Publisher Health

Use of the drug verapamil to treat Type 1 diabetes continues to show benefits lasting at least two years, researchers report in the journal Nature Communications. Patients taking the oral blood pressure medication not only required less daily insulin two years after first diagnosis of the disease, but also showed evidence of surprising immunomodulatory benefits.
Continuing medication was necessary. In the two-year study, subjects who stopped daily doses of verapamil at one year saw their disease at two years worsen at rates similar to those of the control group of diabetes patients who did not use verapamil at all.
Type 1 diabetes is an autoimmune disease that causes loss of pancreatic beta cells, which produce endogenous insulin. To replace that, patients must take exogenous insulin by shots or pump and are at risk of dangerous low blood sugar events. There is no current oral treatment for this disease.
The suggestion that verapamil might serve as a potential Type 1 diabetes drug was the serendipitous discovery of study leader Anath Shalev, M.D., director of the Comprehensive Diabetes Center at the University of Alabama at Birmingham. This finding stemmed from more than two decades of her basic research into a gene in pancreatic islets called TXNIP. In 2014, Shalev’s UAB research lab reported that verapamil completely reversed diabetes in animal models, and she announced plans to test the effects of the drug in a human clinical trial. The United States Food and Drug Administration approved verapamil for the treatment of high blood pressure in 1981.
In 2018, Shalev and colleagues reported the benefits of verapamil in a one-year clinical study of Type 1 diabetes patients, finding that regular oral administration of verapamil enabled patients to produce higher levels of their own insulin, thus limiting their need for injected insulin to regulate blood sugar levels.
The current study extends on that finding and provides crucial mechanistic and clinical insights into the beneficial effects of verapamil in Type 1 diabetes, using proteomics analysis and RNA sequencing.

Examining the spines of Neanderthals, an extinct human relative, may explain back-related ailments experienced by humans today, a team of anthropologists has concluded in a new comparative study.
The analysis centers on the spine’s curvature, which is caused, in part, by a wedging, or angling, of vertebrae and the intervertebral discs — the softer material between the vertebrae.
“Neanderthals are not distinct from modern humans in lumbar wedging and therefore likely possessed curved lower backs like we do,” explains Scott Williams, an associate professor in New York University’s Department of Anthropology and one of the authors of the paper, which appears in the journal PNAS Nexus. “However, over time, specifically after the onset of industrialization in the late 19th century, we see increased wedging in the lower back bones of today’s humans — a change that may relate to higher instances of back pain, and other afflictions, in postindustrial societies.”
Neanderthals have long been thought to have a different posture than modern humans.
“A good part of this perspective derives from the wedging of Neanderthals’ lumbar, or lower, vertebrae — their spines in this region curve less than those of modern humans studied in the U.S. or Europe,” explains Williams.
However, much of this view was based on an analysis of modern humans beginning in the late 19th century — well after the onset of industrialization, which significantly altered our daily lives. Furniture, for instance, became more widely available and desk jobs more prevalent — both of which encouraged sitting and, with it, changes in posture. These changes were coupled with a reduction in high-activity occupations, such as agriculture. In addition, specific afflictions became associated with working conditions that elicit poor posture.

Women with long or irregular periods are known to have a higher risk of type 2 diabetes and heart disease, but researchers found these women may also be at risk for nonalcoholic fatty liver disease (NAFLD), according to a new study published in the Endocrine Society’s Journal of Clinical Endocrinology and Metabolism.
About 24% of U.S. adults have NAFLD, a chronic disease in which excess fat builds up in your liver. This buildup of fat is not caused by heavy alcohol use. NAFLD can progress to chronic liver damage and is associated with a higher risk of death. Diet and exercise are the standard of care for NAFLD as no medicines have been approved to treat the disease.
“Our study results show that long or irregular menstrual cycles may be associated with an increased risk of developing NAFLD, and this link was not explained by obesity,” said Seungho Ryu, M.D., Ph.D., of the Center for Cohort Studies, Total Healthcare Center, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine in Seoul, South Korea. “Previous studies have shown that long or irregular menstrual cycles are associated with type 2 diabetes and cardiovascular disease, but our study is the first to find a link between long or irregular menstrual cycles and NAFLD.”
The researchers studied a data set of 72,092 women under 40 years old. About 28% of these women had long or irregular menstrual cycles, and 7% had NAFLD. The researchers followed up four years later and found new cases of NAFLD occurred in almost 9% of the women. The researchers concluded that there was an association between long or irregular menstrual cycles in young, premenopausal women and an increased risk of NAFLD.
“Young women with long or irregular menstrual cycles may benefit from lifestyle changes to reduce the risk of NAFLD as well as other cardiometabolic diseases,” Ryu said.
Other authors of this study include: In Young Cho, Yoosoo Chang, Jae-Heon Kang, Yejin Kim, Eunju Sung and Hocheol Shin of Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine in Seoul, South Korea; Sarah Wild of the University of Edinburgh in Edinburgh, U.K; and Christopher Byrne of the University of Southampton and the University Hospital Southampton in Southampton, U.K.
The study received funding from Sungkyunkwan University and the Southampton NIHR Biomedical Research Centre.
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Nirsevimab showed 74.5 percent efficacy against medically attended lower respiratory tract infections caused by respiratory syncytial virus (RSV) in healthy infants, according to an international, randomised, placebo-controlled Phase 3 clinical trial. It is the first potential immunization against RSV in the general infant population, with a single dose providing safe protection across the entire RSV season. Results were published in the New England Journal of Medicine.
“These exciting data show that nirsevimab has the potential to offer RSV protection for all infants, which would be a paradigm shift in the approach to this disease,” said site Principal Investigator and co-author William Muller, MD, PhD, Scientific Director of Clinical and Community Trials at Stanley Manne Children’s Research Institute at Ann & Robert H. Lurie Children’s Hospital of Chicago, and Associate Professor of Pediatrics at Northwestern University Feinberg School of Medicine.
RSV is a common, contagious virus that causes seasonal epidemics of lower respiratory tract infections, leading to bronchiolitis and pneumonia in infants. It is also a leading cause of hospitalizations in all infants.
The trial involved healthy term and late preterm (gestational age ?35 weeks) infants entering their first RSV season. Lurie Children’s was among the highest enrolling US sites in the trial.
Nirsevimab is an investigational long-acting monoclonal antibody, being developed by AstraZeneca and Sanofi, designed to protect all infants through their first RSV season with a single dose. Monoclonal antibodies do not require the activation of the immune system to help offer rapid and direct protection against disease.
Currently, the only available preventative option for RSV is palivizumab, which is limited to high-risk infants and provides one-month protection, requiring five injections to cover an RSV season.
A separate Phase 2/3 trial, also published in the New England Journal of Medicine, which evaluated the safety of nirsevimab in infants with congenital heart disease, chronic lung disease and prematurity entering their first RSV season, demonstrated that nirsevimab had a similar safety and tolerability profile compared to palivizumab.Results in this population of infants indicated similar protection against RSV to that in the healthy term and late preterm infants.
“We know that RSV has seen a resurgence with the easing of COVID-19 public health measures. This shows us a broad immunization approach is needed to help mitigate the substantial global burden RSV places on infants, their families and healthcare services,” said Dr. Muller.
Research at Ann & Robert H. Lurie Children’s Hospital of Chicago is conducted through the Stanley Manne Children’s Research Institute. The Manne Research Institute is focused on improving child health, transforming pediatric medicine and ensuring healthier futures through the relentless pursuit of knowledge. Lurie Children’s is ranked as one of the nation’s top children’s hospitals by U.S. News & World Report. It is the pediatric training ground for Northwestern University Feinberg School of Medicine.
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Australian bull ants have evolved a venom molecule perfectly tuned to target one of their predators — the echidna — that also could have implications for people with long-term pain, University of Queensland researchers say.
Dr Sam Robinson and David Eagles from UQ’s Institute for Molecular Bioscience found a bull ant venom component that exploits a pain pathway in mammals, which they believe evolved to stop echidnas attacking the ant’s nests.
“Venoms are complex cocktails and while bull ant venom contains molecules similar to those found in honey bee stings which cause immediate pain, we also found an intriguing new molecule that was different,” Dr Robinson said.
Whilst searching databases for similar amino-acid sequences, Dr Robinson found that the molecule matched the sequence of mammalian hormones related to Epidermal Growth Factor (EGF), and of these, was most closely related to that of the echidna.
“We tested the venom molecule on mammalian EGF receptors and it was very potent — this convinced us that the venom molecule was there to defend against mammals,” he said.
“We went on to show that while it didn’t cause direct pain, the molecule did cause long-lasting hypersensitivity.
“Many small carnivorous marsupials, like bandicoots, eat individual ants, but only the echidna is known to attack bull ant nests and target their young — we think that making the echidna sensitive to pain, in tandem with the immediate ‘bee-sting’ pain, may dissuade it from returning to the nests.
“You can see clearly in the ant’s DNA that it is producing a molecule that mimics a hormone of its natural enemy and is using it as a weapon against it — it brings to mind the ancient proverb ‘to know your enemy, you must become your enemy.'”
The team believes the links between EGF signalling and chronic pain are building momentum and is confident this study could inspire new ways to treat long-term pain.
EGF-inhibitor drugs are readily available on the market and used in anti-cancer therapy to slow tumour growth, with evidence suggesting patients that take them experience less long-term pain.
“We hope that by highlighting the role of this signalling pathway in pain, we can encourage different strategies for pain treatment, especially long-term pain for which treatment is currently limited,” Dr Robinson said.
Video: https://youtu.be/Gh7iwGemJeo
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An analysis of data from a large, nationally representative survey of the US population shows that e-cigarette use is associated with increased odds of prediabetes. The findings, which are reported in the American Journal of Preventive Medicine, published by Elsevier, add important evidence about the health effects of e-cigarettes and can help shape public health best practices.
“Our study demonstrated a clear association of prediabetes risk with the use of e-cigarettes,” explained lead investigator Shyam Biswal, PhD, Department of Environmental Health and Engineering, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA. “With both e-cigarette use and prevalence of prediabetes dramatically on the rise in the past decade, our discovery that e-cigarettes carry a similar risk to traditional cigarettes with respect to diabetes is important for understanding and treating vulnerable individuals.”
According to the Centers for Disease Control and Prevention (CDC), traditional cigarette smokers are 30% to 40% more likely than non-smokers to develop type 2 diabetes, which increases their risk for cardiovascular diseases such as atherosclerotic disorders, stroke, and peripheral vascular diseases. E-cigarettes are sometimes promoted as a risk reduction product for current traditional cigarette smokers. The use of e-cigarettes is rising among younger population, which remains a public health concern.
To determine the association between e-cigarette use and prediabetes, the investigators analyzed 2016-2018 data from the Behavioral Risk Factor Surveillance System (BRFSS). It is the largest annual nationally representative health survey of US adults with data on health outcomes, health-related risk behaviors, preventive services, and chronic medical conditions. Among the 600,046 respondents, 9%, more than 66,000 individuals, were current e-cigarette users who self-reported prediabetes diagnoses. The data also showed that e-cigarette users have a higher prevalence of high-risk lifestyle factors and worse self-related mental and physical health status than non-smokers.
Survey respondents were 50.4% female, 67.7% non-Hispanic White, 12.2% non-Hispanic Black, 5% Hispanic, and 28.6% were age 35 or older. In this representative sample of US adults, e-cigarette use was associated with greater odds of prediabetes compared to those who did not use e-cigarettes or traditional cigarettes.
The association of e-cigarettes with prediabetes heightens significant concerns for public health officials. “We were surprised by the findings associating prediabetes with e-cigarettes because they are touted as a safer alternative, which we now know is not the case,” commented Dr. Biswal. “In the case of cigarette smoking, nicotine has a detrimental effect on insulin action, and it appears that e-cigarettes may also have the same effect.”
Prediabetes is reversible with lifestyle management. Based on these findings, the authors make a compelling recommendation for targeting the reduction in e-cigarette use and education of young adults as a therapeutic lifestyle management strategy for the reduction of diabetes risk.
“Our effort for smoking cessation has led to a decrease in smoking traditional cigarettes. With this information, it is time for us to ramp up our public health efforts to promote the cessation of e-cigarettes,” cautioned Dr. Biswal.
Prediabetes is defined as the presence of impaired fasting glucose (greater than 100-125 mg/dL), impaired glucose tolerance (greater than 140-199 mg/dL two hours after a 75-g oral intake of glucose), or hemoglobin A1c between 5.7&-6.4%), which indicate an intermediate glycemic state between normal glycemia and diabetes. The CDC has reported that prediabetes has become increasingly common in the past few decades, and recent estimates indicate that 38% of American adults have this condition. It is also on the rise among an increasingly younger population. Projections estimate that by 2030, more than 470 million people worldwide will be diagnosed with prediabetes.
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Genomes are made up of thousands of individual pieces — genes — which are expressed at different levels. Researchers have shed light on how the placement of a gene affects its expression, as well as that of its neighbors.
The celebrated physicist Richard Feynman is credited with the quote, “What I cannot create, I do not understand.” As well as informing Feynman’s approach to theoretical physics, it’s a good way of describing the motivations of synthetic biologists, with their interest in building genomes from scratch. By designing and building synthetic genomes, they hope to better understand the code of life. Synthetic biology has been organised around the concept of using DNA sequences as ‘parts’ with reproducible functions. Now, through successful collaborations and the use of cutting-edge tools, EMBL’s Steinmetz Group has gained an important insight into the variation of gene expression that results from the position or context of these DNA parts within the genome.
Explaining the underlying question motivating the work, Amanda Hughes – co-lead author and postdoc in the Steinmetz Group – said, “In synthetic biology, you tend to break things down into modular, ‘plug-and-play’ parts. These are promotor parts, coding regions, and terminator parts. We wanted to test whether these pieces really are ‘plug-and-play,’ functioning the same way in any context, or whether their position affects their function. We wanted to better understand how the linear organisation of genes affects their functions and identify general design principles that could be applied to building genomes.”
A synthetic biology toolbox delivers contextual insights
This work, funded by BMBF and Volkswagen Foundation’s “Life?” initiative, was possible because of two key technologies: synthetic yeast strains from the Sc2.0 consortium and long-read direct RNA sequencing. The strains obtained from the Sc2.0 consortium included a design feature called ‘SCRaMbLE’ that provides the ability to rearrange genes into different locations at a previously unachievable scale. The expertise and tools available in the Genomics Core facility at EMBL, including Oxford Nanopore’s GridION, allowed the team to perform long-read direct RNA sequencing, permitting identification of both the start and end of RNA molecules and their assignment to particular rearrangements. The combination of these cutting-edge technologies was critical to measure full-length RNA molecules from genes across many contexts.
The paper, published in Science showed that context — and in particular transcriptional context — alters the RNA output of a gene. Using long-read direct RNA sequencing, they were able to observe changes in the start, end, and amount of full-length RNA molecules expressed from DNA sequences that had been randomly rearranged in synthetic yeast genomes. Relocating a gene affected the length and abundance of its RNA output; however, these changes were not always explained by the new adjacent DNA sequence. It appeared to be transcription occurring around it, rather than the sequence itself, that altered a gene’s RNA output.
Gleaning general principles from such a large, stochastic dataset was not a trivial task, as the lead author Aaron Brooks explained: “To reach our conclusions, we had to observe genes in many alternative genetic contexts, which were present in the SCRaMbLE strains. Putting the pieces back together, however, was a big effort. We had to generate a massive sequencing dataset, which, in turn, required us to develop new software tools. We had to rely on sophisticated machine learning algorithms to help us understand the complex patterns we were observing.” Modelling a gene’s RNA output based on its new upstream and downstream contexts revealed that features related to surrounding transcriptional patterns predicted RNA boundaries and abundance. For example, if a gene was relocated next to a highly expressed neighbour, its expression also tended to increase.
Defining design principles for building genomes
In addition to illuminating the relationship between RNA abundance and neighbouring gene expression, the researchers also noted a compelling relationship between the end positions of RNAs of convergent genes (genes oriented with ends towards one another). Specifically, they found that the length of an RNA was affected by the proximity and abundance of neighbouring transcripts. Jef Boeke, co-author and Director of the Sc2.0 consortium remarked on these insights: “Deep transcriptional profiling combined with the genomic variations produced using [the] SCRaMbLE system have given us new insights into the flexibility of the yeast genome and pointed out that the rules of where transcripts end can be surprisingly context dependent.”
Ultimately, applying these findings, the researchers were able tune the length of RNA molecules by controlling transcription of a neighbouring gene. The team demonstrated that the lessons learned from studying the transcriptomes of SCRaMbLEd genomes can be applied to engineer genomes with desired functions. The study also proposes a new synthetic biology design concept that the researchers term ‘transcriptional embedding’ that could be used to reversibly tag an RNA, altering its stability, translation into protein, or even localisation. All of this could be accomplished, they believe, by controlling the expression of a convergent, neighbouring gene rather than the gene itself.
“The unbiased and high-throughput nature of the gene reshuffling approach used here leads us to discover functions of genomic sequences in different genomic contexts, something that previously was not possible at scale,” said Lars Steinmetz, group leader at EMBL. “This approach emphasises that context matters in regulating transcript ends — surprisingly, even permitting context-dependent predictions of transcript ends when genes are reshuffled to new locations. Ultimately, the work reveals that there is fine-tuned interlinked regulation between neighbouring genetic elements, spanning multiple genes that determines where transcripts start and stop. The ability to predict these interactions can inform key ‘design principles’ for genome construction; i.e. where are genes best located and how should they be positioned relative to each other. These insights advance tools for engineering transcripts without changing the sequence itself but by modulating neighbouring gene expression.” Their work adds to a growing repertoire of design principles that can be leveraged to realise a grand vision in synthetic biology: designing and building a genome from scratch.

SharecloseShare pageCopy linkAbout sharingThis video can not be playedTo play this video you need to enable JavaScript in your browser.Memory loss, fatigue and trouble concentrating can be symptoms of having had coronavirus.But scientists think people who haven’t had Covid are also suffering increased tiredness, impaired decision-making and a lack of focus due to the pandemic.Experts believe Covid uncertainty and disruption to routines have led to a phenomenon known as “pandemic brain”.A leading behavioural neuroscientist is now calling for more research into it.”People form habits so we see friends on a particular day or enjoy a sport on a particular evening – and that lack of regularity can be quite challenging,” said Dr Emma Yhnell. Has the pandemic affected your brain?”Uncertainty influences the biology of our brains – and generally we can cope with a certain amount of uncertainty but the longer we have it, generally the worse it is for our brain.’My shame over long Covid 18-month work absence’What are the symptoms of long Covid?How our brains are processing the pandemic”Lots of research has looked at the effect of Covid infection on the brain but actually we know that living in a pandemic more generally really has had impacts on our brain function and brain health.”Image source, Getty ImagesThe UK has a population of more than 68 million people and the latest government figures show there have been more than 18.9 million confirmed UK Covid cases since January 2020.Two years ago this month, the Covid-19 crisis was declared a global pandemic and the UK went into stay-at-home lockdown – with more than 160,000 people dying in the UK after testing positive for coronavirus.Image source, Getty ImagesThere are many studies into the long-term impact of having a Covid infection or long Covid – but some who haven’t had the virus believe two years of living with restrictions has had a significant impact.’I was hesitant to hug my mum’Sannan Iqbal said he was “hesitant” to hug his mum during the pandemic as the 22-year-old with cystic fibrosis shielded to protect himself.Image source, Sannan Iqbal He said he felt like he “had a tonne of bricks” on his shoulders with “nowhere to escape” as he tried to avoid getting Covid.”This pandemic has taken its toll on me” said Sannan, who lives with his parents in Cardiff.Image source, Getty Images”I do feel more fatigued, I do feel more anxious, I do feel myself questioning or even triple questioning my decisions.”Sannan, whose condition affects his mobility, remembers being “glued to the television” when Covid hit the UK, trying to understand the restrictions and statistics.Image source, Getty Images”I already have mental health issues because of my disability, so all this added stress and pressure didn’t help,” he told BBC Wales Live.He said his care services were withdrawn during the first lockdown in March 2020, leaving his anxiety levels “sky high”, and affecting his relationship with his parents, who are both key workers. ‘What happens if my parents caught Covid?'”I relied on those services to give me and my parents a bit of respite from each other,” he said.Image source, Getty Images”I was a bit hesitant to even hug my own mother at most points during the pandemic.”What happens if one of my parents caught Covid or were asymptomatic and brought it home? Would I be safe? Would I be able to cope?”Scientists think regular changes in lockdown rules, travel restrictions, worries about getting the virus and limited face-to-face contact with others has affected some people’s brain health.Image source, Getty ImagesFor Abbie Wright, losing her job at an insurance company during the pandemic impacted her routine and affected her focus.’I feel like my memory is gone’ “The uncertainty, it was just awful. And you couldn’t see the end,” said the 27-year-old from Barry in Vale of Glamorgan.”I feel like my memory is gone. Brain fog has been a definite big thing for me. Forgetting words to use in a sentence and forgetting a simple sum.”Image source, Abbie WrightAbbie was diagnosed with borderline personality disorder in October 2019, just months before the pandemic, and the uncertainty meant she stopped doing things that would normally help her.”I love going to the cinema, I love going to concerts,” she said. “That’s a big part of my life – just anything that takes my mind off things. Things that you take for granted and were normal pre-pandemic now just seem alien.Image source, Abbie Wright”Then it’s the anxiety of getting back out there now restrictions are lifting.”More research needed into ‘pandemic brain’ impactNow there are calls for more research into the psychological impact of living through a pandemic for those who didn’t get Covid.”This term ‘pandemic brain’ has cropped up – and the really interesting thing about it is that different people will have different experiences,” said Dr Yhnell, a senior neuroscience lecturer at Cardiff University.”We know people who have experienced chronic stress or chronic anxiety see some changes to their brain in the parts that are involved in decision making and attention.”But we need much more research to determine whether the experience of the pandemic has caused structural changes in people’s brains.”Catch up with Wales Live on BBC iPlayerIf you have been affected by any of the issues in this story, the BBC Action Line has links to organisations which can offer support and adviceTHE STORY OF MIWSIG: Eleri Price and Huw Stephens time travel with Welsh language popMARGINS TO MAINSTREAM: Michael Sheen introduces new writers revealing their truthsMore on this storyVaccinated less likely to develop long CovidIs ending the last Covid rule ‘brave or stupid’?’My shame over long Covid 18-month work absence’

New research from the University of Exeter reports the largest ever whole-genome sequencing project for the potentially fatal yeast infection Candida glabrata from hospitals across Scotland.
Candida glabrata is a type of yeast that can cause disease in humans. It most commonly affects the urinary tract, genitals, mouth, and the bloodstream. If it is not caught, these infections can become deadly. It also has a very high resistance to certain antifungal drugs, so understanding why resistance occurs is key to knowing how to treat it effectively.
The new research, published in Genetics, used samples from eight hospitals in Scotland to sequence the genome of Candida glabrata. This led to the discovery of a variety of new information on the species. This includes information on how they reproduce and the genetic diversity. It also found that genes that make it more likely to be infectious have an advantage for survival, and the drug-resistance genes often evolve within patients.
The discovery of this information gives scientists an advantage when it comes to treating candida glabrata. A better understanding of the genes involved allows researchers to focus their work in ways that were not possible before. It also helps aid understanding on how the pathogen spreads, which is important to identifying infections.
Dr Rhys Farrer, one of the Principal Investigators at the MRC Centre for Medical Mycology at the University of Exeter, said: “Our study sheds new light on the genetic diversity of Candida glabrata. We have demonstrated that this deadly human fungal pathogen is being spread between continents, probably by humans, and recombining to form new populations, which is likely contributing to its high virulence and increasing drug resistance.”
The research was funded by the Medical Research Council and the Wellcome Trust.
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The strategy is supposed to help the nation transition to what some are calling a “new normal,” but it will require funding from Congress.WASHINGTON — The White House unveiled its long-awaited new coronavirus response strategy on Wednesday, aimed at turning the corner on the worst public health crisis in a century while also preparing for the next threat.The plan, meant to help the United States transition to what some are calling a “new normal,” has four main goals: protecting against and treating Covid-19; preparing for new variants; avoiding shutdowns; and fighting the virus abroad.But there is a big hitch: Much of the plan requires funding from Congress. The administration recently told congressional officials it could need as much as $30 billion to sustain the pandemic response. One outside adviser to the White House, Dr. Ezekiel Emanuel, said in an interview that the United States needed to spend much more — on the order of $100 billion over the next year, and billions more after that — to be fully prepared.“Congress has to think of this as an investment in biosecurity for the country,” said Dr. Emanuel, who led a team of experts in developing a far-reaching coronavirus response plan that it shared with the White House. “We should not be penny-wise and dollar-foolish.”The strategy comes on the heels of the president’s State of the Union address on Tuesday night and as new U.S. cases decline, though deaths remain high. President Biden used the speech to spotlight a key component: a new “test to treat” initiative that he said would allow Americans to get tested at a pharmacy and, if they are positive, “receive antiviral pills on the spot at no cost.”Many of the other initiatives in the strategy — including a plan to accelerate research so that vaccines can be developed and deployed within 100 days of variants arising, which was announced in November — are not new. But taken together, they amount to a blueprint for the next phase of the response.“Make no mistake, President Biden will not accept just ‘living with Covid’ any more than we accept ‘living with’ cancer, Alzheimer’s or AIDS,” the plan declares. “We will continue our work to stop the spread of the virus, blunt its impact on those who get infected, and deploy new treatments to dramatically reduce the occurrence of severe Covid-19 disease and deaths.”The health secretary, Xavier Becerra, who has been criticized for keeping too low of a profile, made a rare appearance on Wednesday alongside the health officials who hold the weekly White House briefings.Mr. Becerra highlighted another element of the plan: boosting research into long Covid, the long-term symptoms some people experience after infection. He pledged to open “new centers of excellence” around the country to provide high-quality care to long-Covid patients — which will also require congressional buy-in.A bipartisan group, led by two former governors, has been pressing Mr. Biden to do more for tens of thousands of children in the United States who have lost parents or caregivers to Covid-19, and the White House apparently listened. The plan says the president will direct federal agencies to review their programs to formulate a more coordinated “bereavement response” for such children, who now number around 200,000.“This is all part of our commitment to be there for Americans who have long-term physical and mental health needs caused by Covid,” Mr. Becerra said.The idea behind the strategy is to get the nation out of crisis mode and to a place, Mr. Biden has said, where the virus will no longer disrupt everyday life. It includes a pledge for the administration to work with Congress to “give schools and businesses guidance, tests and supplies to stay open, including tools to improve ventilation and air filtration.”In interviews, experts generally praised the plan as a good step forward. Dr. Rick Bright, the chief executive of the Rockefeller Foundation’s Pandemic Prevention Institute, called it a “great start,” adding that the plan should “serve as a firm foundation to build upon, to extend our preparedness posture beyond Covid.”But Jay A. Winsten, the director of the Harvard Initiative on Media Strategies for Public Health, said the 100-day timeline for vaccine development might not be fast enough for a highly transmissible variant like Omicron. The first Omicron sample was collected in South Africa on Nov. 8, he said; the United States reached the peak of the Omicron wave just 67 days later, on Jan. 14.Mr. Biden came into office more than a year ago with a 200-page plan to combat the pandemic, which was the most pressing challenge in his nascent presidency. But a lot has changed since then.The Coronavirus Pandemic: Key Things to KnowCard 1 of 3A new U.S. strategy.