Researchers discover new member of novel drug family for ‘undruggable’ targets

In the last several years, excitement has surged for a promising class of drugs that work not by inhibiting the action of a molecular target, as most conventional drugs do, but instead by harnessing the cell’s recycling system to destroy the target. However, these unusual compounds, known as molecular glue degraders, have been difficult to find and engineer.

Now, a research team led by scientists at the Broad Institute of MIT and Harvard and the Friedrich Miescher Institute for Biomedical Research in Basel, Switzerland has discovered a new molecular glue degrader called CR8. By dissecting the details of CR8’s molecular mechanism of action, as described in a paper published in Nature, the researchers show how it may be possible to build more of these unique compounds as potential treatments for a variety of diseases.

“We have shown that it is possible to take a conventional kinase inhibitor and, by attaching a particular chemical group, transform it into a molecular glue degrader,” said co-senior author Benjamin Ebert, an institute member in the Broad Cancer Program and the chair of the Department of Medical Oncology at Dana-Farber Cancer Institute. “This offers the potential for creating molecular glue degraders for a much wider range of therapeutic targets than we had initially anticipated.”

Throw away the lock and key

Most drugs use a lock-and-key approach to target proteins, typically enzymes, by directly binding within distinct grooves in the target protein to block its activity. Yet many other kinds of proteins, like transcription factors, lack such binding sites, which has stymied efforts to design drugs against these traditionally “undruggable” targets.

About six years ago, Ebert and his colleagues revealed that a well-known multiple myeloma drug, called lenalidomide, works as a molecular glue degrader. Instead of directly binding to its targets, it operates more stealthily, by recruiting a molecular machine that tags target proteins for destruction in the cell. This machine, known as E3 ubiquitin ligase, attaches a small protein called ubiquitin to the ill-fated targets, which are then degraded by the cell’s recycling system.

To identify more molecular glue degraders, Ebert’s team, led by co-first author Mikolaj Slabicki, a postdoctoral researcher at Broad and the German Cancer Research Center in Heidelberg, studied data on more than 4,500 drugs and compounds from the Broad’s Drug Repurposing Hub, a collection of compounds that have been shown to be safe in humans, including many that are FDA-approved. The scientists combed through these publicly available data to pinpoint drugs that preferentially kill cancer cells with high E3 ubiquitin ligase levels.

“We were always brainstorming in the lab to figure out how we can find more molecular glue degraders,” said Slabicki. “We were incredibly fortunate to have access to such large, robust datasets. We wouldn’t have made this discovery without the dataset generated at the Broad Cancer Program.”

A path to creating more

CR8 is a compound that was originally designed to inhibit enzymes called cyclin-dependent kinases (CDKs), which play important roles in controlling cell growth. The researchers used their bioinformatic approach to discover that CR8’s cell-killing activity correlates with levels of a component of the E3 ubiquitin ligase complex called DDB1.

The team found that CR8 kills cancer cells by inducing degradation of a protein called cyclin K, which is a binding partner of some CDKs, in particular CDK12. CR8 does this by acting like a molecular glue, binding CDK12-cyclin K, and recruiting DDB1 and subsequently other parts of the E3 ubiquitin ligase complex, which results in the tagging of cyclin K for degradation.

Collaborators from the Friedrich Miescher Institute including co-senior author Nicolas Thomä and co-first authors Zuzanna Kozicka and Georg Petzold solved the crystal structure of key components of this CR8-induced protein complex, which revealed new molecular details about the interactions between all the glued-together parts.

The Boston and Basel teams looked at the activity of a drug that’s structurally similar to CR8 and found that it doesn’t lead to cyclin K degradation. The only structural difference between the two compounds is a lone chemical moiety known as a pyridyl substituent, that protrudes out. This moiety, the team concluded, is sufficient to enable CR8 to act like a molecular glue degrader. The finding suggests that chemical modifications of outward-facing parts of inhibitors could turn them into molecular glue degraders of a given protein target.

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Machine learning can give healthcare workers a ‘superpower’

With healthcare organizations around the world leveraging cloud technologies for key clinical and operational systems, the industry is building toward digitally enhanced, data-driven healthcare.

And unstructured healthcare data, within clinical documents and summaries, continues to remain an important source of insights to support clinical and operational excellence.

But there are countless nuggets of important unstructured data – something that does not lend itself to manual search and manipulation by clinicians. This is where automation comes.

Getting insights from unstructured data

Arun Ravi, senior product leader at Amazon Web Services is co-presenting a HIMSS20 Digital presentation on unstructured healthcare data and machine learning, Accelerating Insights from Unstructured Data, Cloud Capabilities to Support Healthcare.

“There is a huge shift from volume- to value-based care: 54% of hospital CEOs see the transition from volume to value as their biggest financial challenge, and two-thirds of the IT budget goes toward keeping the lights on,” Ravi explained.

“Machine learning has this really interesting role to play where we’re not necessarily looking to replace the workflows, but give essentially a superpower to people in healthcare and allow them to do their jobs a lot more efficiently.”

In terms of how this affects health IT leaders, with value-based care there is a lot of data that is being created. When a patient goes through the various stages of care, there is a lot of documentation, a lot of data that is created.

“But how do you apply the resources that are available to make it much more streamlined, to create that perfect longitudinal view of the patient?” Ravi asked. “A lot of the current IT models lack that agility to keep pace with technology. And again, it’s about giving the people in this space a superpower to help them bring the right data forward and use that in order to make really good clinical decisions.”

The unstructured data automation model

This requires responding to a very new model that has come into play. And this model requires focus on differentiating a healthcare organization’s ability to do this work in real time and do it at scale.

“How you incorporate these new technologies into care delivery in a way that not only is scalable but actually reaches your patients and also makes sure your internal stakeholders are happy with it,” Ravi said. “And again, you want to reduce the risk, but overall, how do you manage this data well in a way that is easy for you to scale and easy for you to deploy into new areas as the care model continues to shift?”

So why is machine learning important in healthcare?

“If you look at the amount of unstructured data that is created, it is increasing exponentially,” said Ravi. “And a lot of that remains untapped. There are 1.2 billion unstructured clinical documents that are actually created every year. How do you extract the insights that are valuable for your application without applying manual approaches to it?”

Reducing expense and time

Automating all of this really helps a healthcare organization reduce the expense and the time that is spent trying to extract these insights, he said. And this creates a unique opportunity, not just to innovate but to build new products, he added.

Ravi and his co-presenter, Paul Zhao, senior product leader at AWS, offer an in-depth look into gathering insights from all of this unstructured healthcare data via machine learning and cloud capabilities in their HIMSS20 Digital session. To attend the session, click here.

Twitter: @SiwickiHealthIT
Email the writer: [email protected]
Healthcare IT News is a HIMSS Media publication.

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How to unblock your nose

When your nose is blocked, all you want to do is blow it. However, nothing ever comes out. A blocked nose normally resolves itself, but the process can be sped up with a few simple tricks. Express.co.uk talks you through six ways to unblock your nose.

What causes a blocked nose?

There are a few reasons why you could have a blocked nose.

Normally, a stuffy nose is due to inflamed blood vessels in the sinuses.

These vessels normally become irritated by a cold, the fly, allergies, or a sinus infection.

There are a few easy ways to calm down these vessels and unblock your nose as a result.

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Stay hydrated

Topping up on water throughout the way will ease a congested nose.

Keeping fluids flowing will help to thin the mucus in your nose, and push the fluids out.

Less fluids means less pressure on your sinuses, and this means less inflammation.

Try drinking a warm herbal tea, fresh juice, and cold water.

Hot shower

A hot shower should clear your nose temporarily, and here’s why.

The steam from a shower should thin out the mucus and take down inflammation.

This should allow you to breathe properly through your nose for a short while.

If you don’t have time for a shower, you could steam your face in a hot sink.

Fill the sink with hot water, hover your face over the sink, and place a towel over your head.

You will feel hot, but relax and take in deep breaths of the steam.

Take care not to burn your face on the hot water or steam, though.

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Warm compress

Another trick that involves warm water is using a warm compress.

Soak a towel or flannel in warm water and squeeze the water out again.

Place the damp towel over your nose and forehead, and allow the nasal passages to open up.

The temperature will ease pain and help to relieve inflammation of the nostrils.

Humidifier

Purchasing a humidifier will keep stuffy noses at bay.

A humidifier converts water to moisture, and the moisture fills the air. This makes the air more humid.

Moist air is better for a blocked nose than dry air, so a humidifier could soothe your irritated tissues and swollen vessels.

Humidifiers also thin the mucus in your sinuses, helping to empty the fluids in your nose. This should allow you to breathe easily again.

Keep your humidifier in your room to ease the inflammation while you sleep and relax.

Decongestants

Try a decongestant medication to reduce the swelling and ease pain.

You can opt for a nasal spray decongestant, or a pill decongestant.

An example of a nasal spray decongestant is Sinex.

Most nasal decongestants are available to buy over the counter without a prescription.

However, common decongestant pills, like Sudafed, include pseudoephedrine.

Because of this, they will be kept behind the pharmacy counter.

Antihistamine or allergy medicine

Your stuffy nose could be down to an allergy, so you might want to try taking an antihistamine or allergy medicine.

Both types of medication will reduce swelling and decongest your nose.

Check with your GP to see which medication is suitable of you.

There are even medications which combine both antihistamine and allergy medicine.

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Singer Amy Grant Just Had Open Heart Surgery To Treat A Rare Condition Called PAPVR

  • Christian singer Amy Grant had open heart surgery to treat a rare heart condition.
  • She was recently diagnosed with partial anomalous pulmonary venous return (PAPVR).
  • Because PAPVR is a congenital abnormality, Amy has had this condition since birth.

Singer Amy Grant shared some surprising news with fans this week: She just underwent open heart surgery to correct a rare heart condition called partial anomalous pulmonary venous return (PAPVR) that she’s had since birth.

“Thank you for all the prayers today! Amy’s heart surgery went well and she is recovering in the care of a great team of doctors. More updates to come,” a rep for Amy wrote in a post shared on Amy’s Instagram account on Thursday.

https://www.instagram.com/p/CA_7aHTDzcQ/

The “Every Heartbeat” singer had heart surgery on Wednesday to fix her rare heart condition PAPVR, which her doctor discovered earlier this year, People reported.

PAPVR is a congenital abnormality (meaning someone is born with it) where some of the pulmonary veins connect to the right atrium of the heart. This can cause blood that’s rich in oxygen to flow back to the lungs, instead of to the rest of the body, according to University of Wisconsin-Madison Health’s website. That can lead to symptoms like shortness of breath during heavy exercise.

“She had open heart surgery to correct a condition from birth the doctors discovered during a heart checkup called PAPVR,” Amy’s publicist told People. “Thankfully the doctor said it could not have gone better.”

Amy first shared news of her condition back in February in a statement on Twitter. At the time, she said that her doctor recommended she have her heart health checked out due to her family history. After a “battery of tests,” she was given a diagnosis that she didn’t share at the time. Amy also said at the time that she was “completely asymptomatic” and that her condition was “fixable.” “Instead of concerts and camping trips this summer, I am going to take care of my heart,” she wrote.

Fans were given a heads up on Facebook earlier this week that the surgery would be happening. “With all that is going on in our world that needs our collective prayer, please also join us in praying for Amy this week as she has heart surgery to correct her PAPVR condition,” her team wrote on Facebook.

Treatment for PAPVR is surgery under general anesthesia which, it seems, Amy had. During the surgery, the surgeon cuts open the patient’s breastbone and exposes the heart, according to UW Health. Blood from the heart is redirected to a bypass machine, while the doctor redirects blood flow from the anomalous pulmonary vein to the left atrium. Then, the bypass machine is shut down and the heart starts beating again.

Amy’s publicist told People that her team is “praying for a full and easy recovery over the next days, weeks, and months to come.”

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Stopping the clones may help win skin cancer battle

Targeting large clones of skin cells caused by ultraviolet irradiation (UV) may help reduce skin cancers, according to University of Queensland research.

Professor Kiarash Khosrotehrani said the study found proliferation of these large clones was concentrated around hair pores and not evenly distributed.

“Using genetic engineering of skin epidermal stem cells, we were able to track the growth, regression and cancerisation of individual clones that resulted from UV exposure.

“We found large clones regressed in size as soon as skin irradiation stopped, highlighting the importance of sun protection,” Professor Khosrotehrani said.

Keratinocyte cancers, or basal and squamous cell carcinomas, are one of the main cancers in Australia, affecting one in three people, and are strongly linked to sun exposure.

Dr. Edwige Roy said skin cancers were more likely to be found in large clones.

“While surgery is extremely effective in treating individual keratinocyte cancers, it doesn’t prevent a high proportion of patients from developing subsequent tumours in the same sun damaged area,” Dr. Roy said.

“In Queensland, about four per cent of people experience 10 or more skin cancers every three years.

“For these patients, skin cancer is a chronic disease with multiple surgeries and regular skin checks required during their lifetime.

“While it’s still unclear what processes drive the formation of skin cancer, our study helps clarify the influence of UV irradiation in its development by evaluating clone size dynamics in skin exposed to chronic ultraviolet irradiation,” she said.

“It also considers whether specific clones have more propensity to form skin cancer.

“Our findings have major implications for reducing skin cancer through sun protection and reducing the size of skin clones.

“Chemoprevention treatment could play a significant role in addition to sun protection by reducing the size of skin cancer clones, lowering keratinocyte cancers rates in Australia.”

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Diet, gut microbes affect effectiveness of cancer treatment, research reveals

What we eat can affect the outcome of chemotherapy—and likely many other medical treatments—because of ripple effects that begin in our gut, new research from the University of Virginia suggests.

Scientists found that diet can cause microbes in the gut to trigger changes in the host’s response to a chemotherapy drug. Common components of our daily diets (for example, amino acids) could either increase or decrease both the effectiveness and toxicity of the drugs used for cancer treatment, the researchers found.

The discovery opens an important new avenue of medical research. It could have major implications for predicting the right dose and better controlling the side effects of chemotherapy, the researchers report. The finding also may help explain differences seen in patient responses to chemotherapy that have baffled doctors until now.

“The first time we observed that changing the microbe or adding a single amino acid to the diet could transform an innocuous dose of the drug into a highly toxic one, we couldn’t believe our eyes,” said Eyleen O’Rourke of UVA’s College of Arts & Sciences, the School of Medicine’s Department of Cell Biology and the Robert M. Berne Cardiovascular Research Center. “Understanding, with molecular resolution, what was going on took sieving through hundreds of microbe and host genes. The answer was an astonishingly complex network of interactions between diet, microbe, drug and host.”

How diet affects outcomes

Doctors have long appreciated the importance of nutrition on human health, but the new discovery highlights how what we eat affects not just us, but the microorganisms within us.

The changes that diet triggers on the microorganisms can increase the toxicity of a chemotherapeutic drug up to 100-fold, the researchers found using the new lab model they created with roundworms. “The same dose of the drug that does nothing on the control diet kills the [roundworm] if a milligram of the amino acid serine is added to the diet,” said Wenfan Ke, a graduate student and lead author of a new scientific paper outlining the findings.

Further, different diet and microbe combinations change how the host responds to chemotherapy. “The data show that single dietary changes can shift the microbe’s metabolism and, consequently, change or even revert the host response to a drug,” the researchers report in their paper published in Nature Communications.

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Pollen count: Wearing this on your face may reduce hay fever symptoms if the count is high

Pollen count is based on how many particles there are in a cubic metre of the air. When the count is high or very high, then hay fever sufferers may experience worse symptoms like itchy eyes and a runny nose. The Met Office have forecasted HIGH pollen levels for the South East of England while the Midlands will experience MEDIUM levels. Areas in the North of England including Scotland will experience LOW levels.

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A high pollen count can mean that allergy sufferers can experience worse symptoms which can be irritating.

Hay fever occurs when the immune system mistakes a normally harmless airborne substance for a threat. The body then produces an antibody to attack the threat and releases the chemical known as histamine. It is histamine that causes the allergy symptoms.

Pollen count is usually higher in the summer months when it is warm but also can be high when the weather is damp and windy.

While it is recommended to take medication to help alleviate hay fever symptoms like antihistamines and eye drops, there are other measures that you should take in order to try and help manage your symptoms.

Eye drops can help puffy, itchy red eyes and can be purchased over-the-counter at your local pharmacy.

LloydsPharmacy’s allergy expert has shared their top tip to help you avoid suffering with bad symptoms.

Wearing wraparound sunglasses when you are outdoors can help your eyes stop itching.

This is because the sunglasses will help to keep pollen out of your eyes which causes itchy, red eyes.

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Pollen can spread very easily outside and so keeping your eyes covered fully is essential.

Wrap around sunglasses are recommended as it reduces the risk of pollen entering in any small gaps that there may be.

These types of sunglasses feature a semi-circular frame shape that wraps around your head reducing the distance between your face and the glasses frame.

This limits the opportunity for pollen, dust and irritants to reach the eye.

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However, when the pollen count is high, it is recommended that hay fever sufferers stay inside as much as they can.

This is particularly advised in the early morning and early evening as this is when the pollen count tends to be at its highest.

You should keep windows and doors shut during the day when the count is high to stop pollen getting trapped inside your home.

If it is essential that you go outside, then measures should be taken to help hay fever symptoms.

Another tip in trapping pollen particles is to add a small amount of Vaseline into and around your nostrils.

LloydsPharmcy say this may sound strange and can feel weird for a while but it can help pollen spores entering your nasal passages.

This will help you stop sneezing and should help alleviate symptoms.

You can check the accurate pollen count here: https://www.metoffice.gov.uk/weather/warnings-and-advice/seasonal-advice/pollen-forecast#?date=2020-06-03

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Flu researchers say we should make a NEW antiviral to stop coronavirus

Flu researchers say we should make a NEW antiviral to prevent coronavirus from replicating throughout the body and stop focusing on repurposing old drugs

  • Researchers looked an older treatment for the flu, Tamiflu, and a newer treatment, Xofluza, the first new type of flu drug in 20 years
  • Xofluza limited the amount of time a person was sick by quickly stopping the virus from replicating and spreading throughout the body
  • The team says the same approach needs to work for coronavirus, creating a new drug that stops the virus from multiplying rather then repurposing old drugs
  • In the US, there are more than 1.8 million confirmed cases of the virus and more than 105,000 deaths
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A new antiviral drug should be created to stop the novel coronavirus rather than repurposing old medication, a new study suggests.

Researchers compared an older antiviral treatment that most flu patients know compared to a newer one.

The newer treatment cut the amount of time people were sick with the flu, which limited the spread of the virus, because it stopped the disease from multiplying within an infected person. 

The team, from the University of Texas at Austin, says creating a drug that does the same for the coronavirus in early-stage patients would be more beneficial that trying to get existing drugs to treat late-stage patients.

A newer treatment fro flu Xofluza (blue) limited the amount of time a person was sick by quickly stopping the virus from replicating and spreading throughout the body rather than the older treatment of Tamiflu (green)

The team says the same approach needs to work for coronavirus, creating a new drug that stops the virus from multiplying rather then repurposing old drugs. Pictured: COVID-19 patients are taken into to the Wakefield Campus of the Montefiore Medical Center in the Bronx, New York, April 6

For the study, published in Nature Communications, the team looked at influenza and its implications for COVID, the disease caused by the virus.

Researchers first looked at the effects of Tamiflu, or its generic oseltamivir, one of three drugs the Centers for Disease Control and Prevention has endorsed to treat the flu.  

Then they looked at baloxavir, which is sold under the brand name Xofluza, the first new type of flu drug in 20 years.

The new treatment from the same company that developed Tamiflu, was shown in past studies to cut the amount of time people were sick and reduce the length of a fever. 

While Xofluza didn’t work faster than Tamiflu, it did reduce the level of the virus in patients’ nose and throat quicker. 

The new study showed that the newer treatment limited the amount of time a person was sick by quickly stopping the virus from replicating and spreading throughout the body. 

‘We found that treating even 10 percent of infected patients with baloxavir shortly after the onset of their symptoms can indirectly prevent millions of infections and save thousands of lives during a typical influenza season,’ said Dr Robert Krug, a professor emeritus of molecular biosciences, in a blog that accompanied the paper.  

Krug and his team say that a similar antiviral treatment would help to prevent thousands of infections and deaths from the coronavirus    

‘Imagine a drug that quashes viral load within a day and thus radically shortens the contagious period,’ said Dr Lauren Ancel Meyers, a professor of integrative biology.

‘Basically, we could isolate COVID-19 cases pharmaceutically rather than physically and disrupt chains of transmission.’

Most drugs being researched to treat COVID-19 have focused on existing antivirals that can be given to critically ill patient.

But the team says research should shift towards developing a new antiviral for the coronavirus that is used early on in infection and stops the virus from replicating,  , just as baloxavir does for the flu.

‘It may seem counterintuitive to focus on treatments, not for the critically ill patient in need of a life-saving intervention, but rather for the seemingly healthy patient shortly after a COVID-19 positive test,’ Krug said. 

‘Nonetheless, our analysis shows that the right early-stage antiviral treatment can block transmission to others and, in the long run, may well save more lives.’

In the US, there were more than 1.8 million confirmed cases of the virus and more than 105,000 deaths.

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Podcast: Addressing rumors, conspiracy theories related to coronavirus

A new episode of our podcast, “Show Me the Science,” has been posted. At present, these podcasts are highlighting research and patient care on the Washington University Medical Campus as our scientists and clinicians confront the COVID-19 pandemic.

It seems almost every day brings a new finding about COVID-19, but still, relatively little is understood about the novel coronavirus, the disease it causes or how best to prevent and treat it. Scientific research takes time, but the lack of sound research hasn’t stopped some from filling in the gaps with their own theories about the origins of the virus, potential treatments, vaccines, the usefulness of masks and other matters. In this episode, we discuss some of the strange theories filling social media feeds and even climbing best-seller lists. David Wang, PhD, a professor of molecular microbiology, and of pathology and immunology, discusses the origins of the new coronavirus, as well as what can be learned from past outbreaks. In addition, Michael S. Kinch, PhD, associate vice chancellor and director of the Center for Research Innovation in Biotechnology and the Center for Drug Discovery, discusses fears, particularly fears and rumors often linked to vaccines. Also a professor of radiation oncology and of biochemistry and molecular biophysics, he authored the book “Between Hope and Fear,” about the history of vaccines in medicine.

The podcast, “Show Me the Science,” is produced by the Office of Medical Public Affairs at Washington University School of Medicine in St. Louis.

Full transcript

[music plays]

Jim Dryden (host): Hello and welcome to “Show Me the Science,” a podcast about the research, teaching, and patient care, as well as the student, staff, and faculty at Washington University School of Medicine in St. Louis, Missouri, the Show-Me State. My name is Jim Dryden, and I’m your host this week. We’ve been focusing these podcasts on the COVID-19 pandemic and Washington University’s response, trying to bring you as much information as we can. Unfortunately, much still is unknown about this new coronavirus and the illness it causes. That, however, has not stopped some from trying to fill in the gaps. On social media, unfounded rumors and conspiracies abound about the origins of the virus, the use of masks, vaccines, and other issues. For example, some claim the virus is a bioweapon that was created in a lab in Wuhan, China. But Washington University’s David Wang who studies viruses says that’s extremely unlikely.

David Wang, PhD: Its sequence is different from any virus that we’ve ever seen, so it’s very difficult to imagine that anyone could have engineered it or manufactured it. And there are so many viruses that are very similar to it in nature in bats, that the most logical and simplest conclusion is that it came from nature.

Dryden: Other rumors make the unfounded claim that wearing a mask can make you sick, that vaccines we’ve received earlier in our lifetimes make us more vulnerable to infection with this new virus, even that when a COVID-19 vaccine finally arrives, it may be used as a way to track people and invade their privacy. Washington University’s Michael Kinch has written a book about the history of vaccines in the U.S. It’s called “Between Hope and Fear.”

Michael Kinch, PhD: In looking at the history of medicine, there has always been an irrational fear of vaccination. There was an anti-vax community before there was the first vaccine.

Dryden: This week, speaking with both Kinch and Wang, we’re comparing the rumors and conspiracy theories to the reality that the coronavirus has caused about 100,000 deaths in about three months in the United States. David Wang says this new coronavirus is different from other deadly viruses that have arisen in recent years.

Wang: It’s really because it’s a respiratory virus, and so it can be spread through droplets and particles in the air, and you don’t have to have direct contact. Everyone knows about Ebola virus, but Ebola virus is actually very difficult to transmit. You have to actually come into very close contact with fluids from an infected patient. So if you’re able to keep physically distant from the Ebola patient, then you won’t get infected. For Zika virus, which was in the news a couple years ago, that was transmitted primarily, almost exclusively by mosquitoes. And so it was very difficult for, again, humans to transmit to other humans. The first SARS was very similar to this one. It was less readily transmitted, and so then it was easier to contain by quarantine and isolation of people who were infected and their contacts.

Dryden: We know it’s caused hundreds of thousands of deaths worldwide in only a few months. There are some people who have suggested that something that deadly must have been created on purpose.

Wang: There’s no data to support the idea. It appears, by all accounts, to be a natural virus that emerged, and we’ve been dealing with natural viruses that emerged for the past many decades. It is, in fact, not very lethal compared to viruses like Ebola, which kill somewhere between 50 and 90% of the people who are infected by it. More specifically, the SARS-CoV-2 virus is a totally new virus. Its sequence is different from any virus that we’ve ever seen, so it’s very difficult to imagine that anyone could have engineered it or manufactured it. And there are so many viruses that are very similar to it in nature, in bats that the most logical and simplest conclusion is that it came from nature. There is absolutely no evidence that any parts of it have been manipulated by humans, as far as we can tell.

Dryden: Is there a way that you can explain why you think that?

Wang: I guess people have wanted to use viruses as bioweapons for a long time. During the Cold War, both the United States and the Soviet Union had biological warfare programs. And in those cases, though, they always utilized highly deadly viruses that we knew about. If you were going to engineer a brand-new virus, that’s extraordinarily difficult. But if you were going to do it, you might try to take pieces from the viruses that you knew were very deadly, and there’s no evidence that any parts of any known highly pathogenic viruses have been incorporated into the SARS-CoV-2 genome sequence.

Dryden: This gets compared to the Spanish flu of the World War I era. That, obviously, is a different kind of virus. There have also been other viruses that were relatively widespread and feared like polio, like smallpox. Is there a comparison between this and any of those?

Wang: In history, the most similar comparison is to the Spanish flu from 1918. That’s because it’s also a respiratory virus that transmits quite readily. It kills a significant fraction but not at the extraordinarily high levels of something like Ebola, which again, is something like greater than 50% of the people. So I think that there are a lot of analogies to the 1918 flu, although it’s a very different kind of virus. Our ability to treat and to hopefully develop therapeutics or prevention strategies are far superior now, and so that’s one advantage that we have. I think there is hope that we could have effective drugs that could be developed.

Dryden: The weather’s warming up. I know, again, a different kind of virus, but flu season tends to go away when the weather tends to get warm. Is there any thought that this virus might behave the same way, or is it possible that it will get worse again even with the warm weather?

Wang: I think it’s unlikely that the warm weather is going to help the situation in a significant way. That’s because when you look at other parts of the world, the virus is expanding tremendously in places like Saudi Arabia. Brazil is a hot spot right now, and Brazil’s on the equator. A lot of people can be infected with the virus and transmit the virus even though they don’t have symptoms.

Dryden: Is social distancing still the key as we move into the summer?

Wang: Public health people have done a good job of emphasizing that you have to do this social distancing and be six feet away from people. But I guess I’m concerned now with all this reopening that you have six-feet spacing and people can be sitting in the restaurant, but now you’re there for hours on end and you’re six feet away. This is not the magic bullet because it’s respiratory. Being six feet away from someone who was infected for two hours or three hours is not good. I fear that people have latched onto the six-feet thing as if it’s a magic thing. And if this was Ebola virus, it would be wonderful. You will not get Ebola virus if you’re six feet away, but this is a respiratory virus. And so I fear that — I don’t know, the people who want to open gyms, they’re saying, “Well, we’ll be social distanced. We’ll be six feet away.” So you’ll have people six feet away who are breathing heavily, huffing and puffing, and you’re both on the treadmill for an hour. Everybody’s exhaling forcefully and, yes, you are six feet away, but that’s worthless.

[music plays]

Kinch: I’m Michael Kinch. I’m an associate vice chancellor at Washington University in St. Louis.

Dryden: Kinch directs Washington University’s Center for Research Innovation and Biotechnology and Center of Drug Development. He has studied and written about vaccines throughout our nation’s history. And he says he believes part of the issue with this new coronavirus is that so much still is unknown, and so many people looking to learn more have been willing to accept bad information.

Kinch: Well, I think, obviously, it comes from fear, and I’m not a psychologist. I’m a biologist, but at the end of the day, to put things into perspective, this is an extremely dangerous virus. It is very easily communicated to others, and so we need to be very nervous about this.

Dryden: It seems as if there are a lot of people that don’t think masks protect you or don’t think masks protect others. The question is why do we wear masks?

Kinch: Well, we wear masks, probably if you look at the biology behind it, to prevent a virus that we might have from being transmitted to others. You’re doing service to your neighbor by wearing a mask. So instead of viewing it as something that is harmful to you and it’s inconvenient and everything else that goes with wearing a mask, the reality is that that mask is actually you preventing, hopefully, your spreading the disease to someone else.

Dryden: We wipe down our groceries when we get home, maybe we let the mail sit for a day before we open it, things like that. Are those worthwhile?

Kinch: We tend to become most fearful of the things that we, again, don’t understand as much. The likelihood that the virus is going to be sitting on that pizza box is actually quite low. The bigger fear is that you might communicate that to someone else and cause harm to them. And so we just have to put things into perspective, and right now we’ve got, if anything, perhaps an irrational fear of COVID-19 by some people. And then we have another population of people, a minority of people, that figure, “Well, let fate be what it is. I’m not afraid of this virus. It’s overblown.” The danger of that is that it doesn’t take but a small minority to infect the majority, and that’s what it really comes down to: A small number of people can really cause a lot of harm.

Dryden: We have heard that one reason we’re so susceptible to this is because we’ve all been vaccinated against measles, mumps, rubella, that these vaccines have made us more vulnerable. What are your thoughts?

Kinch: In part of the book that I wrote, which is called “Between Hope and Fear,” in looking at the history of medicine, there has always been an irrational fear of vaccination. And I can actually say and defend the statement that there was an anti-vax community before there was the first vaccine. Part of this fear that we’ve been experiencing today – and there was a documentary, or a supposed documentary, and a book that is on the best-seller list right now that is helping to spread the most recent version of the conspiracy, which is that vaccines are doing some harm. None of the vaccines on the market today have that inherent risk that has been attributed by this supposed documentary and this book to causing COVID-19 or propagating COVID-19. COVID-19 is, unfortunately, an infection that happens normally about every decade or two, naturally coming out of nature about every 10 to 20 years.

Dryden: But this one is worse than SARS was, for instance. Not that it’s worse for the people that are infected because my understanding is that SARS was probably more lethal than this one, but it was contained more quickly than this one was.

Kinch: Yes. So again, that gets back to the fact that all of your listeners need to realize there are two factors that make a disease truly lethal. One is whether it will kill you when you get it, but the other is how easily you transmit it. And when you look at SARS, it was very similar to Ebola, where basically, the disease was so deadly – well, you could argue from an evolutionary standpoint SARS was too deadly. It killed people before they had the ability to communicate the disease to the next person.

Dryden: A moment ago we were talking about your expertise with vaccines and the history of vaccines. Now there’s a rush to make a new one. Is there danger in bringing out a vaccine too quick? And then the second part is because we’re rushing to try to get a vaccine out and because there are people who are suspicious of vaccines, does that add to the paranoia?

Kinch: From the discovery side, it’s really important that we get this right because we need to make sure not just that we can develop a vaccine that elicits antibodies. And the early results that have caused a lot of excitement about some of the early vaccines that are being tested are just that, they’re very early. We don’t know whether they are creating protective antibodies or nonprotective antibodies. We don’t know also whether they’re producing enough of those antibodies to be physiologically useful, and we don’t know how long they’re going to last.

Dryden: The second part of that was just about anti-vax thoughts feeding into the idea that we’re in a hurry to get this vaccine.

Kinch: There has always been an anti-vax movement, every vaccine that’s ever come out. And there’s always been a different angle on it. The current fear is associated, for example, with 5G towers and the rationale behind that, there is no rationale. There’s no objective evidence of anything. And I can tell you that infectious agents could not care less about this part of the electromagnetic spectrum, so there is nothing to it whatsoever.

Dryden: I’m imagining that from the point of view of science, the fact that we’re having these debates that are causing us at some times to move at cross-purposes as a society is probably to the benefit of the virus rather than to the benefit of us.

Kinch: It is important to have these kind of debates. The problem arises when those debates prevent us from being able to move forward. If or when a vaccine is developed, there will be a question about mandatory vaccination. And the urgency and importance of that comes back to what we started off with. The deadliness of this virus is a reflection of its ability to be easily transmitted and to kill with high efficiency. And even if a small population of people opposes being vaccinated, that could still end up endangering a vast number of people, and people will die as a consequence of that.

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Dryden: Both Kinch and Wang say the only way to better understand the virus and COVID-19 illness is to do more studies. They say, unfortunately for those who want quick answers, some of those studies will take some time. But in the meantime, with so many unknowns, there are a few things that are virtually certain. No matter what you’ve seen on social media, masks do protect. Certainly, they provide some protection for others from you. Also, 5G phone towers have nothing to do with this virus, and the virus almost certainly was not built in a laboratory.

“Show Me the Science” is a production of the Office of Medical Public Affairs at Washington University School of Medicine in St. Louis. The goal of this project is to keep you informed and maybe teach you some things that will give you hope. Thanks for tuning in. I’m Jim Dryden. Stay safe.

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UK records lowest daily virus death toll since start of lockdown

This scanning electron microscope image shows SARS-CoV-2 (yellow)—also known as 2019-nCoV, the virus that causes COVID-19—isolated from a patient, emerging from the surface of cells (blue/pink) cultured in the lab. Credit: NIAID-RML

Younger children went back to schools in England on Monday as Britain began to stir back to life, while the government reported the lowest coronavirus death toll since the start of the national lockdown in late March.

Outdoor markets also swung open their gates and car showrooms tried to lure back customers and recoup losses suffered since Britain effectively shut down for business to ward off a disease that has now officially claimed 39,045 lives in the country.

Health Secretary Matt Hancock said Britain was making “significant progress” against the virus after its daily toll dropped to 111—the lowest since the stay-at-home order was issued on March 23.

Reporting of virus cases and fatalities is often lower after a weekend and many people still appeared hesitant to start using public transport or shop.

“It’s very different from usual,” Danish Londoner John Jellesmark said on a visit to the usually bustling Camden Market in the north of the capital.

“It’s still pretty slow. It looks like the market is basically waking up.”

Too much, too soon?

Prime Minister Boris Johnson has set out a timeline that allows two million younger children in England to return to school on Monday and older ones from June 15.

The devolved governments in Scotland and Northern Ireland are eyeing a return in August and September, while Wales is still weighing the benefits of human contact against the dangers of children catching the disease and bringing it home.

A survey conducted by the National Foundation for Educational Research found that primary school leaders expect about half the families to keep their children home.

Principal Claire Syms at the Halley House School in east London said children who do turn up need to feel comfortable in an unfamiliar setting where the desks are spaced out and many around them wear masks.

“We’ve been really conscious about keeping things as normal and as consistent as we can for our children,” Syms told AFP.

“We’re really mindful of their wellbeing and their mental health.”

The UK government has been encouraged by the positive experience of other European countries that have started to return to something resembling normal life.

The House of Commons will debate a government push to get everyone to start voting in person instead of remotely when parliament returns from a break on Tuesday.

But critics of the easing believe the so-called R rate of transmission—estimated nationally at between 0.7 and 0.9—was still dangerously close to the 1.0 figure above which the virus’ spread grows.

‘Unenforceable’

Scientists and lawmakers are not the only ones to express concern that the government’s “cautious and phased” reopening is moving too quickly.

“We’re only able to take these steps because of what we have achieved together so far,” finance minister Rishi Sunak said as he toured Tachbrook Market in central London.

London’s Metropolitan Police Federation chairman Ken Marsh said current rules such as those allowing people to gather in groups of six in England were unenforceable.

“I don’t think the public are taking much notice of what is laid down in front of them,” Marsh told The Daily Telegraph. “They are doing it how they want to do it.”

English parks and beaches have been inundated with people over two successive May weekends that came on the sunniest month ever recorded in Britain.

Police had warned after seeing growing numbers ignore social distancing measures a week ago that they were serious about sanctioning those who gather in large groups.

But some London parks looked like one giant party on Sunday and police issued just a tiny fraction of the fines they had handed out before people were allowed to leave their homes more freely on May 13.

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