Publisher Health

Within the next decade, the novel coronavirus responsible for COVID-19 could become little more than a nuisance, causing no more than common cold-like coughs and sniffles. That possible future is predicted by mathematical models that incorporate lessons learned from the current pandemic on how our body’s immunity changes over time. Scientists at the University of Utah carried out the research, now published in the journal Viruses.
“This shows a possible future that has not yet been fully addressed,” says Fred Adler, PhD, professor of mathematics and biological sciences at the U. “Over the next decade, the severity of COVID-19 may decrease as populations collectively develop immunity.”
The findings suggest that changes in the disease could be driven by adaptations of our immune response rather than by changes in the virus itself. Adler was senior author on the publication with Alexander Beams, first author and graduate student in the Department of Mathematics and the Division of Epidemiology at University of Utah Health, and undergraduate co-author Rebecca Bateman.
Although SARS-CoV-2 (the sometimes-deadly coronavirus causing COVID-19) is the best-known member of that virus family, other seasonal coronaviruses circulate in the human population — and they are much more benign. Some evidence indicates that one of these cold-causing relatives might have once been severe, giving rise to the “Russian flu” pandemic in the late 19th century. The parallels led the U of U scientists to wonder whether the severity of SARS-CoV-2 could similarly lessen over time.
To test the idea, they built mathematical models incorporating evidence on the body’s immune response to SARS-CoV-2 based on the following data from the current pandemic. There is likely a dose response between virus exposure and disease severity. A person exposed to a small dose of virus will be more likely to get a mild case of COVID-19 and shed small amounts of virus. By contrast, adults exposed to a large dose of virus are more likely to have severe disease and shed more virus. Masking and social distancing decrease the viral dose. Children are unlikely to develop severe disease. Adults who have had COVID-19 or have been vaccinated are protected against severe disease.Running several versions of these scenarios showed that the three mechanisms in combination set up a situation where an increasing proportion of the population will become predisposed for mild disease over the long term. The scientists felt the transformation was significant enough that it needed a new term. In this scenario, SARS-CoV-2 would become “Just Another Seasonal Coronavirus,” or JASC for short.
“In the beginning of the pandemic, no one had seen the virus before,” Adler explains. “Our immune system was not prepared.” The models show that as more adults become partially immune, whether through prior infection or vaccination, severe infections all but disappear over the next decade. Eventually, the only people who will be exposed to the virus for the first time will be children — and they’re naturally less prone to severe disease.
“The novel approach here is to recognize the competition taking place between mild and severe COVID-19 infections and ask which type will get to persist in the long run,” Beams says. “We’ve shown that mild infections will win, as long as they train our immune systems to fight against severe infections.”
The models do not account for every potential influence on disease trajectory. For example, if new virus variants overcome partial immunity, COVID-19 could take a turn for the worse. In addition, the predictions rely on the key assumptions of the model holding up.
“Our next step is comparing our model predictions with the most current disease data to assess which way the pandemic is going as it is happening,” Adler says. “Do things look like they’re heading in a bad or good direction? Is the proportion of mild cases increasing? Knowing that might affect decisions we make as a society.”
The research, published as “Will SARS-CoV-2 Become Just Another Seasonal Coronavirus?,” was supported by COVID MIND 2020 and the University of Utah.
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Fast-spreading variants of the COVID-19-causing coronavirus, SARS-CoV-2, carry mutations that enable the virus to escape some of the immune response created naturally or by vaccination. A new study from scientists at Scripps Research, along with collaborators in Germany and the Netherlands, has revealed key details of how these escape mutations work.
The scientists, whose study appears in Science, used structural biology techniques to map at high resolution how important classes of neutralizing antibodies bind to the original pandemic strain of SARS-CoV-2 — and how the process is disrupted by mutations found in new variants first detected in Brazil, the United Kingdom, South Africa and India.
The research also highlights that several of these mutations are clustered in one site, known as the “receptor binding site,” on the spike protein of the virus. Other sites on the receptor binding domain are unaffected.
“An implication of this study is that, in designing next-generation vaccines and antibody therapies, we should consider increasing the focus on other vulnerable sites on the virus that tend not to be affected by the mutations found in variants of concern,” says co-lead author Meng Yuan, PhD.
Yuan is a postdoctoral research associate in the laboratory of senior author Ian Wilson, DPhil, Hansen Professor of Structural Biology and Chair of the Department of Integrative Structural and Computational Biology at Scripps Research.
How ‘variants of concern’ escape immune response
SARS-CoV-2 “variants of concern” include the UK’s B.1.1.7 variants, South Africa’s B.1.351 variants, Brazil’s P.1 variants and India’s B.1.617 variants. Some of these variants appear to be more infectious than the original Wuhan strain. Recent studies have found that antibody responses generated through natural infection to the original strain or via vaccination are less effective in neutralizing these variant strains.

Around the world and within the U.S., the percentage of people wearing masks during the Covid-19 pandemic has varied enormously. What explains this? A new study co-authored by an MIT faculty member finds that a public sense of “collectivism” clearly predicts mask usage, adding a cultural and psychological perspective to the issue.
The study uses a series of datasets about mask usage and public attitudes, along with well-established empirical indices of collectivism, to evaluate the impact of those cultural differences on this element of the pandemic response.
“Our data both within the United States and across the world shows that collectivism is a strong and important predictor of whether people in a region wear masks or not,” says Jackson G. Lu, an assistant professor at the MIT Sloan School of Management and co-author of a new paper detailing the results.
Collectivism broadly refers to the inclination to prioritize a group’s needs over an individual’s concerns, and social scientists have often worked to measure its presence among different populations. The researchers found a culture of collectivism to be a key driver of mask use even after accounting for many other factors, including political orientation, state policies, the severity of Covid-19 outbreaks, and more.
“In collectivistic cultures, people consider wearing masks not only a responsibility or duty, but also, a symbol of solidarity — that we’re standing together and fighting this pandemic together,” Lu says.
The paper, “Collectivism Predicts Mask Use During COVID-19,” appears today in Proceedings of the National Academy of Sciences. The authors are Lu, who is the Mitsui Career Development Professor at MIT Sloan; Peter Jin, a research associate at MIT Sloan; and Alexander S. English, a researcher in the Department of Psychology and Behaviorial Sciences at Zhejiang University in Hangzhou, China.

You might be older — or younger — than you think. A new study found that differences between a person’s age in years and his or her biological age, as predicted by an artificial intelligence (AI)-enabled EKG, can provide measurable insights into health and longevity.
The AI model accurately predicted the age of most subjects, with a mean age gap of 0.88 years between EKG age and actual age. However, a number of subjects had a gap that was much larger, either seemingly much older or much younger by EKG age.
The likelihood to die during follow-up was much higher among those seemingly older by EKG age, compared to those whose EKG age was the same as their chronologic or actual age. The association was even stronger when predicting death caused by heart disease. Conversely, those who had a lesser age gap ? considered younger by EKG — had decreased risk.
“Our results validate and expand on our prior observations that EKG age using AI may detect accelerated aging by proving that those with older-than-expected age by EKG die sooner, particularly from heart disease. We know that mortality rate is one of the best ways to measure biological age, and our model proved that,” says Francisco Lopez-Jimenez, M.D., chair of the Division of Preventive Cardiology at Mayo Clinic. Dr. Lopez-Jimenez is senior author of the study.
When researchers adjusted these data to consider multiple standard risk factors, the association between the age gap and cardiovascular mortality was even more pronounced. Subjects who were found to be oldest by EKG compared to their actual age had the greatest risk, even after accounting for medical conditions that would predict their survival, while those found the youngest compared to their actual age had lower cardiovascular risks.
Mayo Clinic researchers evaluated the12-lead EKG data of more than 25,000 subjects with an AI algorithm previously trained and validated to provide a biologic age prediction. Subjects with a positive age gap — an EKG age higher than their chronological or actual age — showed a clear connection to all-cause and cardiovascular mortality over time. The findings are published in European Heart Journal — Digital Health.
Study subjects were selected through the Rochester Epidemiology Project, an index of health-related information from medical providers in Olmsted County, Minnesota. The subjects had a mean age around 54 and were followed for approximately 12.5 years. The study excluded those with a baseline history of heart attacks, bypass surgery or stents, stroke or atrial fibrillation.
“Our findings open up a number of opportunities to help identify those who may benefit from preventive strategies the most. Now that the concept has been proven that EKG age relates to survival, it is time to think how we can incorporate this in clinical practice.More research will be needed to find the best ways to do it,” says Dr. Lopez-Jimenez.
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Materials provided by Mayo Clinic. Original written by Terri Malloy. Note: Content may be edited for style and length.

A protein that provides essential protection against free radicals inside the cell provokes damaging inflammation when released outside, activating immune cells and worsening damage following a stroke, according to a new study published 20th May, 2021 in the open access journal PLOS Biology by Takashi Shichita of the Tokyo Metropolitan Institute of Medical Science and colleagues.
The protein DJ-1 acts within cells to mop up dangerous molecular fragments called free radicals. It is thought to prevent neurodegeneration by reducing oxidative stress within aging neurons; indeed, an inactivating mutation in the gene that encodes DJ-1 causes one form of Parkinson’s disease (DJ-1 is also known as PARK7 for this reason).
When a cell ruptures, its contents are released into the surroundings, where certain released molecules, called DAMPs (damage-associated molecular patterns) act as alarm signals to activate inflammatory processes, including the attraction of macrophages to clean up the damage. At low levels and for short periods of time, inflammation in the brain can be beneficial. But when the damage is extensive, as in stroke, inflammation can contribute to the problem rather than the solution.
To identify new DAMPs, the authors prepared brain homogenates and then separated the proteins within by molecular weight. They had previously shown that one subset, between 15 and 25 kilodaltons, contained DMAP activity. Here, they identified candidate proteins within that subset by using mass spectrometry, generated the purified proteins, and then added them to cultured macrophages.
One of those proteins was DJ-1, which prompted upregulation of inflammatory cytokines in the macrophages. The researchers showed that this effect was triggered by interaction with Toll-like receptors on the surface of macrophages, membrane proteins known to mediate inflammatory activation. To further confirm DJ-1’s pro-inflammatory potential, the team showed that its DAMP activity depended on the presence of two key sections of the protein’s three-dimensional structure; altering these abolished the effect. Finally, they showed that DJ-1 was released by dying cells during stroke in a mouse model, and that knocking out DJ-1, or blocking it with an antibody, reduced the damage caused by stroke.
“Extracellular DJ-1 is a previously unknown inflammatogenic DAMP,” said Shichita, “and may be a putative target for therapeutic intervention to prevent the progression of inflammatory and neurodegenerative diseases.”
Dr. Shichita notes “DJ-1 has been thoroughly investigated as a cytoprotective antioxidant protein in neurons. However, here we demonstrate that extracellularly released DJ-1 triggers neurotoxic inflammation after ischemic stroke. Intracellular DJ-1 increases in response to oxidative stress in ischemic neurons, but if ischemic stresses result in necrotic cell death, DJ-1 is passively released into the extracellular space. Released DJ-1 interacts with Toll-like receptor 2 (TLR2) and TLR4 in the infiltrating myeloid cells and triggers post-ischemic inflammation, leading to the exacerbated pathologies of ischemic stroke. Thus, extracellular DJ-1 is a previously unknown inflammatogenic DAMP, and may be a putative target for therapeutic intervention to prevent the progression of inflammatory and neurodegenerative diseases.”
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Materials provided by PLOS. Note: Content may be edited for style and length.

Taking more steps per day, either all at once or in shorter spurts, may help you live longer, according to preliminary research to be presented at the American Heart Association’s Epidemiology, Prevention, Lifestyle & Cardiometabolic Health Conference 2021. The meeting is virtual, May 20-21, and offers the latest science on population-based health and wellness and implications for lifestyle.
Walking is one of the safest and easiest ways to improve fitness and health including heart health. The American Heart Association’s fitness guidelines for adults recommend at least 150 minutes per week of moderate or 75 minutes of vigorous physical activity, or a combination of both. Popular fitness apps and step counters make it easy to count steps, so researchers used a wearable step counting device to compare the effects of uninterrupted bouts of steps (10 minutes or longer) to occasional short spurts, such as climbing the stairs and general daily activities throughout the day.
“Technological advances made in recent decades have allowed researchers to measure short spurts of activity. Whereas, in the past we were limited to only measuring activities people could recall on a questionnaire,” said lead study author Christopher C. Moore, M.S., a Ph.D. student in epidemiology at the University of North Carolina at Chapel Hill. “With the help of wearable devices, more research is indicating that any type of movement is better than remaining sedentary.”
From 2011-2015, 16,732 women wore a waist step counter that measured their daily steps and walking patterns for four to seven days. The women were all over age 60 (average age of 72; mostly non-Hispanic white women) and were participants in the Women’s Health Study, a large, national study of heart disease, cancer and other long-term disease prevention.
The researchers divided the total number of steps for each study participant into two groups: 1) 10 minutes or longer bouts of walking with few interruptions; and 2) short spurts of walking during regular daily activities such as housework, taking the stairs, or walking to or from a car. In follow-up, they tracked deaths from any cause for an average of six years, through December 31, 2019.
Researchers found: Overall, 804 deaths occurred during the entire study period of 2011-2019. Study participants who took more steps in short spurts lived longer, regardless of how many steps they had in longer, uninterrupted bouts. The benefits leveled off at about 4,500 steps per day in short spurts. Compared to no daily steps, each initial increase of 1,000 steps per day was associated with a 28% decrease in death during the follow-up period. A 32% decrease in death was noted in participants who took more than 2,000 steps daily in uninterrupted bouts.A prior analysis of the same women reported that those who took 4,500 steps per day had a significantly lower risk of death compared to the least active women. “Our current results indicate that this finding holds even for women who did not engage in any uninterrupted bouts of walking. Taking 2,000 or more additional steps during bouts was associated with further benefits for longevity,” Moore said.
“Older adults face many barriers to participating in structured exercise programs, so some may find it more convenient and enjoyable to increase everyday walking behaviors, like parking slightly further from their destination or doing some extra housework or yardwork,” Moore said.
Since all study participants were older and mostly non-Hispanic white women, more research is needed to determine if the results apply to men, younger women and people from diverse racial and ethnic groups.
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Most able-bodied people take their ability to perform simple daily tasks for granted — when they reach for a warm mug of coffee, they can feel its weight and temperature and adjust their grip accordingly so that no liquid is spilled. People with full sensory and motor control of their arms and hands can feel that they’ve made contact with an object the instant they touch or grasp it, allowing them to start moving or lifting it with confidence.
But those tasks become much more difficult when a person operates a prosthetic arm, let alone a mind-controlled one.
In a paper published today in Science, a team of bioengineers from the University of Pittsburgh Rehab Neural Engineering Labs describe how adding brain stimulation that evokes tactile sensations makes it easier for the operator to manipulate a brain-controlled robotic arm. In the experiment, supplementing vision with artificial tactile perception cut the time spent grasping and transferring objects in half, from a median time of 20.9 to 10.2 seconds.
“In a sense, this is what we hoped would happen — but perhaps not to the degree that we observed,” said co-senior author Jennifer Collinger, Ph.D., associate professor in the Pitt Department of Physical Medicine and Rehabilitation. “Sensory feedback from limbs and hands is hugely important for doing normal things in our daily lives, and when that feedback is lacking, people’s performance is impaired.”
Study participant Nathan Copeland, whose progress was described in the paper, is the first person in the world who was implanted with tiny electrode arrays not just in his brain’s motor cortex but in his somatosensory cortex as well — a region of the brain that processes sensory information from the body. Arrays allow him to not only control the robotic arm with his mind, but also to receive tactile sensory feedback, which is similar to how neural circuits operate when a person’s spinal cord is intact.
“I was already extremely familiar with both the sensations generated by stimulation and performing the task without stimulation. Even though the sensation isn’t ‘natural’ — it feels like pressure and gentle tingle — that never bothered me,” said Copeland. “There wasn’t really any point where I felt like stimulation was something I had to get used to. Doing the task while receiving the stimulation just went together like PB&J.”
After a car crash that left him with limited use of his arms, Copeland enrolled in a clinical trial testing the sensorimotor microelectrode brain-computer interface (BCI) and was implanted with four microelectrode arrays developed by Blackrock Microsystems (also commonly referred to as Utah arrays).
This paper is a step forward from an earlier study that described for the first time how stimulating sensory regions of the brain using tiny electrical pulses can evoke sensation in distinct regions of a person’s hand, even though they lost feeling in their limbs due to spinal cord injury. In this new study, the researchers combined reading the information from the brain to control the movement of the robotic arm with writing information back in to provide sensory feedback.
In a series of tests, where the BCI operator was asked to pick up and transfer various objects from a table to a raised platform, providing tactile feedback through electrical stimulation allowed the participant to complete tasks twice as fast compared to tests without stimulation.
In the new paper, the researchers wanted to test the effect of sensory feedback in conditions that would resemble the real world as closely as possible.
“We didn’t want to constrain the task by removing the visual component of perception,” said co-senior author Robert Gaunt, Ph.D., associate professor in the Pitt Department of Physical Medicine and Rehabilitation. “When even limited and imperfect sensation is restored, the person’s performance improved in a pretty significant way. We still have a long way to go in terms of making the sensations more realistic and bringing this technology to people’s homes, but the closer we can get to recreating the normal inputs to the brain, the better off we will be.”
This work was supported by the Defense Advanced Research Projects Agency (DARPA) and Space and Naval Warfare Systems Center Pacific (SSC Pacific) under Contract No. N66001-16-C-4051 and the Revolutionizing Prosthetics program (Contract No. N66001-10-C-4056).
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Materials provided by University of Pittsburgh. Note: Content may be edited for style and length.

Deaths caused by indirect effects of the pandemic emphasize the need for policy changes that address widening health and racial inequities.
More than 15 months into the pandemic, the U.S. death toll from COVID-19 is nearing 600,000. But COVID-19 deaths may be underestimated by 20%, according to a new, first-of-its-kind study from Boston University School of Public Health (BUSPH), the University of Pennsylvania, and the Robert Wood Johnson Foundation.
Published in the journal PLOS Medicine, the study uses data from the National Center for Health Statistics (NCHS) and the Centers for Disease Control and Prevention (CDC) to estimate the number of deaths in 2,096 counties from January to December 2020 above what would be expected in a normal year, or “excess deaths.” For every 100 excess deaths directly attributed to COVID-19, there were another 20 excess deaths not attributed to COVID-19. In other words, 20 out of every 120 excess deaths, or 17%, were not directly attributed to COVID.
The researchers found that the proportion of these excess deaths not directly attributed to COVID-19 was higher in counties with lower average socioeconomic status and less formal education, as well as in counties located in the South and West. Counties with more non-Hispanic Black residents — who were already at high risk of dying directly from COVID-19 — also reported a higher proportion of excess deaths not assigned to COVID-19.
“Our findings suggest that the impact of the COVID-19 pandemic on mortality has been substantially underestimated in many communities across the US,” says study lead author Dr. Andrew Stokes, assistant professor of global health at BUSPH. “Several factors, including severe testing shortages, overwhelmed health care systems, and a lack of familiarity with the clinical manifestations of COVID-19 has likely led to significant underreporting of COVID-19 on death certificates, especially early in the pandemic. Official COVID-19 death tallies also fail to capture the pandemic’s profound social and economic consequences, including the downstream effects of interruptions in receiving health care, loss of employment, evictions, and social isolation and loneliness.”
In addition to deaths directly from the coronavirus that were not recorded as such, some of the excess deaths are likely from indirect consequences of the COVID crisis, including fear of going to the hospital for another condition, or any number of issues caused or exacerbated by the toll that COVID has taken on the economy and on mental health.
“Counties with high levels of COVID-19 mortality also had exceptionally high levels of mortality in 2020 from other causes of death. This result suggests that the epidemic is responsible for many more deaths than are attributed to COVID-19 alone,” says study senior author Dr. Samuel H. Preston, professor of sociology at the University of Pennsylvania.
“Racial and socioeconomic inequities in U.S. mortality have widened significantly as a result of the COVID pandemic, especially when considering total excess deaths. To protect public health, policymakers must act decisively to address structural racism and reduce income inequality,” says study co-author Dielle Lundberg, a research fellow at BUSPH.
Overall, the study makes clear that county-level measures of direct COVID-19 mortality were not accurate measures of excess mortality in many US counties.
“A more complete accounting of COVID-19 deaths in local communities using excess deaths could lead to increased public awareness and vaccine uptake, particularly in areas where the official death counts suggested the pandemic had a limited impact,” Stokes says.
The study was also co-authored by Dr. Jacob Bor, assistant professor of global health epidemiology at BUSPH, and by Dr. Katherine Hempstead of the Robert Wood Johnson Foundation, and was funded by the Robert Wood Johnson Foundation.
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Materials provided by Boston University School of Medicine. Original written by Michelle Samuels. Note: Content may be edited for style and length.

The most populous boroughs in New York City, Queens and Brooklyn, likely served as the major hub of COVID-19 spread in the spring of 2020, a new study finds.
Led by researchers at NYU Grossman School of Medicine, the new investigation analyzed over 800 coronavirus genetic samples to trace the path of the virus as it traveled across New York City during the pandemic’s deadly first wave. It identified Queens and, to a lesser extent, Brooklyn as the likely origin point of most cases sampled, with more cases circulating within their borders and spreading from these parts of the city into Manhattan and the outer boroughs than in the other direction.
“Our findings appear to confirm Queens’ role as the early epicenter of coronavirus transmission throughout the rest of the New York metropolitan area,” says study co-senior author Ralf Duerr, MD, PhD. “Now that we understand how viral outbreaks can spread between neighborhoods, we can better plan for future contagions and prioritize testing in the most vulnerable areas.”
Duerr, a research assistant professor in the Department of Pathology at NYU Langone Health, notes that if a disease that transmits similarly to the coronavirus strikes New York again, it could likely follow the same basic path through the region.
Although more research is needed to identify the underlying reasons behind the spread, the study researchers suspect that commuting likely played a key role. Duerr notes that 35 percent of Queens and Brooklyn workers travel daily to Manhattan by car, subway, and bus. In addition, both of the city’s main airports, LaGuardia and J.F.K., are located in Queens. That Black and Hispanic Americans, who were hit particularly hard by the pandemic, disproportionally use public transportation and live in these two boroughs may have been another possible factor, says Duerr.
Past studies revealed that the coronavirus first took root in New York in late February 2020, with more than a hundred separate outbreak sources bursting into chains of infection rather than from a single “patient zero.” However, the dynamics of viral spread within and between individual boroughs had remained unclear.

If there’s one take-home message for the general public about the coronavirus vaccines approved in the U.S., it’s that they are remarkably effective.
But Michigan State University’s Morteza Mahmoudi is raising awareness about an important subtlety: The vaccines developed by Moderna and Pfizer-BioNTech appear to work slightly better for men than for women.
Both vaccines use tiny orbs, or nanoparticles, to deliver their active ingredients to cells in our immune systems. For years, Mahmoudi has been studying how and why nanomedicines — therapies that use nanoparticles — can affect patients differently based on their sex and he believes this could be a factor with the vaccines.
The Johnson & Johnson vaccine has also drawn attention to sex differences because its rare blood-clotting side effect has affected predominantly women. The J&J vaccine, however, uses modified adenoviruses rather than nanoparticles to help teach our immune systems to fight off the coronavirus. That said, Mahmoudi has shown in earlier work that viruses can transfect the cells of men and women differently.
Now, he’s focusing on the nanomedicine component. He’s published three peer-reviewed papers calling attention to the role of sex in nanomedicine studies, both in general and as they relate to coronavirus vaccines.
“We need to monitor these sex differences and report them to the scientific community and the public,” said Mahmoudi, an assistant professor in the Department of Radiology and the Precision Health Program. “It can be very helpful in developing future strategies and as we prepare for future threats.”
To develop those future strategies, researchers must better understand what causes patients of different sexes to respond differently to nanomedicines, Mahmoudi said. To that end, Mahmoudi is advocating for systemic changes in how nanoparticles are used and studied in medicine with an article published May 20 in the journal Nature Communications.