Inflammation could be a core feature of depression

inflammation

People with depression have higher levels of inflammation in their bodies than those without depression, regardless of socioeconomic background, ill health or unhealthy behaviors, a study by King’s College London finds.

C-reactive protein (CRP), a marker for inflammation in the body, was found in higher levels in depressed people compared to non-depressed people in the largest ever study into the genetic, environmental, lifestyle, medical pathways leading to inflammation in major depressive disorder (MDD).

The effect was reduced but remained significant when factors known to be related to increased inflammation such as smoking, body mass index (BMI) and trauma were taken into account, adding to the body of evidence that there may be a direct biological link between inflammation and depressive disorders. The study was conducted by researchers funded by the NIHR Maudsley Biomedical Research Center and NARSAD (National Alliance for Research on Schizophrenia & Depression) and it was published in the American Journal of Psychiatry.

Largest study of its kind

In any given week in England 3 in 100 people will have depression. The economic costs of mental illness in England have been estimated at £105.2 billion each year by the government which includes direct costs of services, lost productivity at work and reduced quality of life.

This study used the largest ever community-based sample with information on mental health, inflammation, genome-wide association study (GWAS) data linking genes to certain diseases, environment, lifestyle and physical health with approximately 86 thousand participants.

Researchers analyzed blood samples, genetic data and physical and mental health questionnaires collected by UK Biobank, the large-scale biomedical database and research resource with over half a million UK participants who were recruited between in 2006-2010. Of the 86,000 participants included in the study just under a third (31%) were classified as having major depressive disorder. This percentage is similar to estimates found by other studies on the global prevalence of depression occurring during a person’s lifetime.

The study showed that depressed participants had raised C-reactive protein (CRP) levels in their blood compared to non-depressed participants, and were more likely to have low-grade inflammation, defined as CRP levels in the blood of over 3 mg per liter. Inflammation is a biological response which is predominantly directed to fight infection but also has an important role in regulating behavior. CRP is one marker for inflammation.

Further analysis showed that this increased inflammation in depression is only partially explained by clinical and sociodemographic factors including age, sex, body mass index (BMI) smoking, alcohol consumption, exposure to early life trauma, socio-economic status and self-reported health status.

Genetics x environment

The study found that the greater the genetic risk for depression, the greater the level of inflammation.

The polygenic risk score gives an estimate of how likely an individual is to have a given trait based only on genetics. The researchers calculated polygenic risk score in participants for major depression was strongly associated with levels of CRP. However, this association was no longer present when BMI and smoking were taken into account. In contrast, polygenic risk scores for three immune disorders—biliary cirrhosis, Crohn’s disease and rheumatoid arthritis- are all positively associated with CRP levels even after controlling for BMI and smoking.

First author Maria Pitharouli, Research Associate at the Institute of Psychiatry, Psychology & Neuroscience, King’s College London said: “Our study provides the most conclusive evidence to date that people with depression have proteins in their blood indicating activation of the inflammatory system. Furthermore, through in-depth analysis of data from over 86,000 people we have discovered more about the mechanisms that may be behind the relationship between inflammation and depression.”

Joint senior author, Professor Cathryn Lewis who leads the Social, Genetic and Developmental Psychiatry Center at the Institute of Psychiatry, Psychology & Neuroscience, King’s College London said: “Our study highlights how genetics can be used as a tool for dissecting mental health disorders. Here we’ve shown that the genetic contribution to inflammation in depression comes mostly from eating and smoking habits. That finding is important to help us understand depression better—and one further piece in the jigsaw puzzle towards improving care for people with depression.”

Joint senior author, Professor Carmine Pariante from the National Institute for Health Research Maudsley Biomedical Research Center says: “Our large-scale analysis of data removed socioeconomic background, ill health, unhealthy habits as well as genetic predisposition to immune dysfunction as the only explanations for the relationship between depression and inflammation. By this process of elimination, we show that there may be a core biological process that is behind the association between depression and increased inflammation. If we can identify this process and uncover more detail about its role in the development of depression, we can pave the way for trialing new treatments for this widespread mental health disorder.”

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U.S. COVID Response Could Have Avoided Hundreds of Thousands of Deaths – Research

WASHINGTON (Reuters) – The United States squandered both money and lives in its response to the coronavirus pandemic, and it could have avoided nearly 400,000 deaths with a more effective health strategy and trimmed federal spending by hundreds of billions of dollars while still supporting those who needed it.

That is the conclusion of a group of research papers released at a Brookings Institution conference this week, offering an early and broad start to what will likely be an intense effort in coming years to assess the response to the worst pandemic in a century.

U.S. COVID-19 fatalities could have stayed under 300,000, versus a death toll of 540,000 and rising, if by last May the country had adopted widespread mask, social distancing, and testing protocols while awaiting a vaccine, estimated Andrew Atkeson, economics professor at University of California, Los Angeles.

He likened the state-by-state, patchwork response to a car’s cruise control. As the virus worsened people hunkered down, but when the situation improved restrictions were dropped and people were less careful, with the result that “the equilibrium level of daily deaths … remains in a relatively narrow band” until the vaccine arrived.

Atkeson projected a final fatality level of around 670,000 as vaccines spread and the crisis subsides. The outcome, had no vaccine been developed, would have been a far-worse 1.27 million, Atkeson estimated.

The economic response, while mammoth, also could have been better tailored, argued University of California, Berkeley economics professor Christine Romer. She joins former Treasury Secretary Lawrence Summers and several others from the last two Democratic administrations in criticizing the spending authorized since last spring, including the Biden team’s $1.9 trillion American Rescue Plan.

While she said the federal government’s more than $5 trillion in pandemic-related spending won’t likely trigger a fiscal crisis, she worries that higher-priority investments will be deferred because of allocations to initiatives like the Paycheck Protection Program.

Those forgivable small business loans were “an interesting and noble experiment,” but were also “problematic on many levels,” including an apparent cost of hundreds of thousands of dollars for each job saved, she said.

“Spending on programs such as unemployment compensation and public heath was exactly what was called for,” she wrote, but other aspects, particularly the generous one-time payments to families, were “largely ineffective and wasteful.”

“If something like the $1 trillion spent on stimulus payments that did little to help those most affected by the pandemic ends up precluding spending $1 trillion on infrastructure or climate change in the next few years, the United States will have made a very bad bargain indeed,” Romer wrote.

Biden administration officials, including Treasury Secretary Janet Yellen, argue the full package was needed to be sure all workers and families are kept economically intact until the job market recovers.

In a separate paper, Minneapolis Federal Reserve researchers Krista Ruffini and Abigail Wozniak concluded the federal programs largely did what they intended by supporting income and spending, with the impact seen in how consumption changed in response to the approval and lapse of different government payments.

But they also found room for improvement.

Evidence of the PPP’s effectiveness in job retention, for example, was “mixed,” they found, and increases in food assistance didn’t account for things like higher grocery prices.

“Food insecurity remained elevated throughout 2020,” they noted.

The aim now, they said, should be on determining what worked in order to make the response to any similar crisis more effective.

“The 2020 social insurance system response had many successes,” they said. “Given the scope and scale of the pandemic response, it is critical we continue to evaluate these efforts to understand the full extent of their reach, which populations were helped, who was left out.”

SOURCE: https://brook.gs/31iIjSA BPEA Spring 2021 Conference, March 25, 2021.

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Feeling rundown? It could raise your odds for severe COVID

Feeling rundown?  it could raise your odds for severe COVID

Groggy during the day? Feeling burned out at work? That could put you at increased risk for COVID-19 and more severe illness, a new study suggests.

“We found that lack of sleep at night, severe sleep problems and high level of burnout may be risk factors for COVID-19” for frontline health care workers, according to a team led by Dr. Sara Seidelmann, an assistant professor of clinical medicine at Columbia College of Physicians and Surgeons, Stamford Hospital, Conn.

One expert who wasn’t connected to the research said the findings made sense.

“This study reconfirms several items that have been suspected about the relationship of sleep, stress and infectious diseases,” said Dr. Thomas Kilkenny, who directs sleep medicine at Staten Island University Hospital in New York City. “The researchers demonstrate, in a very comprehensive way, that both sleep deprivation through lack of sleep increases both the risk of developing COVID 19 but also the duration of the illness.”

Prior research has found that poor sleep and job burnout are linked with a greater risk for a variety of viral and bacterial infections, so the authors of this new study wanted to find out if they’re also risk factors for COVID-19.

In this latest study, published March 22 in the journal BMJ Nutrition Prevention & Health, they analyzed the responses of nearly 2,900 health care workers in the United States, France, Germany, Italy, Spain and Britain. All had participated in an online survey from July 17 to Sept. 25, 2020. Of those health care workers, 568 reported having gotten infected with the new coronavirus.

The health care workers averaged between 6 and 7 hours of sleep a night.

The study couldn’t prove cause-and-effect, but after the researchers accounted for other factors, they concluded that every extra hour of sleep at night was associated with a 12% lower risk of the worker getting COVID-19.

However, when that extra hour of shuteye took place was crucial. An extra hour of sleep via daytime napping was associated with a 6% higher risk of getting COVID-19, the team noted in a journal news release.

According to Kilkenny, that shows that “staffers that needed to take naps during the day—a surrogate for lack of sleep—were also at an increased risk for the disease.”

About 1 in 4 (24%) of the people who went on to contract COVID-19 had already reported long-term difficulties sleeping at night, compared with about 1 in every 5 (21%) of those who hadn’t gotten the illness.

Seidelmann’s group also found that 5% of those with COVID-19 had three or more sleep problems—including difficulties falling asleep, staying asleep, or needing to use sleeping pills on three or more nights of the week—compared with 3% of those without COVID-19.

People with those three sleep problems were 88% more likely to develop COVID-19 than those with no sleep problems, the study found.

Another finding was that 5.5% of those with COVID-19 reported daily work burnout, compared with 3% of those without COVID-19. Compared to those with no burnout, those with daily burnout had twice the risk of getting COVID-19, and they were about 3 times more likely to have severe COVID-19 and to take longer to recover.

Dr. Harly Greenberg is chief of pulmonary, critical care and sleep Medicine at Northwell Health, in Great Neck, N.Y. He wasn’t involved in the research, but said it “adds to the mounting literature that sleep is much more than simply withdrawing from the environment; rather it is an essential and active biological process that restores brain function including memory, mood, cognition and resiliency to stress.”

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Why do we need booster shots, and could we mix and match different COVID vaccines?

Why do we need booster shots, and could we mix and match different COVID vaccines?

The COVID vaccine rollout is now underway in Australia and around the world. It’s incredible we’ve been able to develop and produce safe and effective vaccines so quickly—but the current crop of vaccines might not protect us forever.

Fortunately, researchers are already developing and testing booster shots. So what are booster shots, and when might we need them?

First a prime, then a boost

The first time you give someone a dose of vaccine against a particular infection, it’s called a prime. You’re getting your immune response ready to roll.

Each time you give another dose against that same infection, it’s called a boost. You’re building on immunity you already have from the first dose.

Importantly, giving smaller doses in multiple shots is often better than a large dose of vaccine in a single shot. This is because our immune system builds on our immunity like bricks in a wall; each level needs to be laid before the next layer is built.

Booster shots take advantage of a phenomenon called “immunological memory”. Our immune cells essentially remember vaccines we’ve previously received, and respond much more quickly and vigorously to subsequent shots, building our immunity to levels at which we can be confident we’ll be protected.

When might I need a boost?

There are three different situations in which you might need a boost.

First, several doses of a vaccine can be given relatively quickly, one after another, to rapidly build someone’s immunity against a given infection. A good example is the whooping cough vaccine. It’s initially given at around two, four and six months of age to rapidly build immunity in infants, who are most at risk from whooping cough.

This is also the approach most COVID vaccines use. The first shot gets your immune system going but immunity is unreliable. The second shot leads to more consistent protection.

Second, we can give a booster shot if immunity drops over time, or “wanes,” to restore someone’s immunity to optimal levels. For example, we know immunity to tetanus can drop over time, so we recommend tetanus boosters every ten years.

Immunity appears to be strong three months after the Moderna vaccine and six months after the AstraZeneca vaccine, but we don’t yet have a full picture of how long immunity to COVID-19 lasts after vaccination. Scientists will continue to monitor this to determine if and when we’ll need these type of boosters for COVID.

Third, if the virus “mutates” or changes substantially over time, this can make it challenging for our immune cells to recognize the virus, effectively lowering our immunity again. A good example here is the influenza vaccine. The ‘flu virus can change a lot from year to year so, to make sure immunity remains high, we give annual boosters tailored to new strains.

On the front foot with viral variants

SARS-CoV-2, the virus that causes COVID-19, has already undergone a number of changes. We’re still learning how this might affect the efficacy of different vaccines.

But vaccine manufacturers are already adjusting their COVID vaccines to better target new variants. Moderna, for example, has just administered the first doses of an updated vaccine to volunteers in a new clinical trial. They’re intending to find out how well it works against B.1.351, the variant first identified in South Africa.

The updated vaccines tweak the “antigen”—the molecule used by our immune cells to target a specific virus. But they can use the same basic design and manufacturing processes.

As a result, they probably won’t have to go through the full gamut of clinical testing again. Regulatory hurdles are similarly streamlined with updated ‘flu vaccines.

Rapid development of these updated vaccines will put us on the front foot in our fight against COVID-19.

More of the same, or something a little different?

With boosting, you can end up with a higher level of immunity if you wait longer between doses. This is because our immune cells need a rest before they can respond to additional doses. We’ve seen this with the AstraZeneca vaccine where a longer delay between doses, up to 12 weeks, leads to much better protection.

It’s also possible we could generate greater immunity if we use different vaccines, one after the other, rather than repeating the same vaccine. This is called heterologous prime boosting.

We’re not sure why a mix-and-match approach can be more potent. But it’s possible combining two different vaccines—which give the same antigen target but stimulate the immune system in different ways—could better focus our immune cells’ attention on the right target.

We haven’t really taken advantage of heterologous vaccines in real-world settings yet. The first clinical heterologous vaccine was an Ebola vaccine approved in May 2020, while the Sputnik V COVID vaccine is also a heterologous vaccine.

But that could change. While there are now multiple approved COVID vaccines, vaccine rollout has been challenging. In the United Kingdom, the official policy is to use the same vaccine for both shots. But if the vaccine used for the first shot is not known or not available, people can still receive a booster with what is available.

Meanwhile, a clinical trial in the UK is evaluating the immune response when the Pfizer vaccine is followed by the AstraZeneca vaccine, and vice versa, as compared two doses of the same vaccine.

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Targeted immunotherapy could boost radiotherapy response

Targeted immunotherapy could boost radiotherapy response

Cancers that are resistant to radiotherapy could be rendered susceptible through treatment with immunotherapy, a new study suggests.

Manipulating bowel cancers based on their “immune landscape” could unlock new ways to treat resistant tumors.

Cancers can evolve resistance to radiotherapy just as they do with drugs.

The new study found that profiling the immune landscape of cancers before therapy could identify patients who are likely to respond to radiotherapy off the bat, and others who might benefit from priming of their tumor with immunotherapy.

Inflammation predicts radiotherapy response

Scientists at The Institute of Cancer Research, London, in collaboration with the University of Leeds and The Francis Crick Institute, studied inflammation in bowel tumor samples taken before and after radiotherapy from 53 patients. They aimed to understand how tumor immune activity before and after radiotherapy differs between patients who respond well and those who respond poorly to treatment.

The study is published in the Journal for ImmunoTherapy of Cancer and was supported by the NIHR Biomedical Research Centre at The Royal Marsden NHS Foundation Trust and the ICR, and the Medical Research Council.

The team showed that the effectiveness of radiotherapy partly depends on the level of inflammation within tumors before and after treatment.

In the study, patients who showed a poor response to radiotherapy—with no substantial falls in numbers of tumor cells—started with chronically inflamed tumors, with high levels of activity in 40 immune genes. The level of inflammation within their tumors showed minimal changes following radiotherapy.

In contrast, good responders—who saw a marked drop in the number of tumor cells during radiotherapy—started with a relatively low inflammation tumor landscape which revved up following treatment. Here, there was a significant increase in the activity of 198 immune genes including genes representing immune cells that can directly kill tumor cells.

Careful timing of immunotherapy alongside radiotherapy could unlock resistant cancers

Together, the findings show that carefully timing a combination of immunotherapy and radiotherapy, based on an assessment of the cancer’s immune landscape, could provide a way forward for treating resistant cancers.

Although the study was carried out specifically in bowel cancer the researchers believe the findings could be relevant for other types of the disease too, particularly for cancers where surgery is not an option and radiotherapy is particularly important.

Increasing evidence shows that radiotherapy not only works by causing DNA damage and cell death in cancer cells but also in potentially a similar way to a vaccine—priming the immune system to recognize tumor cells and ramp up an immune response to attack them.

This work is part of growing activity at the ICR and in radiotherapy and immunology which includes the RadNet radiotherapy research network, in collaboration with The Royal Marsden.

Immunotherapy and radiotherapy could prove a highly potent mixture

Study leader Dr. Anguraj Sadanandam, leader of the Systems and Precision Cancer Medicine Team at the ICR, said:

“Radiotherapy has revolutionized cancer treatment and is the most effective way of curing cancer other than surgery.

“Our study has shown that the immune landscape and levels of inflammation within cancers is crucial to determining how they respond to radiotherapy. It suggests that combining radiotherapy with immunotherapy could prove a highly potent mixture—improving our ability to eliminate hard-to-treat cancers further still.

“Now we want to improve our understanding of how to combine and sequence radiotherapy and immunotherapy together to maximize the treatment response for the individual biology of each patient.”

Study co-author Dr. Anna Wilkins, Clinical Research Fellow in the Clinical Trials and Statistics Unit at the ICR, now at The Francis Crick Institute, said:

“Radiotherapy is an important curative treatment option for many patients with cancer. We are starting to understand how the immune response is important for radiotherapy to work most effectively.

“Our study suggests that by targeting specific non-cancer cells that block this immune response we can further improve radiotherapy responses in patients.”

Dr. Nick West, Clinical Academic Fellow at the University of Leeds and Honorary Consultant in Gastrointestinal Pathology, said:

“Radiotherapy is commonly used in patients with rectal cancer and there are currently no validated biomarkers that reliably predict how well the cancer will respond. Patients who do not respond well to radiotherapy may still experience significant side effects despite no clinical benefit.

“This study suggests that we can potentially improve the response in these patients through modulation of the immune system, which is a very exciting development. The study also showed that a novel technique developed at the University of Leeds, tumor cell density, can be used to objectively measure the degree of tumor response to radiotherapy.”

Tuning the radiotherapy response through immunotherapy

Professor Paul Workman, Chief Executive of the ICR said:

“This fascinating study adds to the evidence that the effectiveness of radiotherapy is closely intertwined with the involvement of the immune system. It’s now clear that the radiotherapy response in cancer cells and surrounding tissues can empower a patient’s own immune system to recognize and destroy their tumor.

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Replacing your furnace filter could help protect from COVID-19

Replacing your furnace filter could help protect from COVID-19

Until a vaccine is readily available, a high-efficiency furnace filter used along with other precautions could help protect people from COVID-19 while they spend time together indoors.

Dr. Yue-Wern Huang, director of S&T’s Laboratory of Environmental Toxicology and a professor of biological sciences, is studying bioaerosols—the particles people release when they speak, sing or cough. He and his team of researchers are observing how viruses travel through the air, how time and environmental conditions affect the viability of viruses, and how proper ventilation can help control viral spread.

“As particles travel in time and distance, their physical properties such as size continue to change due to environmental factors like humidity and temperature,” says Huang. “The viability of pathogens contained within these bioaerosols is largely unknown right now.”

Huang uses a portal chamber and a walk-in chamber to create simulations and then studies the behavior of bioaerosols by collecting and analyzing pathogens on various filters. He uses bioaerosols that contain pathogens similar to SARS-CoV-2, the virus that causes COVID-19.

Working with Huang at S&T is Dr. Yang Wang, assistant professor of civil, architectural and environmental engineering, and Dr. Guang Xu, associate professor of mining engineering. The project is funded by a $330,000 grant from the National Science Foundation.

“This research project is an excellent example of in-depth collaboration between very different disciplines,” says Huang. “Dr. Wang is a particle physicist who knows all about aerosol physics, while Dr. Xu is an expert in mining ventilation. We put together our three areas of expertise to create a unique team to successfully pursue this research during the COVID-19 pandemic.”

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U.K. COVID variant may be more lethal, and could become dominant U.S. strain by March

U.K. COVID variant may be more lethal, and could become dominant U.S. strain by march

(HealthDay)—Even as efforts to vaccinate Americans gain steam, more evidence has emerged that suggests a coronavirus variant already known to spread faster is also likely to be more deadly.

The B.1.1.7 variant, which is thought to have originated in Britain, is already firmly entrenched in America and could soon become the dominant strain, according to Dr. Rochelle Walensky, director of the U.S. Centers for Disease Control and Prevention.

Speaking Sunday on CBS’ “Face the Nation,” she said “we know now that, or we estimate now that about 4% of disease in this country is related to B.1.1.7,” she said. “And we have projections that it may be the dominant strain by the end of March.”

Her warning came on the heels of research released by British scientists that shows B.1.1.7 might be more likely to trigger more lethal cases of COVID-19.

As reported Saturday by The New York Times, the new study was posted Friday on a U.K. government website. The scientists stressed that, as has always been the case, the vast majority of COVID-19 cases are not fatal, and their new research is based on only a small proportion of deaths in Britain.

Still, “the overall picture is one of something like a 40 to 60 percent increase in hospitalization risk, and risk of death,” Neil Ferguson, an epidemiologist and scientific adviser to the British government, told the Times on Saturday.

B.1.1.7 is known to have spread to at least 82 countries and is thought to be transmitted between 35 and 45 percent more easily than other variants of coronavirus already found in the United States, the Times said.

Newer data

The British team first signaled more than a month ago that they thought there was a “realistic possibility” that B.1.1.7 might also be more lethal, based on a small amount of preliminary data. With more data now in hand, they say they have a 55 to 75 percent degree of confidence in the latest finding.

Exactly why the variant causes more death isn’t clear. It could cause higher viral loads within the body, making treatment tougher. Muge Cevik, an infectious disease expert at the University of St. Andrews in Scotland and a scientific adviser to the British government, told the Times the variant may also “transmit disproportionately in settings with frailer people,” such as nursing homes, because it is more transmissible.

Vaccines already being distributed in the United States are believed to be effective against B.1.1.7, so Walensky said it’s imperative that the massive rollout already underway continues. At the same time, and in the face of other new variants, other steps are underway, she told CBS.

Pharmaceutical companies are tweaking their research to fight the B.1.1.7 variant, she said, and the CDC is monitoring how people who’ve already gotten the Pfizer or Moderna vaccines are faring.

“But we’re not waiting for that,” she said. “We’re doing the science to scale up different vaccines in case we either need bivalent vaccines, that is a vaccine that has two different strains, or booster vaccines. Both are happening.”

In the meantime, she said, Americans need to continue with tried-and-true ways of curbing viral spread such as social distancing and mask-wearing.

“So what I would say is now is the time to not let up our guard. Now is the time to double down, still with 100,000 cases a day, still with over two and a half times the cases we had over the summer,” Walensky said.

Big boost in vaccine supply

The United States will have enough COVID-19 vaccines to inoculate 300 million Americans by summer, President Joe Biden announced Thursday.

During a tour of the National Institute of Health’s Viral Pathogenesis Laboratory, where the Moderna COVID-19 vaccine was created, Biden said his administration had secured the delivery of 600 million doses of the Moderna and Pfizer vaccines over the next five months, the Associated Press reported.

“We’re now on track to have enough supply for 300 million Americans by the end of July,” he announced.

The country is already on pace to exceed Biden’s goal of administering 100 million vaccine doses in his first 100 days in office, with more than 26 million shots delivered during his first three weeks in office, the AP reported.

“That’s just the floor,” Biden said. “Our end goal is beating COVID-19.”

If a third coronavirus vaccine, from drugmaker Johnson & Johnson, is approved for emergency use by the U.S. Food and Drug Administration at the end of February, the pace of vaccinations should accelerate even further.

Biden emphasized that his administration is doing everything possible to increase vaccine supply and the country’s capacity to deliver injections into arms.

To date, the Biden administration has deployed active-duty troops to man mass vaccination sites in several states, as it looks to lay the groundwork for increasing the rate of vaccinations once more supply is available.

On the NIH tour, Biden was shown the lab bench where researchers sequenced the coronavirus and developed the precursor of the Moderna vaccine, the AP reported.

Just days after Chinese scientists shared the genetic blueprint of the new coronavirus in January of last year, the NIH had sent instructions to Moderna to brew up doses and scientists were already setting up the key lab and animal tests that would eventually prove they were on the right track, the AP reported.

All Americans could get vaccine by April: Fauci

Any American will be able to start getting vaccinated by April, the nation’s leading infectious diseases expert predicted earlier this month.

During an interview on the “Today Show,” Dr. Anthony Fauci said that month will be “open season” for vaccinations, as increased supplies of the vaccines will allow most people to get shots to protect against COVID-19.

Fauci, who serves as science adviser to President Joe Biden, added that the rate of vaccinations will greatly accelerate in the coming months. Why? He credited forthcoming deliveries of the two approved vaccines, the potential approval of a third vaccine and measures taken by the Biden administration to increase capacity to deliver doses.

“By the time we get to April,” it will be “open season, namely virtually everybody and anybody in any category could start to get vaccinated,” Fauci noted.

Despite that good news, he cautioned it will take “several more months” to actually deliver shots to Americans, but herd immunity could be achieved by late summer. As of Monday, more than 70 million doses have been distributed, while nearly 53 million Americans have been vaccinated. More than 14 million people have gotten their second shot.

Meanwhile, fully vaccinated Americans can now skip quarantines if they are exposed to someone infected with COVID-19, new federal guidelines say.

“Fully vaccinated persons who meet criteria will no longer be required to quarantine following an exposure to someone with COVID-19,” the U.S. Centers for Disease Control and Prevention said in updated guidance posted Wednesday on its website.

There was one caveat: At least two weeks must have passed since the second shot, because it takes that long to build full immunity. But the CDC says it’s not known how long protection lasts, so people who had their last shot three months ago or more should still quarantine if they are exposed or show symptoms, the agency added.

“This recommendation to waive quarantine for people with vaccine-derived immunity aligns with quarantine recommendations for those with natural immunity,” the CDC said. People who have been vaccinated should still watch for symptoms for 14 days after they have been exposed to someone who is infected, the agency added.

That doesn’t mean vaccinated people should stop practicing social distancing, the CDC noted.

“At this time, vaccinated persons should continue to follow current guidance to protect themselves and others, including wearing a mask, staying at least 6 feet away from others, avoiding crowds, avoiding poorly ventilated spaces, covering coughs and sneezes, washing hands often, following CDC travel guidance, and following any applicable workplace or school guidance, including guidance related to personal protective equipment use or SARS-CoV-2 testing,” the agency said.

A global scourge

By Monday, the U.S. coronavirus case count passed 27.6 million while the death toll passed 485,000, according to a Times tally. On Monday, the top five states for coronavirus infections were: California with nearly 3.5 million cases; Texas with more than 2.5 million cases; Florida with over 1.8 million cases; New York with more than 1.5 million cases; and Illinois with over 1.1 million cases.

Curbing the spread of the coronavirus in the rest of the world remains challenging.

In India, the coronavirus case count was nearly 10.9 million by Monday, a Johns Hopkins University tally showed. Brazil had over 9.8 million cases and more than 239,000 deaths as of Monday, the Hopkins tally showed.

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Immune response to insulin could identify, help treat those at risk for type 1 diabetes

diabetes

Researchers from the Barbara Davis Center for Childhood Diabetes at the University of Colorado Anschutz Medical Campus have found that immune responses to insulin could help identify individuals most at risk for developing Type 1 diabetes.

The study, out recently in the Proceedings of the National Academy of Sciences, measured immune responses from individuals genetically predisposed to developing Type 1 diabetes (T1D) to naturally occurring insulin and hybrid insulin peptides. Since not all genetically predisposed individuals develop T1D, researchers sought to examine T-cell immune responses from the peripheral blood that could occur before the onset of clinical diabetes.

“We want to know why people develop T1D, and this research has helped provide a lot more information and data as to what it looks like when genetically at-risk individuals are headed towards clinical diagnosis,” says Aaron Michels, MD, the study’s lead researcher, Associate Professor of Medicine at CU Anschutz and researcher at the Barbara Davis Center. “Ideally, you want to treat a disease when it’s active, so this is a need in our field to understand when people have an immune response directed against insulin producing cells.”

Researchers collected blood samples from genetically at-risk adolescents every 6 months for two years. Inflammatory T-cell responses to hybrid insulin peptides correlated with worsening blood glucose measurements and progression to T1D development. The results indicate an important advancement in identifying the risk of T1D early as well as the potential for intervention.

“There are now therapies used in research studies that have delayed the onset of clinical type 1 diabetes,” says Michels. “Patients with these specific immune responses, may benefit from immune intervention to delay T1D onset and possibly prevent it for years.”

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Coronavirus: why combining the Oxford vaccine with Russia’s Sputnik V vaccine could make it more effective

Coronavirus: why combining the Oxford vaccine with Russia's Sputnik V vaccine could make it more effective

When the efficacy of the Oxford/AstraZeneca vaccine was announced in late 2020, there was some confusion. The overall efficacy of the vaccine at stopping people developing symptomatic COVID-19, two weeks after the second dose, was 70%. But this wasn’t the whole picture.

This figure was based on averaging the results from two groups. In one group, which was given two full doses, the vaccine was 62% effective at stopping people developing symptoms. But in the second group, a dosing error meant that volunteers received a half dose followed by a full one. This ended up being 90% protective against developing COVID-19.

This was intriguing. Why would giving people less of the vaccine lead to a more effective immune response? The answer to this may lie in the design of the vaccine, and could mean that there are ways to make this vaccine—and others that use the same design—more effective.

How the Oxford vaccine works

Vaccines work by exposing the immune system to recognisable parts—or “antigens”—of pathogens that cause disease, such as bacteria or viruses. The immune system then mounts a response. Immune cells called B cells make antibodies to destroy the pathogen. Sometimes T cells can also be called into action, which eliminate our own cells that have been infected with the pathogen.

Some B and T cells then remember the antigens for the future. At some future point, if the person is exposed to the pathogen, these long-lasting memory cells can quickly order more antibodies to be made to destroy the pathogen and attack infected cells.

In effect, the principle of vaccination is to “mimic” an infection, but in a controlled way so that immunity is generated without causing illness. After a few weeks, once T cells and B cells have been generated, the person vaccinated will be protected. For certain vaccines, this requires two doses, as in some people the first dose alone won’t generate complete immunity. The booster dose ensures as many people as possible acquire protection.

In the case of the coronavirus vaccines, a number of methods are used to present the virus’s antigens to the immune system. Some, such as the Sinopharm and Sinovac vaccines in China, simply present the body with a whole, inactivated version of the coronavirus. But others instead instruct the vaccinated person’s own cells to produce a specific part of the coronavirus: the spike protein on its outer surface, which is a particularly recognisable antigen.

These vaccines do this by delivering the part of the coronavirus’s genetic code that encodes the spike protein into the cells of the body, which then read the code and start making the protein. Some, such as the Pfizer/BioNTech and Moderna vaccines, deliver the code in the form of messenger RNA (mRNA). Others use a harmless virus to get the genetic code inside cells; the Oxford vaccine uses chimpanzee adenovirus, genetically altered so that it’s unable to reproduce, called ChAdOx1. These are known as viral-vector vaccines.

How design could affect efficacy

It’s not yet known why the reduced-dose regimen of the Oxford vaccine showed better efficacy in trials, but it could be down to the viral vector.

When a person is given a viral-vector vaccine, as well as generating an immune response against the coronavirus’s spike protein, the immune system will also mount a response against the viral vector itself. This immune response may then destroy some of the booster dose when it is subsequently delivered, before it can have an effect. This has long been recognised as a problem.

However, a lower first dose might not allow for a strong anti-vector immune response to develop, which could leave the booster dose unscathed and lead to greater overall efficacy. If it turns out that this is the case, then future work will need to establish the optimum dosing regimen for generating the strongest immune response.

The Russian Sputnik V vaccine acknowledges that immunity to the viral vector could be a problem, but comes up with a different solution. It uses two different human adenoviruses—Ad26 and Ad5 (out of the 50 that affect humans) – for its two vaccine doses. This heterologous (or hybrid) vaccine, with different vectors for prime and booster vaccinations, is less likely to have one jab generate an immune response against the viral vector that then interferes with the other. The vaccine is therefore less likely to have a reduced efficacy.

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New 'iron lung' ventilator could revolutionise Covid treatment

New ’21st Century iron lung’ ventilator designed by British experts could revolutionise Covid treatment by taking patients out of intensive care wards

  • Exovent was modelled on the ‘iron lung’ used to battle 20th century polio crisis
  • Device said to be more comfortable, cheaper and needs fewer staff to manage
  • The device has already successfully been tested on six healthy adults 

British experts have designed a new type of ventilator that may allow more patients with severe Covid-19 to be treated outside of intensive care, easing pressure on hospitals hit hard by the coronavirus crisis.

The pandemic has put immense pressure on the NHS, with figures from earlier this month showing how the number of coronavirus patients in hospital was almost twice the level during the darkest days of the first wave last year. 

The researchers said that their device, known as exovent, is more comfortable for the patient, cheaper than those currently being used in intensive care units (ICU), and requires fewer staff to manage it.

Exovent is a negative pressure ventilator – which means it works by lowering the pressure outside the body to allow lung tissue to expand and function in a way that resembles normal breathing.

The device, which is modelled on the ‘iron lung’ used to battle the polio crisis in the 20th century, works differently from the conventional positive pressure ventilators which, instead, push air into the lungs. 

The device has already successfully been tested on six healthy adults, although it will need to be put through its paces in a full clinical trial before it can be put into general use. 

Researchers found it was ‘able to deliver both an increased lung expansion to people breathing spontaneously, and powerful ventilation to take over people’s breathing entirely, using only moderate negative pressures’.

British experts have designed a new type of ventilator, known as exovent, that may allow more patients with severe Covid-19 to be treated outside of intensive care

As positive pressure devices became much smaller, cheaper and more convenient over the years, research into negative pressure devices was mostly abandoned since the 1950s.

However, the scientists behind exovent said that negative pressure devices are far less intrusive than either positive pressure ventilation, where a tube is inserted into the windpipe, or continuous positive airway pressure (CPAP), where oxygen is delivered through a tightly-fitting face mask.

Patients do not need to be sedated and can take food and medication by mouth, as well as talk to loved ones on the phone when using exovent, they added.

The new ventilator was previously endorsed by the family of the late theoretical physicist Stephen Hawking.

He died in 2018 after battling motor neurone disease since 1963 and relied on a ventilator to stay alive.

His family told the Sunday Telegraph: ‘As the family of a ventilated man, we know the life and death difference that access to this kind of medical technology makes.’

Exovent is a negative pressure ventilator – which means it works by lowering the pressure outside the body to allow lung tissue to expand and function in a way that resembles normal breathing

The device, which is modelled on the ‘iron lung’ (pictured) used to battle the polio crisis in the 20th century, works differently from the conventional positive pressure ventilators which, instead, push air into the lungs

During the first wave of the coronavirus crisis last year, private firms rushed to offer to build new ventilators amid fears that hospitals would run out of the machines as coronavirus hospitalisations increased dramatically. 

Ian Joesbury, the chief executive of exovent, said: ‘We are really excited to be unveiling this life-saving system which is a cutting-edge reinvention of pre-existing technology.

What is a ventilator? 

A machine that helps people breathe.

It puts oxygen directly into patients’ lungs and removes carbon dioxide from them. 

A breathing tube connects the ventilator machine to your body. 

One end of the tube is placed into the lung’s airways through down the throat or nose. 

In some serious cases, the tube is connected directly to the windpipe through a small cut in the throat. 

Surgery is needed to make the hole in the neck. This is called a tracheostomy.

Patients are heavily sedated so they can’t fight the sensation of being unable to breathe on their own. 

Ventilators are used to help a person breathe if they have lung disease or another condition that makes breathing difficult.

They can also be used during and post-surgery.

‘As the patient does not need to be sedated it opens up alternative treatment options that may allow more patients with Covid-19 to be treated outside of intensive care.’

A team of anaesthetists, nurses and engineers were involved in the design of the exovent chamber, which consists of a base fitted on to a standard hospital bed.

A pump unit is connected to the base by hoses and pressure around the torso can be adjusted using a control unit.

The patient’s torso can be monitored through a window and accessed through portholes.

The device was tested on six healthy adults in the presence of three senior anaesthetists.

According to the researchers, exovent ‘was able to deliver both an increased lung expansion to people breathing spontaneously, and powerful ventilation to take over people’s breathing entirely, using only moderate negative pressures’.

However, they said that a clinical trial is required to fully test the device.

They believe exovent can also help people with other respiratory diseases such as pneumonia or chronic obstructive pulmonary disease (COPD).

According to the team, an exovent device costs approximately £8,000, making it cheaper than existing positive-pressure devices, which cost around £15,000 for CPAP machines and more than £30,000 for intensive care ventilators.

The researchers said they are planning to submit their exovent design to the Medicines and Healthcare products Regulatory Agency (MHRA), which regulates medical devices in the UK.

In the meantime, the details of the device have been published in the journal Anaesthesia.

The family of the late theoretical physicist Stephen Hawking (pictured) said: ‘As the family of a ventilated man, we know the life and death difference that access to this kind of medical technology makes’

A SHORT HISTORY OF THE IRON LUNG

An iron lung is a non-invasive negative-pressure ventilator, used to artificially maintain respiration during an acute polio infection.

They were first used in the 1920s and work by producing pressure on the lungs that causes them to expand and contract so that patients can breathe.

In most cases it would only be used for one or two weeks, until the patient could breathe independently, but some polio survivors with permanent respiratory paralysis rely on them daily. 

They are now all but obsolete, replaced by positive-pressure ventilators such as modern day respirators.

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