public health – E JEMED http://e-jemed.org/ Tue, 08 Mar 2022 02:45:00 +0000 en-US hourly 1 https://wordpress.org/?v=5.9.3 https://e-jemed.org/wp-content/uploads/2021/05/default1-150x150.png public health – E JEMED http://e-jemed.org/ 32 32 Study offers insight into molecular biology of the brain in patients with bipolar disorder https://e-jemed.org/study-offers-insight-into-molecular-biology-of-the-brain-in-patients-with-bipolar-disorder/ Tue, 08 Mar 2022 02:45:00 +0000 https://e-jemed.org/study-offers-insight-into-molecular-biology-of-the-brain-in-patients-with-bipolar-disorder/ In an in-depth study of one of the largest postmortem brain samples ever, scientists from the Lieber Institute for Brain Development, in collaboration with researchers from the Johns Hopkins School of Medicine and the Bloomberg School of Public Health , identified significant differences in gene expression in two specific brain regions of hundreds of patients […]]]>

In an in-depth study of one of the largest postmortem brain samples ever, scientists from the Lieber Institute for Brain Development, in collaboration with researchers from the Johns Hopkins School of Medicine and the Bloomberg School of Public Health , identified significant differences in gene expression in two specific brain regions of hundreds of patients with bipolar disorder.

The findings, published today in Natural neuroscience, represent the first time that researchers have been able to apply the discipline and tools of genetic research to brain samples from hundreds of patients with bipolar disorder (BD), a chronic, often debilitating, almost always incurable behavioral syndrome. The findings suggest that bipolar disorder may stem from chemical and structural changes in brain cells that affect how they communicate with each other.

This is the first deep dive into the molecular biology of the brain in people who have died from bipolar disorder; the study of real genes, not urine, blood or skin samples. If we can understand the mechanisms behind BD, if we can figure out what’s wrong with the brain, then we can start developing new targeted treatments for what has long been a mysterious disease. »


Dr. Thomas Hyde of the Lieber Institute and co-author of the article

Bipolar disorder is a severe mental illness characterized by extreme mood swings, with bouts of mania alternating with bouts of depression. It usually appears in people in their 20s and 30s and stays with them for life. It affects approximately 2.8% of the adult US population, or about 7 million people, at a terrible cost, with patients facing higher suicide rates, poorer quality of life and lower productivity than that of the general population. Some estimates put the annual cost of bipolar disease in the United States at $219.1 billion, or $88,443 per person per year. Treatment usually involves psychotherapy and medication and sometimes electroconvulsive therapy. While medications can be helpful in treating bipolar disorder, many patients find that they have bothersome side effects, and for some patients the medications don’t work at all. To develop more effective ways to treat this disease, it is important to understand the biology behind it.

Because the brain is a complex organ with many distinct anatomical and functional regions – and varied gene expression patterns – the scientists limited their study to two key regions of the limbic system, which plays a vital role in regulating behavior, emotions and memory. The regions were the amygdala and the subgenal anterior cingulate cortex (sACC), evidence of which strongly suggests underlying mood regulation and the pathophysiology of bipolar disorder.

Using advanced laboratory techniques, researchers measured levels of messenger RNA, an index of activated and expressed genes, in brain samples from the largest group of patients and normal controls ever assembled for the study. bipolar disorder (511 brain samples from 295 individual donors). ).

The abundance of tissue samples allowed the researchers to observe much more significant differentially expressed genes than had been detected in previous studies. In fact, they observed nearly eight times as many differentially expressed genetic characteristics in sACC compared to amygdala, suggesting that sACC may play a particularly important role – both in the regulation of mood in general and in comics in particular.

The researchers compared genes from control brains with those from individuals with bipolar disorder and found abnormalities in two gene families: one containing synapse-related genes and the second related to immune and inflammatory function. The synapse is the site where nerve cells communicate with each other, while immune and inflammatory genes are also involved in synapse function in the brain. Taken together, these findings suggest that bipolar disorder is caused by chemical and structural changes at the synapse, altering communication between brain cells. This miscommunication manifests as severe mood swings between depression and mania.

The authors of the article highlighted the importance of solving the mysteries of bipolar disorder through advances such as those achieved through basic research.

“This is a road map, not a treasure map,” said Daniel R. Weinberger, MD, chief executive and director of the Lieber Institute and co-author of the study. “We have a much better understanding of where to go as we dig to make new discoveries and develop new treatments.”

“There is finally a study using modern technology and our current understanding of genetics to find out how the brain is doing,” Dr Hyde added. “We know that BD tends to run in families, and there is strong evidence that there are inherited genetic abnormalities that put an individual at risk for bipolar disorder. Unlike conditions such as sickle cell disease, bipolar disorder does not result from a single genetic disease, rather most patients have inherited a group of variants spread over a number of genes.

Dr. Hyde noted that a major clinical study conducted by the National Institutes of Health, known as the Psychiatric Genetics Consortium, involving tens of thousands of people with bipolar disorder as well as normal control subjects, identified 31 variations of the genome that increase the risk. of illness. The current study from the Lieber Institute continues this progress at the genetic level in hundreds of brains.

“By examining messenger RNA in the brains of people with bipolar disorder, we were able to identify several genes that have alterations in the amount of messenger RNA they produce,” Dr. Hyde said. “By identifying these individual genes, we can begin to define the molecular changes that cause highly erratic moods. Ultimately, these findings promise new treatments targeting the abnormal chemical makeup in the brains of people with bipolar disorder.”

“Bipolar disorder, also known as manic-depressive disorder, is a very damaging and paradoxical condition, Dr. Weinberger said. “It can make people very productive so they can run countries and businesses, but it can also throw them into the meat grinder of dysfunction and depression. Patients with BD can live on two hours of sleep by night, saving the world with their abundance of energy, then become so self-destructive that they spend their family’s fortune in a week and lose all their friends as they spiral down. Bipolar disorder also has shared genetic links with other psychiatric disorders, such as schizophrenia, and is implicated in the overuse of drugs and alcohol.”

Dr Weinberger added: “Because society values ​​manic productivity, BD is often not viewed as the terrible disease that it is. But it can be a tragic affliction.”

Source:

Lieber Institute for Brain Development

Journal reference:

10.1038/s41593-022-01024-6

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Aging is still one of the greatest mysteries in biology https://e-jemed.org/aging-is-still-one-of-the-greatest-mysteries-in-biology/ Tue, 25 Jan 2022 14:38:30 +0000 https://e-jemed.org/aging-is-still-one-of-the-greatest-mysteries-in-biology/ My mother lived beyond the mark of the century. In fact, she died a week after her 101st birthday. But she didn’t become one of those mentally and physically robust centenarians that researchers love to study. At the time of her death, my mother was frail and almost bedridden. Dementia twisted his mind, osteoarthritis crushed […]]]>

My mother lived beyond the mark of the century. In fact, she died a week after her 101st birthday. But she didn’t become one of those mentally and physically robust centenarians that researchers love to study. At the time of her death, my mother was frail and almost bedridden. Dementia twisted his mind, osteoarthritis crushed his right knee, then his heart gave out.

Even with health issues, her attitude remained strong. She loved to dance and she was a badass in the gym until she was in her nineties. No matter what happened to her body – she also survived two bouts of breast cancer – her youthful appearance made my mother smile, even when she was weak and in hospice.

Every organism ages, even bacteria. Why aging occurs, however, is still one of biology‘s greatest mysteries. Researchers have offered many theories for why we age, but here’s the most common explanation: Damage begins in our cells from early exposure to everything from environmental toxins to pathogens to bad weather. diet and even lifestyle choices like smoking. Over decades, the altered cells weaken tissues and organs, leading to a decline in sparks throughout the body.

Biologically, we age at different rates; some of us age faster or slower than others, and our chronological age (how long we’ve actually been there) can be out of step with our biological age. To measure these differences, the researchers developed molecular clocks, blood tests that track markers on our DNA. These estimates can tell us how much aging has occurred up to a given time, predict lifespan, and whether those years will be healthy. Another blood test measure tells us how fast or fast we age. This knowledge can anticipate who is most at risk for age-related diseases, such as heart disease, and tell researchers whether or not interventions are working.

Some people at 75 are athletic and independent, while others may need help with daily living. But aging is more than the changes our cells accumulate over time, or the gradual accumulation of molecular damage. We also age mentally and our attitudes matter. How we view aging can help or hurt our own health and impact how we as a society view aging, and these views affect us all. “Aging is not just about living longer; we want healthier aging,” says Allaattin Kaya, a researcher specializing in cellular aging and longevity at Virginia Commonwealth University in Richmond.

“The more we understand about aging, the more the public will understand and the more we will see support for aging,” said Patricia M. D’Antonio, vice president of policy and professional affairs at The Gerontological Society of America in Washington, DC. “We are not falling off a cliff because our society is aging.”

The Why and How of Aging

Our risks of heart disease, cancer and diabetes increase over time. The new field of geroscience aims to understand why by focusing on the basic mechanisms of aging: how aging affects disease and how disease affects aging at the molecular and genetic level. Studying aging is complicated, says D’Antonio, because most people end up with multiple chronological conditions later in life.

My mother was in pretty good shape until her 100th birthday. Shortly after, she caught pneumonia. Doctors said it was mild, but she was sick enough to spend a few days in the hospital. She never regained her old strength and her life sitting in a chair turned into frailty, one of the physical signs of aging. Experts call it functional aging, which indicates how fast we can walk, how many times we get up and down from a chair. She also lost her resilience, another molecular marker of aging.

In general, biological aging reflects changes that occur in our cells, blood chemistry and organ function also change over time, says Daniel Belsky, a genetic epidemiologist at Columbia University Mailman School of Public Health. Determining our biological age and rate of aging can help predict a person’s life expectancy and whether those years will be healthy.

Belsky and a team of researchers have designed a molecular tool that measures the rate of aging. This tool can tell you if you are aging faster or slower compared to a calculated standard. They based the algorithm on data collected at multiple points over the years, from 1,000 babies born in 1972 in Dunedin, New Zealand. The measurement is more like a speedometer than a clock, Belsky says. This tool has also been tested in a clinical trial that studied calorie restriction. In this study, the algorithm was able to show that the treatment group had a slower rate of aging.

While these tools give researchers a way to measure such interventions, they are still in the early stages. “We are closer to the start than the end of the development of these biomarkers,” says Belsky

Those golden years

Our attitudes can also impact how we age. These biases start when we’re young, says Di’Antonio. Negative attitudes toward aging are everywhere you look, from birthday cards to commercials to sitcoms.

Age biases can turn us against older people, so we blame them for their health issues, such as type 2 diabetes, Di’Antonio says. People will say, “If only you had eaten well, you wouldn’t have all these problems now,” she says. These attitudes ignore the fact that people can live their lives in areas without grocery stores or even sidewalks. Working three jobs just to survive financially may leave no time for exercise.

Di’Antonio leads the Reframe Aging project, an effort to change the public’s understanding of aging, but changing attitudes will take a generation of work, she said.

Beyond that, our own perceptions of aging can affect our behavior and, therefore, our health. If we think of ourselves as too old for a particular activity, for example, it can cause us to become disengaged and sedentary. Or the constant stress of aging can also have physical and mental consequences. “Beliefs play a huge role in what we do and how we feel about what we do,” says Lindsay Ryan, research associate at the University of Michigan, Ann Arbor.

But research also shows health benefits in people with positive self-perceptions about aging. Plus, it’s normal to have both negative and positive self-perceptions about getting older, Ryan says. “Older people may face declining health and social loss, but can still find satisfaction and meaning in their relationships and activities.”

My mother knew both sides of this double-edged sword. She stayed strong until she couldn’t anymore. At 90, she was healthy enough for knee replacement surgery, but chose not to have the operation – and that’s the kind of choice we should all have. Although I may not live to see my 100th birthday, I hope that mental and physical strength will age as my mother did.

This article was written with the support of a Journalism Fellowship from the Gerontological Society of America, the Journalists Network on Generations, and the John A. Hartford Foundation.

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Third Round of Presidential Interdisciplinary Seed Grants Awarded https://e-jemed.org/third-round-of-presidential-interdisciplinary-seed-grants-awarded/ Tue, 18 Jan 2022 14:12:19 +0000 https://e-jemed.org/third-round-of-presidential-interdisciplinary-seed-grants-awarded/ How can nanotechnology and big data be used to improve the diagnosis of infectious viruses like SARS-CoV-2? This is one of the questions that will be explored with funding provided by a third round of Presidential Interdisciplinary Seed Grants. Eleven grants totaling $1.5 million were awarded in November 2021 to recipients of the third round […]]]>

How can nanotechnology and big data be used to improve the diagnosis of infectious viruses like SARS-CoV-2?

This is one of the questions that will be explored with funding provided by a third round of Presidential Interdisciplinary Seed Grants.

Eleven grants totaling $1.5 million were awarded in November 2021 to recipients of the third round of Presidential Interdisciplinary Seed Grants. Overall, the awards went to faculty from 13 UGA departments, centers, programs, schools and colleges.

The program was launched in 2017, with a second round of grants in 2019, through a partnership between UGA Research and UGA Public Service and Outreach. The teams from the first two rounds were very successful in securing external funding to continue the work initiated through these seed grants.

“I am thrilled with the continued success of this program as the University of Georgia seeks ways to grow our research enterprise and expand the impact of our faculty,” said President Jere W. Morehead. “Research funding opportunities such as the Presidential Interdisciplinary Seed Grants are investments in the future of our state, our nation, and the world as well as our university.”

A total of 89 faculty teams submitted research proposals in the third round, targeting important local, national or global challenges that align with UGA’s goals. 2025 Strategic Plan. Examples include areas identified by the Provost’s Task Force on Academic Excellence (Precision Agriculture, Security, Climate and Environment, Brain and Behavioral Sciences, and Data Science and AI), as well as those requiring collaboration. between social/behavioural and biomedical faculties.

“UGA faculty are finding creative ways to explore the challenges that affect our daily lives,” said Karen Burg, vice president for research. “We look forward to seeing how their collaborations across the board will lead to new approaches and innovative solutions.”

A project co-led by Lisa Renzi Hammond and Jenay beer will develop a UGA center focused on addressing statewide disparities in prevention and access to health care for Alzheimer’s disease and related dementias (ADRD).

Lisa Renzi-Hammond (Photo by Peter Frey/UGA)

“SARD will impose an annual burden of $1 trillion on the health care system by 2050,” said Renzi-Hammond, co-lead researcher and associate professor at the College of Public Health. “Rural Georgia has limited education and programs to prevent MADR, limited opportunities to participate in clinical research, and limited access to diagnostic and support resources, but the risk factors – advanced age, poor nutrition, poverty , comorbidities, obesity, etc. – are more important. frequent.”

“We envision a Georgia in which everyone has access to early, accurate diagnosis and treatment,” said Jenay Beer, co-principal investigator and associate professor in the College of Public Health and School of Social Work. “To achieve this goal, we have established the Center for Research and Education in Cognitive Aging, which will provide statewide community dementia prevention education, caregiver training of health and the development of a digital health infrastructure for diagnosis, as well as an adapted geographical and cultural post-training. diagnostic support, connection to care and treatment, and opportunities to participate in cutting-edge research.

Assistant Professor Jenay Beer sits next to an interactive companion robot. (Photo by Peter Frey/UGA)

The team has already begun offering dementia education workshops in four Archway Partnership communities: Grady, Hart, McDuffie and Washington counties. This funding will expand their program to two additional Archway communities. The Archway Partnership is a public service and outreach unit of UGA.

Renzi-Hammond and Beer are senior professors at UGA’s Institute of Gerontology. The team also includes Denise Dixon Everson (UGA Extension, Faculty of Agricultural and Environmental Sciences); Bernadette Heckman (College of Education); Donald Scott (Augusta University/UGA Medical Partnership); Sharon Ligget (Archway Partnership); Devin Lavender (College of Pharmacy); Timothy Heckman and Grace Bagwell Adams (College of Public Health); Laurent Doux (Franklin College of Arts and Sciences); Alexander Scherr (Law School); and Tiffany Washington (School of Social Work).

“I am encouraged by the number of faculty across campus who will collaborate to address some of our state’s challenges,” said Jennifer Frum, vice president of public service and outreach. “Part of UGA’s mission, as the state’s land-grant and maritime-grant institution, is to extend our knowledge and expertise to help communities thrive.”

Yiping Zhao is Emeritus Research Professor of Physics at UGA’s Franklin College of Arts and Sciences. (Photo by Andrew Davis Tucker/UGA)

A project, led by the Principal Investigator Yiping Zhao, aims to combine nano-optics and machine learning techniques to develop a rapid, portable and cost-effective point-of-care method to detect viruses – such as SARS-CoV-2 – and bacterial infections in patients.

“Mitigation of epidemic and pandemic diseases like COVID-19 will require improved diagnostic methods,” said Zhao, research professor emeritus of physics at Franklin College of Arts and Sciences. “Preliminary results have shown that our approach can provide direct and differential detection of important respiratory viruses within 20 minutes.”

Zhao’s team includes Ralph Trip and Hemant Naikare (College of Veterinary Medicine), Xianyan Chen (Franklin College of Arts and Sciences) and external collaborators.

Additional proposals that have received funding from the Presidential Interdisciplinary Seed Grant include:

  • “Integrated Approaches to Treat Current and Future High-Consequence Biological Agents.” Franklin E. Leach III (Senior Investigator, College of Public Health, Center for Complex Carbohydrate Research); Fred Quinn, Danny Mead, Jeff Hogan and Eric Lafontaine (College of Veterinary Medicine); and Ryan Weiss and Michael Tiemeyer (Franklin College of Arts and Sciences, CCRC).
  • “The THRIVE Project: Developing a Mother-Centered ‘Lay Doula’ Communication Intervention to Improve Outcomes for Black Mothers.” Soroya McFarlane (Senior Researcher, Franklin College of Arts and Sciences); Andrea Swartzendruber and Tamora Callands (College of Public Health); and external collaborators.
  • “From the Ethics of AI to the Aesthetics of AI: Artificial Intelligence and Aesthetic Damage.” Aaron Meskin (Senior Researcher, Franklin College of Arts and Sciences); Peng Yuan Wang, Rosanna Smith and Caroline Salge (Terry College of Business); David Saltz, Isabelle Wallace and Katie Geha (Franklin College of Arts and Sciences); and Anne-Abraham (College of Education).
  • “Molecular-Level Biodosimetry for National Security: Proteomics, Glycomics, Epigenetic, and Metabolomics Approaches for the Quantitative Assessment of Low-Dose Radiation Exposure.” Olin “Gene” Rhodes (Principal Investigator, Savannah River Ecology Laboratory, Odum School of Ecology); Franklin Leaching (College of Public Health, Center for Complex Carbohydrate Research), Michael Tiemeyer and Lance Wells (Franklin College of Arts and Sciences, CCRC); and Ben Parrot (SREL, Odum School of Ecology).
  • “Assessing the agrivoltaic potential of emerging perovskite-based solar cells for greenhouse applications.” Susanne Ullrich (Senior Researcher, Franklin College of Arts and Sciences); Tho Nguyen (Franklin College of Arts and Sciences), Marc van Iersel (College of Agricultural and Environmental Sciences), Maric Boudreau and Richard Watson (Terry College of Business), and Tom Lawrence (Higher School of Engineering).
  • “An interdisciplinary school health center in partnership with the Clarke County School District, the University of Georgia, and the University of Augusta/University of Georgia Medical Partnership.” (Suzanne Lester, Principal Investigator, AU/UGA Medical Partnership); Theresa Rohr Kirchgraber, Carrie Kelly Marguerita Tresa Chappell, Lia Bruner and John Chin (AU/UGA Medical Partnership); Edward Delgado-Romero (College of Education); Megane Ford (College of Family and Consumer Sciences); and Jason Cade (Law School).
  • “Aflatoxin Research and Mitigation Center of Excellence in Georgia.” (Harald Scherm, Principal Investigator, College of Agricultural and Environmental Sciences); Thirimachos Bourlai, Jaime Camelio and Changing “Charlie” Li (College of Engineering); Robert Kemerait, Christiane Pilon, Glen Rains and George Vellidis (College of Agricultural and Environmental Sciences); and Alicia Peduzzi (Warnell School of Forestry and Natural Resources).
  • “Bloom and Doom: Is Increased Risk of Harmful Algal Blooms an Inevitable Consequence of Global Change? Assessing Risks and Exploring Strategies in Georgia from Biological and Social Perspectives.” (Cory Struthers, Principal Investigator, School of Public and International Affairs); Peter Hazelton (Warnell School of Forestry and Natural Resources); michelle ritchie (College of Public Health); and Alex Strauss and Krista Caps (Odum School of Ecology).
  • “Developing New Storm Design Criteria for Natural Hazard Planning Research and Practice.” (Scott Pepin, Principal Investigator, Carl Vinson Institute of Government, a UGA Public Service and Outreach Unit); Brian Bledsoe (College of Engineering); Marshal Shepherd, John Knox, Pam Knox, Lynne Seymour and Thomas Mote (Franklin College of Arts and Sciences); and michelle ritchie (College of Public Health).
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New rules on fly ash disposal are “positive step”, but experts say health and ecological risks persist https://e-jemed.org/new-rules-on-fly-ash-disposal-are-positive-step-but-experts-say-health-and-ecological-risks-persist/ Thu, 06 Jan 2022 01:30:33 +0000 https://e-jemed.org/new-rules-on-fly-ash-disposal-are-positive-step-but-experts-say-health-and-ecological-risks-persist/ [ad_1] New Delhi: Thermal and lignite-fired power plants that do not use 100% of the fly ash they generate in an “ecological” way will now be subject to sanctions, under a new set of rules notified by Narendra Modi’s government. Fly ash is the residue from the combustion of coal which, if disposed of improperly, […]]]>


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New Delhi: Thermal and lignite-fired power plants that do not use 100% of the fly ash they generate in an “ecological” way will now be subject to sanctions, under a new set of rules notified by Narendra Modi’s government.

Fly ash is the residue from the combustion of coal which, if disposed of improperly, is hazardous to health and the environment due to the concentrated presence of heavy metals.

The notification from the Union’s Ministry of the Environment, Forests and Climate Change intends to “establish a global framework for the use of ash, including an environmental compensation system based on the polluter pays principle”. This is a first in the country.

Thermal power plants must use 100% of their annual fly ash production over a three-year cycle to avoid penalties, the Dec. 31 notification says, adding that “at no time” should usage drop below 80 %.

Factories that fail to achieve 100% utilization levels during this period will be required to pay Rs 1,000 to the Central Pollution Control Board (CPCB) per tonne of unused ash.

The notification recognizes “legacy ash”, or the build-up of fly ash by thermal power plants over decades, indicating that they are to be used over a period of 10 years from the time the notification becomes applicable, from April 1, 2022. The inherited ash must be processed “beyond” the annual ash production by power plants, the notification said.

India has over 200 coal-fired power plants which generate a huge amount of fly ash. According to the Central Electricity Authority, India’s coal-fired power plants generated 232.56 million tonnes of fly ash in 2020-2021. Although 93 percent of it has been used, millions of tonnes accumulated over the years go unused.

A to study by think-tank Center for Science and Environment in March 2021 found that more than half of India’s power plants were not making full use of their fly ash and falling behind previous government targets.

The new notification will replace the 1999 notification which originally established rules for the use of fly ash. It will also replace the various modifications of the 1999 notification made in 2003, 2009 and 2016, all of which were aimed at managing the generation of fly ash.


Read also : The world has a new path to sustainable energy and net zero emissions – “green hydrogen”


“Ecological” use

The latest notification is largely similar to the draft which was released for public comment in April 2021.

The dumping of fly ash on the ground must be avoided and it must be treated in an “ecological” manner, says the new notification.

It lists “the only” ways fly ash can be used, which include making bricks, tiles, cement, building roads, and exporting to other countries. It also allows the “filling of low areas”, the filling of empty mines and “agriculture in a controlled manner based on soil analyzes”.

The notification adds that the compensation money collected by the CPCB for ash that has not been used will be used “for the safe disposal of unused ash” as well as for research on ash products.


Read also : Solid waste could play an important role in the supply of airlines


What the experts say

According to experts, the introduction of a penalty for non-compliance and recognition of inherited ash is a step in the right direction, but there are other aspects that the notification does not adequately address.

“The notification calls low-lying area filling an environmentally friendly method of using fly ash, but more often than not, it is a euphemism to dump ash irresponsibly. Dumping of ash into low-lying areas can result in serious ecological consequences, ”said Sehr Raheja, researcher at Manthan Adhyayan Kendra, a civil society organization that wrote to the government in April last year, when comments on the draft notification were requested.

A report by Manthan found that there had been eight major fly ash breaches between 2019 and 2021, leading to destruction and contamination.

While the notification states that all annual and old ashes are to be used, it also makes provision for ashes stored in dikes and ponds – structures built for the disposal of large amounts of ash – stating that as long as this storage is “stabilized” or recovered by growing plantations, CPCB certified coal-fired power stations may be excluded from the 10-year period.

“We are also concerned that this will create a loophole for coal-fired power plants not to use their legacy ashes,” Raheja added.

The Think tank Center for Policy Research (CPR) also submitted comments in April of last year, stating that a 10-year deadline to comply with 100% use of legacy ash “alleviates the legal burden of compliance but allows illegal dumping of overloaded ash dikes to continue »Despite the risk of accidents and contamination.

The CPR also said that the draft notification did not address the issue of the generation of fly ash, which is the underlying cause of the build-up and environmental damage. He also urged the government to recognize that fly ash poses a danger to public health.

“It is essential to take political action to link the use of fly ash to measures taken by the government to prevent illness and death and to provide health services. The environmental regulations that emerge from this ‘fly ash as a health risk’ approach have the potential to identify remedies to address the impact of the legacy and prevent future violations of the law, ”wrote the CPR in its comments.

However, the final notification does not include this point.

(Edited by Amit Upadhyaya)


Read also : 1260-150 – why power lines are the ‘greatest threat’ to the Indian great bustard


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The science behind the rapid spread of Omicron https://e-jemed.org/the-science-behind-the-rapid-spread-of-omicron/ Sat, 18 Dec 2021 10:30:00 +0000 https://e-jemed.org/the-science-behind-the-rapid-spread-of-omicron/ [ad_1] As Omicron has quickly become the dominant variant of the coronavirus in South Africa and the UK, scientists are starting to piece together what gives it its evolutionary advantage. Researchers are further refining and expanding their findings, but Omicron’s increased transmissibility appears to be a combination of several properties: it appears to be able […]]]>


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As Omicron has quickly become the dominant variant of the coronavirus in South Africa and the UK, scientists are starting to piece together what gives it its evolutionary advantage.

Researchers are further refining and expanding their findings, but Omicron’s increased transmissibility appears to be a combination of several properties: it appears to be able to bind more easily to and break down in human respiratory cells; it seems to replicate faster once in our body; and it can substantially evade the immunity acquired from a previous infection or vaccination.

These advantages mean that Omicron is spreading across the world at a tremendous rate. Since scientists in South Africa first reported its presence last month, it has been detected in 77 countries and is likely present in most others, according to the World Health Organization.

Cases of Omicron have been detected in the United States, across Europe and Africa, and in China, which maintains strict border controls and a strict regime to handle even tiny epidemics.

“Omicron is spreading at a rate that we haven’t seen with any previous variant,” WHO Secretary-General Tedros Adhanom Ghebreyesus recently said.

In New York and New Jersey, Omicron is estimated to account for around 13% of Covid-19 cases in the week to December 11.


Photo:

Ed Jones / Agence France-Presse / Getty Images

There are signs that the variant is associated with less severe disease than earlier versions of the virus. Scientists warn, however, that the severity can vary from place to place depending on factors such as immunity levels and characteristics of the population, and that while it is not as dangerous, its ease of transmission means that Omicron could still cause waves of illness and death.

There are more and more examples of Omicron’s surprising transmissibility. After a Christmas party on November 26 for a renewable energy company at an Oslo restaurant, 80 of 111 guests tested positive for the coronavirus, with genetic sampling suggesting all were likely Omicron, according to the Norwegian Institute of public health.

In Hong Kong, a 36-year-old man was identified as one of the first known cases of Omicron on November 13 at one of the city’s quarantine hotels. Five days later, a 62-year-old man remaining in the room across the hall also tested positive for the variant, although he had no contact with his neighbor. The researchers concluded that the variant must have crossed the hallway.

In the UK, Omicron replaced Delta as the dominant variant of the coronavirus in England and Scotland in less than a month and it is only a few days behind Denmark, according to Danish health authorities. It is already the dominant variant in Ontario, Canada, accounting for 51% of new cases, according to a panel of scientists advising the provincial government. British health data suggests Omicron cases are doubling across much of the country in less than two days.

In the United States, the Delta variant accounted for about 96% of cases across the country in the week to December 11, while the Omicron variant accounted for about 3%. Some regions have higher figures: in New York and New Jersey, Omicron is estimated to account for around 13% of Covid-19 cases.

Behind Omicron’s rapid spread is a host of mutations that give it an advantage over older variants.

A number of studies indicate that Omicron is more resistant to current vaccines than previous variants of Covid, although boosters seem to be helping. WSJ’s Daniela Hernandez gets exclusive insight inside a lab testing how antibodies interact with Omicron. Photographic illustration: Tom Grillo

Of the approximately 50 mutations in Omicron, at least 30 are on the spike protein, the structure that helps the virus infiltrate cells and is also the primary target of vaccines.

Laboratory tests in South Africa, Sweden, the United Kingdom and the United States have shown that the ability of antibodies to prevent the variant from entering cells is lower than with other strains, which which gives Omicron a much better chance of infecting people who have already been vaccinated or infected. This means that it can spread quickly even in highly vaccinated populations.

Modeling released Friday by researchers at Imperial College London estimates the risk of re-infection with Omicron to be 5.4 times greater than with Delta, suggesting limited protection against a previous infection. The study, which was not peer-reviewed, also reported a reduction in vaccine efficacy against Omicron infection after two doses, compared to Delta.

Almost 70% of the UK population is fully vaccinated, but Omicron has propelled a record number of cases, prompting the government to ask people to work from home where possible, to limit mixing with other households in the days leading up to Christmas and receiving booster shots to build additional immunity. Denmark and Norway have also tightened public health restrictions to fend off a wave of cases.

A Covid-19 research lab in South Africa, where scientists first reported the presence of Omicron.


Photo:

Waldo Swiegers / Bloomberg News

“If the virus is able to partially evade the immune response induced either by a previous infection with another variant or by vaccines, then it can become infected and spread more efficiently.” This is what we see with the Omicron variant, ”said Lawrence Young, virologist and professor of molecular oncology at the University of Warwick.

A growing body of evidence suggests that Omicron’s mutations may also give it inherent transmission benefits in addition to its ability to evade the body’s immune responses.

A study, not yet peer-reviewed, conducted by researchers in Hong Kong found that Omicron infects and multiplies 70 times faster than the Delta variant in the airways, which could explain why the new variant appears to be transmitted. faster.

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Things were different in the lungs, however, researchers found that Omicron replicates less efficiently in the lungs than the original version of the virus, which may help explain why Omicron has been linked to less severe disease in many. people it infects.

Another study, also not yet peer-reviewed, appears to corroborate the findings of the Hong Kong team: researchers showed that an Omicron pseudovirus – a synthetic version of the Omicron variant – was better at infecting cells than a Delta pseudovirus and the original version of the virus.

If the virus multiplies faster, “it can start spreading to others sooner,” said Julian Tang, clinical virologist and professor of respiratory medicine at the University of Leicester.

British public health officials say Omicron’s benefits mean the interval between one newly infected person becoming infectious to others appears to be shorter with Omicron, perhaps three days compared to six or more with Delta. They also estimated that the risk of someone passing the virus to another member of their household is three times higher with Omicron than with Delta.

One metric epidemiologists use to measure a virus’s transmissibility is its effective reproduction number, or R, the average number of people an infected person will infect. This will vary from place to place depending on the levels of immunity and the public health policies in place to control transmission. The higher the value, the more transmissible the virus is.

Nearly 70% of Britain’s population is fully vaccinated, but Omicron has propelled a record number of cases, prompting the government to ask people to get vaccinated.


Photo:

tolga akmen / Agence France-Presse / Getty Images

Susan Hopkins, who heads the UK Health Security Agency, told lawmakers in the UK Parliament on Thursday that her agency estimates Omicron’s current R-value to be between 3 and 5. The overall R-value of the UK outbreak is about 1 to 1.2, she says.

This high level of transmission is problematic, say scientists, even though Omicron is found to cause milder disease, especially in people who have been vaccinated or with a degree of immunity from a previous infection. Booster shots have been shown to increase protection against infection. Scientists are generally optimistic that vaccines will help ward off serious illness and death with Omicron.

An article awaiting peer review by disease modellers at the London School of Hygiene and Tropical Medicine, described several possible scenarios for the coming months in England as Omicron continues to spread, which varied in the how far the variant could evade immunity and how effective the boosters were. slowing down of infection. All of the scenarios indicate many more cases, hospital admissions and deaths.

“We better be careful not to predict it’s less serious, so it’s going to be better,” said Anthony Fauci, chief medical adviser to President Biden, in an interview with The Journal podcast of the Wall Street Journal. , published Thursday.

“Because if you infect a lot more people, the lack of severity could be overcome by having a lot more people infected. “

Write to Jason Douglas at jason.douglas@wsj.com and Sarah Toy at sarah.toy@wsj.com

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UK provides clues as to how Omicron could play in the US https://e-jemed.org/uk-provides-clues-as-to-how-omicron-could-play-in-the-us/ Fri, 10 Dec 2021 18:03:00 +0000 https://e-jemed.org/uk-provides-clues-as-to-how-omicron-could-play-in-the-us/ [ad_1] LONDON — The UK is emerging as a testing ground in the battle for dominance between the new Omicron variant of the coronavirus and Delta, the earlier strain that is currently the cause of most infections in the US- United and Europe. How Britain Behaves Against Omicron will offer clues to the United States […]]]>


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LONDON — The UK is emerging as a testing ground in the battle for dominance between the new Omicron variant of the coronavirus and Delta, the earlier strain that is currently the cause of most infections in the US- United and Europe.

How Britain Behaves Against Omicron will offer clues to the United States and the rest of the industrialized world about how the variant behaves in a highly vaccinated population, how sick people get and whether its dozens of mutations have given Omicron a sufficient edge on the scalable scale to deprive Delta of the hosts it needs to stay on top.

South Africa alerted the world to Omicron in late November and is seeing a rapid rise in infections with the new variant.

But scientists say it may not be a reliable model for what could happen with Omicron in the US and Europe, as it has lower vaccine coverage, a younger population, and the variant is not. not compete with a lot of Delta cases. It’s summer in the southern hemisphere too, and the virus tends to spread more easily when people are clustered indoors in the winter. Many South African cases have been mild.

New hospitalization data published in South Africa has indicated that Omicron causes a milder infection than previous variants, even though it spreads faster.

Michelle Groome, who heads the public health division of the South African National Institute of Communicable Diseases, told a press conference on Friday that researchers found a disconnect between infections and hospitalizations compared to previous strains , with fewer hospitalizations among those infected and a slight increase in the number of deaths. She warned that the results could be due to the limited sample size at the start of the wave.

The UK is more like the US and will likely be a better guide to how Omicron plays out – and not for the first time, having been hit by the Alpha variant earlier than North America. Its population is older than that of South Africa, vaccination coverage is widespread and, since an almost complete reopening in the summer, it has experienced a sustained but manageable period of Delta cases, hospital admissions and death. It also has a sophisticated surveillance system to monitor variants, and its doctors and scientists are posting tons of data and analysis on Covid-19.

Scientists and vaccine makers are studying Omicron, a variant of Covid-19 with around 50 mutations, which has been detected in many countries after spreading to southern Africa. Here’s what we know as the United States and others enforce travel restrictions. Photo: Fazry Ismail / EPA-EFE / Shutterstock

Now, with more confirmed cases than the US or anywhere in Europe, the UK is facing Omicron. Prime Minister Boris Johnson reimposed some public health restrictions in England this week in a bid to stem the spread of the new variant, as public health officials warned Omicron was set to cause a million infections in Britain by the end of the month. Omicron cases are doubling every two or three days, public health officials say, pointing to the variant’s potential to displace Delta as the more common variant within weeks.

Still, there are unanswered questions about the extent of Omicron’s transmission advantage over Delta, and to what extent it can evade immunity conferred by a previous infection or vaccination. Another pressing question is whether vaccination will protect people against serious illnesses. Delta could prove difficult to dislodge. The unfolding of the Omicron wave in the UK should provide some answers, scientists say. Omicron has been detected in 23 US states, according to the Centers for Disease Control and Prevention.

Omicron samples in Elandsdoorn, South Africa.


Photo:

Jérôme Delay / Associate Press

“It is impossible to understand what is going on here without knowing what is going on in the UK, South Africa and other places where the variant has appeared,” said Philip Landrigan, director of the Health Program. global public and the common good. at Boston College.

Confirmed cases of Omicron in the UK totaled 1,265 on Friday, up from 448 the day before. Health Secretary Sajid Javid said this week that the true number of infections could be closer to 10,000 and the variant is rapidly gaining ground.

Scientists on a panel advising the government said on Wednesday that without certain restrictions, Omicron hospital admissions could reach 1,000 per day by the end of the year if the variant continues to spread to its current pace. This would add to the number of admissions caused by Delta. The seven-day average of new Covid-19 cases in the UK was 49,200 on Friday – a weekly rate of over 500 per 100,000 people – and hospitalizations are around 790 per day.

The panel sketched out six scenarios for how the Omicron phase of the pandemic could play out.

The first three, which the modelers advising the government say are the most likely, are that Omicron has a transmission advantage over Delta and may partially evade immunity conferred by vaccination or a previous infection. , thereby expanding the pool of people who may be infected. These advantages mean that Omicron would ultimately outperform Delta, just as Delta would push back earlier variants such as the Alpha.

A Covid-19 testing clinic in London.


Photo:

Stephen Chung / Zuma Press

“The only way one infection leads another to extinction is when they compete for the same resources – sensitive people,” said Matt Keeling, director of the Zeeman Institute for Systems Biology and Infectious Disease Epidemiology Research at the University of Warwick.

The difference between the three scenarios is the severity of the situation in terms of the number of infected people who need to be hospitalized. While scientists are optimistic that vaccines will continue to protect most people against serious illness with Omicron, the grim prognosis is that even though the number of admissions linked to each Omicron case is lower than that of Delta, The other benefits of the variant mean the scale of the epidemic could still lead to an upsurge in serious illness, stretching the capacity of the state-run national health service to cope. A greater severity of the disease would mean a more deadly wave.

“Omicron made the road a little colder”


– Graham Medley, Professor of Infectious Disease Modeling at the London School of Hygiene and Tropical Medicine

In an effort to slow Omicron, Mr Johnson on Wednesday asked the British to work from home where possible, wear masks in indoor public spaces and prepare to show proof of vaccination or a Covid-19 test negative to enter nightclubs and other places.

The remaining scenarios, according to the panel, are less likely. In one, Omicron does not have a greater ability than Delta to circumvent immunity, but has a transmission advantage. That would mean it would eventually displace Delta, but Britain’s immunity bulwark is keeping the outbreak in check.

In another, Omicron turns out to be less dangerous than expected due to continued exposure to Delta, which was not as prevalent in South Africa when the new variant appeared, bolsters protection against Omicron. The last possibility is that Delta will stay on top and Omicron will break out sporadically during small outbreaks. This happened with the Beta variant, which also spread quickly in South Africa but never established itself in Britain or the United States.

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Evidence from laboratory studies suggests that booster shots should improve people’s protection against Omicron. The UK has given boosters to nearly 22 million people, or one-third of its population, and the government has expanded those eligible to anyone over 18 and shortened the interval between second doses and reminders at three months.

Graham Medley, professor of infectious disease modeling at the London School of Hygiene and Tropical Medicine and co-chair of the panel’s modeling group, compared the last phase of the pandemic to driving a car. Vaccines, booster shots, and precautions such as wearing masks act as seat belts and safety checks, reducing a person’s risk of being injured in an accident.

“Omicron made the road a little bit colder,” he said.

Corrections and amplifications
An earlier version of this article said the UK coronavirus case rate was nearly 500 per 100,000 people, without specifying that this was a weekly rather than a daily figure. With an update based on data from Friday, the weekly case rate now exceeds 500 per 100,000 people. (Corrected December 10, 2021)

Write to Jason Douglas at jason.douglas@wsj.com

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Athens News Matters: Dr John Drake discusses new Omicron variant of COVID-19 | WUGA https://e-jemed.org/athens-news-matters-dr-john-drake-discusses-new-omicron-variant-of-covid-19-wuga/ Fri, 03 Dec 2021 22:08:47 +0000 https://e-jemed.org/athens-news-matters-dr-john-drake-discusses-new-omicron-variant-of-covid-19-wuga/ [ad_1] The science of disease modeling can give public health officials clues as to how far and how quickly diseases like the coronavirus can spread, and their severity. Omicron is yet another variant of COVID-19, and researchers and public health officials are actively working to find more information on this new twist in the ongoing […]]]>


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The science of disease modeling can give public health officials clues as to how far and how quickly diseases like the coronavirus can spread, and their severity.

Omicron is yet another variant of COVID-19, and researchers and public health officials are actively working to find more information on this new twist in the ongoing coronavirus saga.

The thing we need to understand now is how Omicron is going to react to the pressure of vaccines.

As public health officials scramble to locate the virus, other researchers plan to model the future of the disease and its spread.

Dr John Drake, professor at the Odum School of Ecology at the University of Georgia and director of the University Center for Infectious Disease Ecology, joins Chris Shupe of WUGA to talk about the science behind the prediction the behavior of pathogens and what the future might look like. stand for the new Omicron variant of Covid.

This transcript has been edited for clarity

Chris Shupe:

Welcome to Athens News Matters.

Dr. John Drake:

Hello, Chris.

CS:

So, before we get into the actual variant, let’s quickly review the process of modeling an infectious disease. What key factors are considered when creating a model for a disease?

JD:

Basically what a model is is a representation of what we think is happening in a process in nature. So, with infectious diseases, we could, for example, develop a model of transmission or movement of the virus in space. And in fact, in the case of Omicron, one of the things that I think will be the most useful in the coming weeks are the scalable models.

CS:

Hmm. That looks interesting. Tell me a little more about the evolutionary models.

JD:

The virus itself has a genome. And as an RNA virus, this genome mutates a lot. The variants we have seen arise when there are specific mutations that give the virus new properties. If we have a model of how these changes happen, then maybe we can infer some things about how fast they spread.

CS:

I suspect there is nothing really easy about any of this. But is it a little easier to model a variant of a pre-existing disease than, say, a new infectious agent?

JD:

Certainly. So when SARS-CoV-2, which is the virus that causes COVID-19, was first discovered in late 2019 and early 2020, we knew very little about its transmission. How come people catch it from each other? Of course, the thing we need to understand now is how Omicron is going to react to the vaccine pressure. Our vaccines have been developed to target earlier variants, including Alpha and Delta. We don’t yet know how well they will work against Omicron. And there are some clues in the genetic sequence of the Omicron virus that suggest it might not work as well against Omicron as it does against Delta.

CS:

Interesting. I know we have the current COVID models. What more can these models suggest when we look at Omicron?

JD:

Well, one of the things we know from modeling exercises is that it’s very, very difficult to keep a virus out of one place. But there was a very rapid response all over the world restricting the movement of people. And I guess to some extent that might be helpful as far as Omicron is concerned, to save some time while we develop our answer. But one of the things the models show us is that it’s not an effective long-term response.

CS:

Thinking back to COVID-19, in general, tell us a bit more about how these models actually helped officials decide certain steps to try to contain the virus.

JD:

One of the things I think they are very useful for is looking at the effectiveness of different practices and policies. So, for example, the effectiveness of face masks, which we know are effective against all variants. Another thing that we can use models for is decision support. So we can ask “if then” questions. One of the things the models have shown us is that if we were to deploy vaccines more effectively, if we would have higher vaccine coverage, then containment would actually be much more achievable. But there is also the will of the people to receive these vaccines, and the models cannot solve that problem for us.

CS:

Well I know there is so much we don’t know, especially about this new variant. But from what you know, what are some of the concerns we should have about this new variant?

JD:

So, most of what we know about Omicron at this point comes from the sequence of genes. We know that major vaccine manufacturers like Pfizer and Moderna, and Johnson & Johnson are studying the effectiveness of their vaccines against the Omicron variant. And we can expect the data from these companies to be probably within a week to 10 days. One thing that is really important is that there have been 32 distinct mutations associated with a single gene known as “S” because it encodes the spike protein. The spike protein is important because it is found on the immune response and therefore the standard vaccine target. So that’s why it’s entirely possible that Omicron is what people call an escape variant.

In addition to these mutations that could confirm immune evasion, there is another interesting angle called S-Gene Target Failure. S, or spike, is just one of the genes targeted by PCR. And in some of those PCR tests, the S gene fails. We are therefore unable to detect the spike protein. And so when that happens what you have is a PCR test that says there is something special about this variant. I expect that many countries around the world will use S-Gene Target Failure to try to follow Omicron’s path during the outbreak, and I expect that here in the United States, we will mainly focused on genome sequencing.

CS:

So what does all of this mean for our listeners as we all head for the holidays?

JD:

You know Chris, the thing to remember is that the biggest threat in the United States is still the Delta variant. And we know the vaccine works great to protect against Delta. People who have not been vaccinated should be vaccinated if they are eligible. And then the other thing is that masks and physical distancing work against all variants.

CS:

Fair enough. Dr John Drake is Professor at UGA and Director of the University Center for Infectious Disease Ecology. Thanks for stopping by.

JD:

Thanks, Chris. It’s my pleasure.

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The omicron variant is a mystery. Here’s how science will solve it https://e-jemed.org/the-omicron-variant-is-a-mystery-heres-how-science-will-solve-it/ Thu, 02 Dec 2021 20:45:29 +0000 https://e-jemed.org/the-omicron-variant-is-a-mystery-heres-how-science-will-solve-it/ [ad_1] From last Friday, the race was on, between a virus and information about it. And for a while, information circulated faster, although there was hardly any. Scientists in South Africa have identified a new variant of the virus that causes COVID-19 – within days the World Health Organization named it the omicron sci-fi spy […]]]>


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From last Friday, the race was on, between a virus and information about it. And for a while, information circulated faster, although there was hardly any.

Scientists in South Africa have identified a new variant of the virus that causes COVID-19 – within days the World Health Organization named it the omicron sci-fi spy – and due to the abundant assortment of mutations in its spike protein, the nanomechanical tentacle that attaches and cracks in cells, scientific alarms have started to sound.

But to be clear, these were the “We should check this” alarms, not the “Everyone’s crazy” alarms. Apparently, they look alike, however. The panic has taken hold as scientists have identified the omicron in 18 countries, triggering travel bans, border closures, stock market crashes and, in the United States, holiday weekend worries that world returns to March 2020. Researchers in South Africa and Botswana have found most of the cases so far, although this may be an artefact of their research; Dutch authorities announced on Tuesday that the first case they could identify was 11 days before the identification of omicron in South Africa.

This means that the omicron variant is widespread and mysterious – a palimpsest wrapped in a hologram draped in a Rorschach test – because no one knows anything yet. Public health officials cannot yet say whether it is more virulent or more transmissible than the delta, which since last summer has crowded out most other variants of SARS-CoV-2. So panic; or not. It’s yours. Because now scientists have to work on the problem.

Things scientists don’t know, but need to know: How efficiently does the omicron move from person to person? Can he escape the immunity conferred by a previous infection or by vaccines? Does this cause more serious illness? “We need many types of data,” says Angela Rasmussen, coronavirologist at the Vaccines and Infectious Diseases Organization-International Vaccine Center in Saskatchewan, Canada. This means obtaining genomic and epidemiological data, understanding the immunological differences of the variant, and collecting statistics on groundbreaking infections and hospitalizations.

This is all going to be complicated, because a crucial piece of information is missing: how long has omicron been around the world. These new Dutch data suggest it lasted longer than health planners initially hoped. Whether it’s the start of a wave – or the middle or end of a wave that no one has noticed – is key. “It seems to have been detected early in a recovery, at a time when everyone was focusing on the delta,” says John Connor, a microbiologist at Boston University and a researcher at the National Emerging Infectious Diseases Laboratories. “The advantage of having this information early is that the rest of the world can start looking at all the questions raised by a new variant: are our diagnostics still working? Does it seem like the immune response generated by vaccines can still neutralize this? virus?”

If this is just the beginning, say, then everyone with omicron could still be a tight-knit bunch, demographically or biologically speaking. This could make the variant more dangerous – moving faster or making people sicker – if this group were, for some reason, more vulnerable than the general population. Or the opposite could be true. To figure this out, disease dynamics researchers could do “forensic accounting” to see how previous waves like the delta have behaved and compare that to what’s happening with the omicron. It could tell if they are underestimated or overestimated how bad an omicron wave could be. “If I had evaluated delta using only the period of time that is approximately now, how much of a mistake would I have been?” Says Matthew Ferrari, director of the Center for Infectious Disease Dynamics at Penn State University.

In short: Based on early data, scientists knew very little about delta. Now they know it by heart. They will need the same patience to understand omicron. As a first step, more details on the genetic structure of the variant, initially generated by scientists in South Africa, could help with the first ideas about the behavior of the variant as it spreads. “We can then deduce from genetics how this virus can escape neutralization of antibodies, whether or not it will escape vaccines,” said Deenan Pillay, virologist at University College London. But that’s just an inference, he adds: “You can never know, but you can make a calculated assessment based on what we know about the genetics of other variants.”

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Prevent the evolution of SARS-CoV-2 by targeting low probability stochastic events https://e-jemed.org/prevent-the-evolution-of-sars-cov-2-by-targeting-low-probability-stochastic-events/ Thu, 25 Nov 2021 02:36:00 +0000 https://e-jemed.org/prevent-the-evolution-of-sars-cov-2-by-targeting-low-probability-stochastic-events/ [ad_1] The rapidity with which severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants are emerging poses a threat to obtaining herd immunity against coronavirus disease 2019 (COVID-19). Multiple point mutations are often responsible for the emergence of these new variants of SARS-CoV-2 which are associated with traits such as increased duration of infection, transmissibility and […]]]>


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The rapidity with which severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants are emerging poses a threat to obtaining herd immunity against coronavirus disease 2019 (COVID-19). Multiple point mutations are often responsible for the emergence of these new variants of SARS-CoV-2 which are associated with traits such as increased duration of infection, transmissibility and immune evasion. In many cases, the emergence of variants has been associated with a longer duration of infections in immunocompromised individuals and patients treated with convalescent plasma.

Various previous studies have shown that people with impaired immune function can create a favorable environment by eliminating high levels of SARS-CoV-2 for weeks. This allows the virus to undergo beneficial phenotypic changes that allow it to evade the immune response.

To study: Long-term control of SARS-CoV-2 infections may slow viral progression and reduce the risk of treatment failure. Image Credit: PHOTOCREO Michal Bednarek / Shutterstock.com

About the study

In a recent Scientific reports item, the authors explored the emergence of more suitable SARS-CoV-2 variants using a stochastic evolutionary modeling framework during long-term infections. By discerning the factors responsible for the evolutionary process of SARS-CoV-2, the authors of this study predict that their findings could aid in the development of biomedical interventions that can control the pandemic.

In the present study, several different steps were used to generate new advantageous variants which are stochastic and occur largely by chance. The first step involved creating genetic diversity within infected individuals through stochastic events.

Extensive sequencing studies have shown that within the host, the SARS-CoV-2 viral population exists as a quasispecies due to de novo mutations during infection. These studies have also established the role of genetic drift and intra-host transmission bottlenecks in the movement of the virus from one area of ​​the body to another.

Genetic diversity helps the development and expansion of beneficial mutations due to natural selection in individuals infected with SARS-CoV-2. Comparatively, genetic drift hampers the expansion of beneficial viral mutations to small population sizes.

The next step involved the transmission of viral variants generated in a COVID-19 patient to new hosts. Stochasticity was introduced during this process to trigger infection in a new host by the low number of viral particles, thus creating a tight transmission bottleneck. Intervention studies can be designed to slow viral progression by viewing these stochastic factors as a potential weakness.

Study results

The authors simulated stochastic viral evolution using a modified Wright-Fisher model and observed that during a typical length SARS-CoV-2 infection, which typically lasts about 23 days, the Viral variants with point mutations increased the probability of replication by 20–50%. Their expansion was also higher than the variants with neutral or weakly deleterious fitness effects, thus leading to an increased probability of transmission of at least one viral particle with a beneficial mutation specific to a new host.

These results suggest that new SARS-CoV-2 lines with unique beneficial mutations are rapidly established at the population level due to the selection of beneficial point mutations in COVID-19 patients. The data also showed that patients with longer periods of higher viral load were able to more effectively transmit more adapted SARS-CoV-2 variants.

It has been observed that as the number of COVID-19 patients with longer SARS-CoV-2 infections increases, the rate at which newer, more suitable variants with two mutations also increases. Overall, the simulation results showed that the evolution of SARS-CoV-2 can be hindered by targeting the various low probability stochastic events that are crucial for the emergence of the SARS-CoV-2 variant. .

Conclusion and limits

The results of the present study suggest practical methods for controlling long-term SARS-CoV-2 infections that will be important in slowing the rate of viral progression. Here, the authors also show that the expected frequency of variant generation events will be sufficient to cause a substantial threat to public health.

There are some limitations associated with this model. The authors speculated that the patients were initially infected with wild-type viruses only and did not take into account the genetic variation existing in the population that could be responsible for beneficial viral mutations. The model also did not take into account the variation of certain parts of the viral replication cycle, which may act as additional stochastic events that may affect viral evolution.

Understanding the mechanism behind the evolution of SARS-CoV-2 allows us to design strategies that can tip the scales in this evolving arms race and ultimately allow us to control the spread of SARS-CoV-2 ”

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Ecology, evolution and overflow of the bat coronavirus https://e-jemed.org/ecology-evolution-and-overflow-of-the-bat-coronavirus/ Wed, 24 Nov 2021 12:21:00 +0000 https://e-jemed.org/ecology-evolution-and-overflow-of-the-bat-coronavirus/ [ad_1] Bat coronaviruses have repeatedly spread in human populations. This fallout will most likely continue to be a threat to public health. Study: Ecology, evolution and spread of bat coronaviruses. Image Credit: Colin Seddon / Shutterstock In a review published in Nature Reviews Microbiology, the authors gather information on the ecology and evolution of bat […]]]>


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Bat coronaviruses have repeatedly spread in human populations. This fallout will most likely continue to be a threat to public health.

Study: Ecology, evolution and spread of bat coronaviruses. Image Credit: Colin Seddon / Shutterstock

In a review published in Nature Reviews Microbiology, the authors gather information on the ecology and evolution of bat coronaviruses. They are also discussing the overflow of these coronaviruses from bats to other hosts, including humans.

Distribution of bat coronaviruses

Coronaviruses have been detected in 16% of bat species. There are 21 bat families, and alphacoronaviruses and beta-coronaviruses have been detected in 14 bat families in at least 69 countries on six continents. The apparent absence of coronavirus in particular bat families is likely due to insufficient sampling rather than a true absence.

Viruses showing high sequence similarity to the three recently emerged human coronaviruses have all been identified in bats. These include the Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV), SARS-CoV-2, and the Middle East Respiratory Syndrome Coronavirus (MERS-CoV).

Coronavirus infection in bats

Are bat species universally tolerant of coronavirus infections?

There have been very few studies. In bats experimentally infected with coronaviruses, some bats exhibited slight tissue damage, swelling of the nasal mucosa, and lung infection. The virus or viral RNA could be detected in the respiratory tract and / or intestines. However, the infected bats did not show obvious clinical signs of infection.

What are the immune responses of bats to coronavirus infections?

There are very few studies and bats do not always produce antibodies against the virus after infection. Bats have limited humoral responses, making it difficult to use serum antibody levels to identify infections with certain pathogens.

In bats, coronaviruses may have the ability to infect the respiratory tract and gastrointestinal tract. Many in vitro The studies provide some insight into the potential for spillover of specific viruses, but they give limited insight into the susceptibility of bats at the organism level.

In addition, studies making such inferences should be interpreted with caution, as it is impossible to predict whether these viruses cause persistent infections in bats without in vivo studies.

Prevalence of coronaviruses in bat populations

The prevalence of coronaviruses is estimated by the proportion of bats with viral RNA detectable in stool or fecal or oral swabs. These data show a strong temporal and spatial variability. Coronavirus excretion peaks in summer or fall in Australia and China, during dry seasons in Central Africa and Asia, and during wet seasons in West or Southeast Africa. Although the trends differ, seasonal variations are constantly observed between the different studies. Thus, the observed seasonal variations are most likely due to resource availability, reproductive cycles and host behavior.

Nutritional stress during times of resource scarcity has been implicated in the shedding of other bat viruses. Additionally, the effects differ among bat species and viral variants. The size, density and composition of bat colonies could also affect the prevalence of the virus by altering transmission rates. Several species of bats often roost together. This affects the viral infection of different bat hosts.

The size and location of roosts appear to affect the risk of virus spread between host species. If the list is dense, the chances of overflow are high and vice versa. Reproductive cycles also influence the prevalence and transmission of viruses in bat colonies. There may be age-related differences in the susceptibility and competence of the infection.

Co-infections in bats

Co-infections with multiple pathogens can influence transmission to other bats and spillover hosts. Cross-immunity against infection by related pathogens could reduce susceptibility or transmission. Conversely, compromises in an immune response against one pathogen could increase susceptibility and facilitate transmission of another. Co-infection of bats with multiple coronaviruses simultaneously, or the co-circulation of multiple virus genotypes in a roost, can result in interactions that affect the timing, location and intensity of virus shedding.

Viral genetic diversity and evolution

Coronaviruses have the largest genome among RNA viruses. Mutations and recombinations generate genetic diversity, expanding viral evolution and increasing the potential for changes in infected cell types, host range and pathogenicity.

Recognition of host receptors

Coronaviruses enter the host cell because of the spike protein. The receptor binding domain (RBD) of the spike protein binds to the host receptor. HCoV-NL63, SARS-CoV and SARS-CoV-2 bind to angiotensin-converting enzyme 2 (ACE2).

The interaction between RBD and the host receiver is like a key and a lock. The specific structures of the RBD virus and host receptors partly determine the infectivity of different hosts. Thus, the direct overflow of the coronavirus from bats to other mammals would therefore be regulated by the structures of the receptors of the host cell and the viral identity of the RBD.

The evolution of the virus which facilitates the binding of human receptors may decrease the binding of the original host receptors. This change of host can promote sustained human-to-human transmission and is characteristic of pandemic viruses.

The distribution of host receptors within a host’s cell types determines which tissues will be infected. This has an impact on pathogenesis and transmission. In humans, ACE2 is expressed primarily in the epithelial cells of many tissues, including the respiratory tract, kidneys, heart, and digestive tract. Therefore, SARS-CoV-2 has a multisystem pathology.

Host proteases

In addition to receptors, host proteases are needed to activate the virus spike protein to allow entry. This cleavage can determine zoonotic viral potential and human-to-human transmissibility. Coronavirus spike proteins have several cleavage sites for host proteases. The distribution and activity of these proteases differ according to cell types and physiological conditions. Therefore, protease expression patterns also contribute to the host range of coronaviruses.

Factors affecting overflow

Human-bat interactions differ in space, time, nature and intensity. Some bat species rarely encounter humans, while others have frequent contact. Land use change, animal husbandry and domestication, and human encroachment on wild lands have been linked to the emergence of infectious diseases. Changes in the quality of habitat for bats can also affect their overall health and viral circulation due to stress. Low food availability due to climate change and deforestation is also increasing viral shedding. It is observed that the excretion of the coronavirus in horseshoe bats is higher in human-dominated landscapes than in natural landscapes.

In addition, legal and illegal wildlife trade results in the transport of viruses over long distances with hosts that are maintained under stressful and unsanitary conditions, possibly increasing excretion and transmission.

Direct bat-to-man overflow

There is no conclusive evidence of direct infections from bats to humans with coronaviruses. This is probably due to inadequate monitoring rather than a true lack of fallout. Infections occur in rural areas or in low-resource countries, where human-bat contact can be common and may eventually go unnoticed. Additionally, infections with certain bat coronaviruses may be asymptomatic in humans or may be mistaken for other common illnesses.

Very few human exposures lead to infection and even less to subsequent transmission. Studies indicate that these viruses do not spread effectively among humans.

Overflow via intermediate hosts

Other animals may provide opportunities for the transmission of coronavirus from bats to humans. Once infected with bats, bridge hosts can promote the spread of the virus to humans through increased exposure or high viral loads. This will lead to a higher likelihood of human exposure to infectious doses of the virus. In addition, bridging hosts can also allow viral evolution which results in new or improved zoonotic capacity.

The ecological and evolutionary conditions that facilitated the overflow of SARS-CoV-2 remain unknown. The first SARS-CoV-2 transmission event may have occurred directly from bats or via a relay host. Most likely, this was a direct transmission from bats to humans.

Humans can also play the role of bridge hosts. Humans have infected domestic cats and dogs with SARS-CoV-2, potentially acting as reservoirs for new variants. This evidence of reverse zoonosis or backfire requires further research to illustrate the potential of other wild animal species to become new viral reservoirs.

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