women, you just can’t predict it," Mr Gellatly explains.
Men determine the sex of a baby depending on whether their sperm is carrying an X or Y chromosome. An X chromosome combines with the mother’s X chromosome to make a baby girl (XX) and a Y chromosome will combine with the mother’s to make a boy (XY).
The Newcastle University study suggests that an as-yet undiscovered gene controls whether a man’s sperm contains more X or more Y chromosomes, which affects the sex of his children. On a larger scale, the number of men with more X sperm compared to the number of men with more Y sperm affects the sex ratio of children born each year.
Sons or daughters?
A gene consists of two parts, known as alleles, one inherited from each parent. In his paper, Mr Gellatly demonstrates that it is likely men carry two different types of allele, which results in three possible combinations in a gene that controls the ratio of X and Y sperm;
Men with the first combination, known as mm, produce more Y sperm and have more sons.
The second, known as mf, produce a roughly equal number of X and Y sperm and have an approximately equal number of sons and daughters.
The third, known as ff produce more X sperm and have more daughters.
“The gene that is passed on from both parents, which causes some men to have more sons and some to have more daughters, may explain why we see the number of men and women roughly balanced in a population. If there are too many males in the population, for example, females will more easily find a mate, so men who have more daughters will pass on more of their genes, causing more females to be born in later generations,” says Newcastle University researcher Mr Gellatly.
More boys born after the wars
In many of the countries that fought in the World Wars, there was a sudden increase in the number of boys born afterwards. The year after World War I ended, an extra two boys were born for every 100 girls in the UK, compared to the year before the war started. The gene, which Mr Gellatly has described in his research, could explain why this happened.
As the odds were in favour of men with more sons seeing a son return from the war, those sons were more likely to father boys themselves because they inherited that tendency from their fathers. In contrast, men with more daughters may have lost their only sons in the war and those sons would have been more likely to father girls. This would explain why the men that survived the war were more likely to have male children, which resulted in the boy-baby boom.
In most countries, for as long as records have been kept, more boys than girls have been born. In the UK and US, for example, there are currently about 105 males born for every 100 females.
It is well-documented that more males die in childhood and before they are old enough to have children. So in the same way that the gene may cause more boys to be born after wars, it may also cause more boys to be born each year.
How does the gene work?
The trees (above) illustrate how the gene works. It is a simplified example, in which men either have only sons, only daughters, or equal numbers of each, though in reality it is less clear cut. It shows that although the gene has no effect in females, they also carry the gene and pass it to their children.
In the first family tree (A) the grandfather is mm, so all his children are male. He only passes on the m allele, so his children are more likely to have the mm combination of alleles themselves. As a result, those sons may also have only sons (as shown). The grandsons have the mf combination of alleles, because they inherited an m from their father and an f from their mother. As a result, they have an equal number of sons and daughters (the great grandchildren).
In the second tree (B) the grandfather is ff, so all his children are female, they have the ff combination of alleles because their father and mother were both ff. One of the female children has her own children with a male who has the mm combination of alleles. That male determines the sex of the children, so the grandchildren are all male. The grandsons have the mf combination of alleles, because they inherited an m from their father and f from their mother. As a result, they have an equal number of sons and daughters (the great-grandchildren).
Gellatly et al. Trends in Population Sex Ratios May be Explained by Changes in the Frequencies of Polymorphic Alleles of a Sex Ratio Gene. Evolutionary Biology, Dec 11, 2008; DOI: 10.1007/s11692-008-9046-3
Vitamin D levels appear to play role in COVID-19 mortality rates
After studying global data from the novel coronavirus (COVID-19) pandemic, researchers have discovered a strong correlation between severe vitamin D deficiency and mortality rates.
Led by Northwestern University, the research team conducted a statistical analysis of data from hospitals and clinics across China, France, Germany, Italy, Iran, South Korea, Spain, Switzerland, the United Kingdom (UK) and the United States.
The researchers noted that patients from countries with high COVID-19 mortality rates, such as Italy, Spain and the UK, had lower levels of vitamin D compared to patients in countries that were not as severely affected.
This does not mean that everyone -- especially those without a known deficiency -- needs to start hoarding supplements, the researchers caution.
"While I think it is important for people to know that vitamin D deficiency might play a role in mortality, we don't need to push vitamin D on everybody," said Northwestern's Vadim Backman, who led the research. "This needs further study, and I hope our work will stimulate interest in this area. The data also may illuminate the mechanism of mortality, which, if proven, could lead to new therapeutic targets."
The research is available on medRxiv, a preprint server for health sciences.
Backman is the Walter Dill Scott Professor of Biomedical Engineering at Northwestern's McCormick School of Engineering. Ali Daneshkhah, a postdoctoral research associate in Backman's laboratory, is the paper's first author.
Backman and his team were inspired to examine vitamin D levels after noticing unexplained differences in COVID-19 mortality rates from country to country. Some people hypothesized that differences in healthcare quality, age distributions in population, testing rates or different strains of the coronavirus might be responsible. But Backman remained skeptical.
"None of these factors appears to play a significant role," Backman said. "The healthcare system in northern Italy is one of the best in the world. Differences in mortality exist even if one looks across the same age group. And, while the restrictions on testing do indeed vary, the disparities in mortality still exist even when we looked at countries or populations for which similar testing rates apply.
"Instead, we saw a significant correlation with vitamin D deficiency," he said.
By analyzing publicly available patient data from around the globe, Backman and his team discovered a strong correlation between vitamin D levels and cytokine storm -- a hyperinflammatory condition caused by an overactive immune system -- as well as a correlation between vitamin D deficiency and mortality.
"Cytokine storm can severely damage lungs and lead to acute respiratory distress syndrome and death in patients," Daneshkhah said. "This is what seems to kill a majority of COVID-19 patients, not the destruction of the lungs by the virus itself. It is the complications from the misdirected fire from the immune system."
This is exactly where Backman believes vitamin D plays a major role. Not only does vitamin D enhance our innate immune systems, it also prevents our immune systems from becoming dangerously overactive. This means that having healthy levels of vitamin D could protect patients against severe complications, including death, from COVID-19.
"Our analysis shows that it might be as high as cutting the mortality rate in half," Backman said. "It will not prevent a patient from contracting the virus, but it may reduce complications and prevent death in those who are infected."
Backman said this correlation might help explain the many mysteries surrounding COVID-19, such as why children are less likely to die. Children do not yet have a fully developed acquired immune system, which is the immune system's second line of defense and more likely to overreact.
"Children primarily rely on their innate immune system," Backman said. "This may explain why their mortality rate is lower."
Backman is careful to note that people should not take excessive doses of vitamin D, which might come with negative side effects. He said the subject needs much more research to know how vitamin D could be used most effectively to protect against COVID-19 complications.
"It is hard to say which dose is most beneficial for COVID-19," Backman said. "However, it is clear that vitamin D deficiency is harmful, and it can be easily addressed with appropriate supplementation. This might be another key to helping protect vulnerable populations, such as African-American and elderly patients, who have a prevalence of vitamin D deficiency."
Backman is the director of Northwestern's Center for Physical Genomics and Engineering and the associate director for Research Technology and Infrastructure at the Robert H. Lurie Comprehensive Cancer Center at Northwestern University.
Ali Daneshkhah, Vasundhara Agrawal, Adam Eshein, Hariharan Subramanian, Hemant Kumar Roy, Vadim Backman. The Possible Role of Vitamin D in Suppressing Cytokine Storm and Associated Mortality in COVID-19 Patients. medRxiv, Posted April 30, 2020; [link]
Increasing abdominal girth and shrinking muscles are two common side effects of aging. Researchers at the University of Bonn have discovered a receptor in mice that regulates both effects. Experiments with human cell cultures suggest that the corresponding signaling pathways might also exist in humans. The study, which also involved researchers from Spain, Finland, Belgium, Denmark and the USA, has now been published in the journal Cell Metabolism.
On their surface, cells carry numerous different "antennas," called receptors, which can receive specific signal molecules. These then trigger a specific reaction in the cell. One of these antennas is the A2B receptor. The surfaces of some cells are virtually teeming with it, for example in the so-called brown adipose tissue. Brown adipose tissue, unlike its white-colored counterpart, is not used to store fat. Instead, it burns fat and thereby generates heat.
"In our publication we took a closer look at the A2B receptors in brown adipose tissue," explains Prof. Dr. Alexander Pfeifer from the Institute of Pharmacology and Toxicology at the University Hospital Bonn. "In the course of this we discovered an interesting association: The more A2B a mouse produces, the more heat it generates." Which means the A2B antennas somehow seem to increase the activity of the brown fat cells. But a second observation was even more exciting: Despite their increased fat burning, the animals weigh hardly less than mice with fewer receptors. "They are slimmer, but at the same time have more muscles," explains Pfeifer.
Muscles like a young mouse
In fact, the researchers were able to show that the muscle cells of mice also carry the A2B receptor. When this is stimulated by a small molecule agonist, muscle growth in the rodents is increased. "The receptor regulates both fat burning and muscle development," emphasizes Pfeifer's colleague Dr. Thorsten Gnad, the lead author of the study.
As they age, mice increasingly lose muscle mass -- similar to humans. And just like us, they also tend to gain a lot of fat around the hips over the years. However, if they receive the agonist that activates the A2B receptor, these aging effects are inhibited: Their oxygen consumption (an indicator of energy dissipation) increases by almost half; moreover, after four weeks of treatment they have as much muscle mass as a young animal. "A2B activation can therefore reverse both aging effects to a certain extent," explains Gnad.
In order to see whether the results were also meaningful for humans, the researchers examined human cell cultures and tissue samples. They found that in people with a large number of A2B receptors, the brown adipose tissue works at a higher rate. At the same time, their muscle cells consume more energy, which may indicate that they are also more active and may be more likely to be regenerated.
"Obesity is a growing problem worldwide," emphasizes Prof. Pfeifer. "Every extra pound not only increases the risk of developing diabetes, but also the risk of high blood pressure, vascular damage and therefore heart attacks and strokes. These problems are further exacerbated by muscles that shrink over the years, as they further reduce the body's energy requirements both at rest and in motion." In addition, poor muscle strength has an immense impact on the everyday life of older people, as they are increasingly restricted in their mobility.
The pharmacologists explain that the prospect of having a receptor on hand that might be able to slow down both of these age-related phenomena is therefore highly exciting. However, further research would first have to show to what extent the human mechanisms actually resemble those in mice. Additionally, there is currently no activator of A2B approved for use in humans. This means that little is known about any side effects of such a treatment. "We found no signs of adverse reactions in mice," says Pfeifer. "However, the meaningfulness of the results is, of course, also limited on this matter."
Gnad emphasizes that the success of the study is also the result of good cooperation with numerous international partners: "Nowadays, it is almost impossible to work on complex issues comprehensively without such cooperation."
Thorsten Gnad, Gemma Navarro, Minna Lahesmaa, Laia Reverte-Salisa, Francesca Copperi, Arnau Cordomi, Jennifer Naumann, Aileen Hochhäuser, Saskia Haufs-Brusberg, Daniela Wenzel, Frank Suhr, Naja Zenius Jespersen, Camilla Scheele, Volodymyr Tsvilovskyy, Christian Brinkmann, Joern Rittweger, Christian Dani, Mathias Kranz, Winnie Deuther-Conrad, Holger K. Eltzschig, Tarja Niemi, Markku Taittonen, Peter Brust, Pirjo Nuutila, Leonardo Pardo, Bernd K. Fleischmann, Matthias Blüher, Rafael Franco, Wilhelm Bloch, Kirsi A. Virtanen, Alexander Pfeifer. Adenosine/A2B Receptor Signaling Ameliorates the Effects of Aging and Counteracts Obesity. Cell Metabolism, 2020; DOI: 10.1016/j.cmet.2020.06.006
Illustration of black hole, warped spacetime (stock image).
The revolution in our understanding of the night sky and our place in the universe began when we transitioned from using the naked eye to a telescope in 1609. Four centuries later, scientists are experiencing a similar transition in their knowledge of black holes by searching for gravitational waves.
In the search for previously undetected black holes that are billions of times more massive than the sun, Stephen Taylor, assistant professor of physics and astronomy and former astronomer at NASA's Jet Propulsion Laboratory (JPL) together with the North American Nanohertz Observatory for Gravitational Waves (NANOGrav) collaboration has moved the field of research forward by finding the precise location -- the center of gravity of our solar system -- with which to measure the gravitational waves that signal the existence of these black holes.
The potential presented by this advancement, co-authored by Taylor, was published in the journal the Astrophysical Journal in April 2020.
Black holes are regions of pure gravity formed from extremely warped spacetime. Finding the most titanic black holes in the Universe that lurk at the heart of galaxies will help us understand how such galaxies (including our own) have grown and evolved over the billions of years since their formation. These black holes are also unrivaled laboratories for testing fundamental assumptions about physics.
Gravitational waves are ripples in spacetime predicted by Einstein's general theory of relativity. When black holes orbit each other in pairs, they radiate gravitational waves that deform spacetime, stretching and squeezing space. Gravitational waves were first detected by the Laser Interferometer Gravitational-Wave Observatory (LIGO) in 2015, opening new vistas on the most extreme objects in the universe. Whereas LIGO observes relatively short gravitational waves by looking for changes in the shape of a 4-km long detector, NANOGrav, a National Science Foundation (NSF) Physics Frontiers Center, looks for changes in the shape of our entire galaxy.
Taylor and his team are searching for changes to the arrival rate of regular flashes of radio waves from pulsars. These pulsars are rapidly spinning neutron stars, some going as fast as a kitchen blender. They also send out beams of radio waves, appearing like interstellar lighthouses when these beams sweep over Earth. Over 15 years of data have shown that these pulsars are extremely reliable in their pulse arrival rates, acting as outstanding galactic clocks. Any timing deviations that are correlated across lots of these pulsars could signal the influence of gravitational waves warping our galaxy.
"Using the pulsars we observe across the Milky Way galaxy, we are trying to be like a spider sitting in stillness in the middle of her web," explains Taylor. "How well we understand the solar system barycenter is critical as we attempt to sense even the smallest tingle to the web." The solar system barycenter, its center of gravity, is the location where the masses of all planets, moons, and asteroids balance out.
Where is the center of our web, the location of absolute stillness in our solar system? Not in the center of the sun as many might assume, rather it is closer to the surface of the star. This is due to Jupiter's mass and our imperfect knowledge of its orbit. It takes 12 years for Jupiter to orbit the sun, just shy of the 15 years that NANOGrav has been collecting data. JPL's Galileo probe (named for the famed scientist that used a telescope to observe the moons of Jupiter) studied Jupiter between 1995 and 2003, but experienced technical maladies that impacted the quality of the measurements taken during the mission.
Identifying the center of the solar system's gravity has long been calculated with data from Doppler tracking to get an estimate of the location and trajectories of bodies orbiting the sun. "The catch is that errors in the masses and orbits will translate to pulsar-timing artifacts that may well look like gravitational waves," explains JPL astronomer and co-author Joe Simon.
Taylor and his collaborators were finding that working with existing solar system models to analyze NANOGrav data gave inconsistent results. "We weren't detecting anything significant in our gravitational wave searches between solar system models, but we were getting large systematic differences in our calculations," notes JPL astronomer and the paper's lead author Michele Vallisneri. "Typically, more data delivers a more precise result, but there was always an offset in our calculations."
The group decided to search for the center of gravity of the solar system at the same time as sleuthing for gravitational waves. The researchers got more robust answers to finding gravitational waves and were able to more accurately localize the center of the solar system's gravity to within 100 meters. To understand that scale, if the sun were the size of a football field, 100 meters would be the diameter of a strand of hair. "Our precise observation of pulsars scattered across the galaxy has localized ourselves in the cosmos better than we ever could before," said Taylor. "By finding gravitational waves this way, in addition to other experiments, we gain a more holistic overview of all different kinds of black holes in the Universe."
As NANOGrav continues to collect ever more abundant and precise pulsar timing data, astronomers are confident that massive black holes will show up soon and unequivocally in the data.
Taylor was partially supported by an appointment to the NASA Postdoctoral Program at JPL. The NANOGrav project receives support from the NSF Physics Frontier Center award #1430284 and this work was supported in part by NSF Grant PHYS-1066293 and by the hospitality of the Aspen Center for Physics. Data for this project were collected using the facilities of the Green Bank Observatory and the Arecibo Observatory.
M. Vallisneri, S. R. Taylor, J. Simon, W. M. Folkner, R. S. Park, C. Cutler, J. A. Ellis, T. J. W. Lazio, S. J. Vigeland, K. Aggarwal, Z. Arzoumanian, P. T. Baker, A. Brazier, P. R. Brook, S. Burke-Spolaor, S. Chatterjee, J. M. Cordes, N. J. Cornish, F. Crawford, H. T. Cromartie, K. Crowter, M. DeCesar, P. B. Demorest, T. Dolch, R. D. Ferdman, E. C. Ferrara, E. Fonseca, N. Garver-Daniels, P. Gentile, D. Good, J. S. Hazboun, A. M. Holgado, E. A. Huerta, K. Islo, R. Jennings, G. Jones, M. L. Jones, D. L. Kaplan, L. Z. Kelley, J. S. Key, M. T. Lam, L. Levin, D. R. Lorimer, J. Luo, R. S. Lynch, D. R. Madison, M. A. McLaughlin, S. T. McWilliams, C. M. F. Mingarelli, C. Ng, D. J. Nice, T. T. Pennucci, N. S. Pol, S. M. Ransom, P. S. Ray, X. Siemens, R. Spiewak, I. H. Stairs, D. R. Stinebring, K. Stovall, J. K. Swiggum, R. van Haasteren, C. A. Witt, W. W. Zhu. Modeling the Uncertainties of Solar System Ephemerides for Robust Gravitational-wave Searches with Pulsar-timing Arrays. The Astrophysical Journal, 2020; 893 (2): 112 DOI: 10.3847/1538-4357/ab7b67
In the wake of the COVID-19 pandemic, the U.S. Centers for Disease Control and Prevention recommends that people wear masks in public. Because N95 and surgical masks are scarce and should be reserved for health care workers, many people are making their own coverings. Now, researchers report in ACS Nano that a combination of cotton with natural silk or chiffon can effectively filter out aerosol particles -- if the fit is good.
SARS-CoV-2, the new coronavirus that causes COVID-19, is thought to spread mainly through respiratory droplets when an infected person coughs, sneezes, speaks or breathes. These droplets form in a wide range of sizes, but the tiniest ones, called aerosols, can easily slip through the openings between certain cloth fibers, leading some people to question whether cloth masks can actually help prevent disease. Therefore, Supratik Guha at the University of Chicago and colleagues wanted to study the ability of common fabrics, alone or in combination, to filter out aerosols similar in size to respiratory droplets.
The researchers used an aerosol mixing chamber to produce particles ranging from 10 nm to 6 μm in diameter. A fan blew the aerosol across various cloth samples at an airflow rate corresponding to a person's respiration at rest, and the team measured the number and size of particles in air before and after passing through the fabric. One layer of a tightly woven cotton sheet combined with two layers of polyester-spandex chiffon -- a sheer fabric often used in evening gowns -- filtered out the most aerosol particles (80-99%, depending on particle size), with performance close to that of an N95 mask material. Substituting the chiffon with natural silk or flannel, or simply using a cotton quilt with cotton-polyester batting, produced similar results. The researchers point out that tightly woven fabrics, such as cotton, can act as a mechanical barrier to particles, whereas fabrics that hold a static charge, like certain types of chiffon and natural silk, serve as an electrostatic barrier. However, a 1% gap reduced the filtering efficiency of all masks by half or more, emphasizing the importance of a properly fitted mask.
The authors acknowledge use of the U.S. Department of Energy's Center for Nanoscale Materials user facility at Argonne National Laboratory and funding from the U.S. Department of Defense's Vannevar Bush Fellowship.
Abhiteja Konda, Abhinav Prakash, Gregory A. Moss, Michael Schmoldt, Gregory D. Grant, Supratik Guha. Aerosol Filtration Efficiency of Common Fabrics Used in Respiratory Cloth Masks. ACS Nano, 2020; DOI: 10.1021/acsnano.0c03252
Research out today in the journal Cell shows that a specific change in the SARS-CoV-2 coronavirus virus genome, previously associated with increased viral transmission and the spread of COVID-19, is more infectious in cell culture. The variant in question, D614G, makes a small but effective change in the virus's 'Spike' protein, which the virus uses to enter human cells.
Bette Korber, a theoretical biologist at Los Alamos National Laboratory and lead author of the study, noted, "The D614G variant first came to our attention in early April, as we had observed a strikingly repetitive pattern. All over the world, even when local epidemics had many cases of the original form circulating, soon after the D614G variant was introduced into a region it became the prevalent form."
Geographic information from samples from the GISAID COVID-19 viral sequence database enabled tracking of this highly recurrent pattern, a shift in the viral population from the original form to the D614G variant. This occurred at every geographic level: country, subcountry, county, and city.
Two independent lines of experimental evidence that support these initial results are included in today's paper. These additional experiments, led by Professor Erica Ollmann Saphire, Ph.D., at the La Jolla Institute, and by Professor David Montefiori, Ph.D., at Duke University, showed that the D614G change increases the virus's infectivity in the laboratory. These new experiments, as well as more extensive sequence and clinical data and improved statistical models, are presented in the Cell paper. More in vivo work remains to be done to determine the full implications of the change.
The SARS-CoV-2 virus has a low mutation rate overall (much lower than the viruses that cause influenza and HIV-AIDS). The D614G variant appears as part of a set of four linked mutations that appear to have arisen once and then moved together around the world as a consistent set of variations.
"It's remarkable to me," commented Will Fischer of Los Alamos, an author on the study, "both that this increase in infectivity was detected by careful observation of sequence data alone, and that our experimental colleagues could confirm it with live virus in such a short time."
Fortunately, "the clinical data in this paper from Sheffield showed that even though patients with the new G virus carried more copies of the virus than patients infected with D, there wasn't a corresponding increase in the severity of illness," said Saphire, who leads the Gates Foundation-supported Coronavirus Immunotherapy Consortium (CoVIC).
Korber noted, "These findings suggest that the newer form of the virus may be even more readily transmitted than the original form -- whether or not that conclusion is ultimately confirmed, it highlights the value of what were already good ideas: to wear masks and to maintain social distancing."
Research partners from Los Alamos National Laboratory, Duke University, and the University of Sheffield initially published work on this analysis on the bioRxiv site in an April 2020 preprint. That work also included observations of COVID-19 patients from Sheffield that suggested an association of the D614G variant with higher viral loads in the upper respiratory tract.
"It is possible to track SARS-CoV-2 evolution globally because researchers worldwide are rapidly making their viral sequence data available through the GISAID viral sequence database," Korber said. Currently tens of thousands of sequences are available through this project, and this enabled Korber and the research team to identify the emergence of the D614G variant.
GISAID was established to encourage collaboration among influenza researchers, but early in the epidemic the consortium established a SARS-CoV-2 database, which soon became the de facto standard for sharing outbreak sequences among researchers worldwide.
The study, "Tracking changes in SARS-CoV-2 Spike: evidence that D614G increases infectivity of the COVID-19 virus" was supported by the Medical Research Council (MRC) part of UK Research & Innovation (UKRI the National Institute of Health Research (NIHR); Genome Research Limited, operating as the Wellcome Sanger Institute; CoVIC, INV-006133 of the COVID-19 Therapeutics Accelerator, supported by the Bill and Melinda Gates Foundation, Mastercard, Wellcome; private philanthropic support, as well as the Overton family; a FastGrant, from Emergent Ventures, in aid of COVID-19 research; and the National Institute of Allergy and Infectious Diseases, National Institutes of Health, Department of Health and Human Services, under Interagency Agreement No. AAI12007-001-00000, and the Los Alamos Laboratory Directed Research and Development program.
Additional study authors included S. Gnanakaran, H. Yoon, J. Theiler, W. Abfalterer, N. Hengartner, E.E. Giorgi, T. Bhattacharya, B. Foley, K.M. Hastie, M.D. Parker, D.G. Partridge, C.M. Evans, T.M. Freeman, T.I. de Silva, C. McDanal, L.G. Perez, H. Tang, A. Moon-Walker, S.P. Whelan, C.C. LaBranche.
B. Korber, W.M. Fischer, S. Gnanakaran, H. Yoon, J. Theiler, W. Abfalterer, N. Hengartner, E.E. Giorgi, T. Bhattacharya, B. Foley, K.M. Hastie, M.D. Parker, D.G. Partridge, C.M. Evans, T.M. Freeman, T.I. de Silva, C. McDanal, L.G. Perez, H. Tang, A. Moon-Walker, S.P. Whelan, C.C. LaBranche, E.O. Saphire, D.C. Montefiori, on behalf of theSheffield COVID-19 Genomics Group. Tracking changes in SARS-CoV-2 Spike: evidence that D614G increases infectivity of the COVID-19 virus. Cell, July 2, 2020; DOI: 10.1016/j.cell.2020.06.043