Posts Tagged ‘COVID-19’

Fluorsecence microscopy image of human epithelial cells form the colon and infected with the novel coronovirus shows production of filopodia (white) extending our from the cell surface and containing viral particlea.

Most of us have already absorbed the idea that the coronavirus does some weird and sinister things to the human body that are unlike most other respiratory viruses known to man. But now a new study finds yet another unsettling thing that the virus appears to do to help spread from cell to cell.

A new study by an international team led by UC San Francisco finds that cells infected with SARS-CoV-2 quickly begin to grow new arms or dendrites — referred to clinically as filopodia — which are themselves studded with fresh virus particles. These filopodia then seek to reach into and through the walls of neighboring cells, thereby infecting them. And this appears to be a second mode that the virus has for replicating and spreading itself in the body.

As the LA Times reports via the study, up until now, researchers believed that this virus spread itself like most other viruses, by docking itself onto healthy cells, invading, and then turning those cells into copying machines. A team in UCSF’s Quantitative Biosciences Institute led by systems biologist Nevan Krogan launched a project in February to rapidly identify existing drugs and compounds that might treat or slow the spread of the coronavirus. They published initial findings in late April pointing to 10 existing drugs and experimental compounds that showed promise in lab settings when it came to targeting the human proteins this virus most needs to survive.

The latest study is an extension of that work, and Krogan is one of the lead authors of the paper published today in the journal Nature. The important new finding, Krogan and the team hope, will lead to some rapid study of several existing cancer treatments that themselves inhibit the growth of filopedia — thereby shutting down this second means that the virus is using to invade cells.

“It’s just so sinister that the virus uses other mechanisms to infect other cells before it kills the cell,” Krogan says, speaking to the LA Times.

Krogan says that while other viruses — including HIV and the family of viruses that cause smallpox — also use filopedia as mechanisms of spreading infection, the way this virus so rapidly prompts the growth of these tentacles is highly unusual. And the shape of them, branching off the cell and each other like trees, is also apparently strange. Other infectious diseases like HIV don’t cause these kinds of prolific, mutant growths.

Expanding the earlier list of promising drugs, the latest study points to seven cancer drugs already in use that could prove effective against COVID-19. Those include a drug already being used to treat acute myeloid leukemia called Xospata (generic name: gilteritinib); the experimental drug Silmitasertib, which is being studied as a treatment for bile duct cancer and one form of childhood brain cancer; and ralimetinib, another cancer drug which was developed by Eli Lilly to treat multiple forms of cancer.

“We’ve tested a number of these kinase inhibitors and some are better than remdesivir,” Krogan says, via the Milwaukee Journal-Sentinel.

Another experimental drug called Dinaciclib was found by the research team to stop the virus’s assault on a family of kinases called CDKs, which are responsible for cell growth and dealing with DNA damage.

Other infectious disease researchers are just waking up to the revelations of the paper, but most reactions seem fairly excited. While much research is being done on shutting down virus proteins, Krogan’s field of study, called proteomics, instead focuses on the less-likely-to-mutate human proteins involved in helping the virus do its dirty work.

“This paper shows just how completely the virus is able to rewire all of the signals going on inside the cell,” says University of Wisconsin-Madison medical professor Andrew Mehle to the Journal-Sentinel. “That’s really remarkable and it’s something that occurs very rapidly (as soon as two hours after cells are infected).”

And Lynne Cassimeris, a professor of biological sciences at Lehigh University, calls the latest findings “an amazing leap.” “We know that the virus has to be manipulating these human proteins,” Cassimeris says. “Now we have a list of what is changing over time.”

While Krogan’s lab at UCSF got this research off the ground just as the pandemic was emerging in February, there were 70 authors listed on the latest paper, with Krogan as the lead. The work was also done by scientists at Mt. Sinai Hospital in New York, Rocky Mountain Labs in Montana, the Pasteur Institute in Paris, and the University of Freiburg in Germany

https://sfist.com/2020/06/26/ucsf-researchers-discover-how-coronavirus-makes-zombies-of-human-cells-causes-them-to-sprout/

Thanks to Kebmodee for bringing this to the It’s Interesting community.

By Ryan Prior

Every morning, Dr. David Fajgenbaum takes three life-saving pills. He wakes up his 21-month-old daughter Amelia to help feed her. He usually grabs some Greek yogurt to eat quickly before sitting down in his home office.

Then he spends most of the next 14 hours leading dozens of fellow researchers and volunteers in a systematic review of all the drugs that physicians and researchers have used so far to treat Covid-19. His team has already pored over more than 8,000 papers on how to treat coronavirus patients.

The 35-year-old associate professor at the University of Pennsylvania Perelman School of Medicine leads the school’s Center for Cytokine Storm Treatment & Laboratory. For the last few years, he has dedicated his life to studying Castleman disease, a rare condition that nearly claimed his life.

Against epic odds, he found a drug that saved his own life six years ago, by creating a collaborative method for organizing medical research that could be applicable to thousands of human diseases.

But after seeing how the same types of flares of immune-signaling cells, called cytokine storms, kill both Castleman and Covid-19 patients alike, his lab has devoted nearly all of its resources to aiding doctors fighting the pandemic.

During a cytokine storm, the body’s overactive immune response begins to attack its own cells rather than just the virus. When that inflammatory response occurs in Covid-19 patients, cytokines are often the culprit for the severe lung damage, organ failure, blood clots or pneumonia that kills them.

Having personal experience tamping down his own cytokine responses gives him a unique insight.
“I’m alive because of a repurposed drug,” he said.

Now, repurposing old drugs to fight similar symptoms caused by a novel virus has become a global imperative.


Researchers from Fajgenbaum’s lab gather in a video call to discuss Covid-19 treatment data.

A global repository for Covid-19 treatment data

Researchers working with his lab have reviewed published data on more than 150 drugs doctors around the world have to treat nearly 50,000 patients diagnosed with Covid-19. They’ve made their analysis public in a database called the Covid-19 Registry of Off-label & New Agents (or CORONA for short).

It’s a central repository of all available data in scientific journals on all the therapies used so far to curb the pandemic. This information can help doctors treat patients and tell researchers how to build clinical trials.

The team’s process resembles that of the coordination Fajgenbaum used as a medical student to discover that he could repurpose Sirolimus, an immunosuppressant drug approved for kidney transplant patients, to prevent his body from producing deadly flares of immune-signaling cells called cytokines.

The 13 members of Fajgenbaum’s lab recruited dozens of other scientific colleagues to join their coronavirus effort. And what this group is finding has ramifications for scientists globally.

Based on their database, the team published the first systematic review of Covid-19 treatments in the journal Infectious Diseases and Therapy in May.

In that first analysis of the data, the team reviewed 2,706 journal articles published on the topic between December 1, 2019, and March 27, 2020. Just 155 studies met the team’s criteria for being included in the meta-review based on standards such as the size of the cohort, the nature of the study and the end points researchers chose for concluding their inquiries.

“It’s frustrating because we all want a drug that works for everyone,” he said. But that isn’t happening because the coronavirus affects people in ways that are much more complex.

They’re sorting through oceans of data

The first key thing to consider, Fajgenbaum said, was the huge variety of Covid-19 patient experiences. It’s hard to zero in on one particular therapy because there can be such significant differences in the timing of when the drug is administered, how severely Covid-19 strikes a given individual and the stage at which the disease has progressed.

Any change in one of those variables can render an otherwise effective drug impotent. But with massive amounts of patients, the clinical data was bearing out a few noticeable themes, he said.

First, the Covid-19 patients with more severe cytokine storms were more likely to need drugs targeted toward suppressing the immune system. Those with less severe cytokine storms were likely to benefit from an immune-boosting drug.

Outside of drugs designed to boost or suppress the immune system, another major category is antiviral therapies. Various antivirals hit the “viral cascade,” Fajgenbaum said. Some work by stopping the virus from infecting cells, others by halting replication within cells. Other antivirals act in between cells and the virus.

Keeping the database is a huge undertaking, given how stunning the pace of global scientific progress and collaboration has been in the face of the disease’s human toll.

“We set the really ambitious goal of just getting this started,” Fajgenbaum said.

In the three months since the cutoff date for their first paper, the team has reviewed more than 5,000 additional papers published by scientists around the world.

One of their biggest challenges has been fitting the puzzle pieces of the different studies. With each study designed differently, one data set can’t necessarily be grafted neatly onto another. That’s especially tricky when most people diagnosed with Covid-19 eventually get better anyway. It’s hard to parse out if a particular drug was effective and saved lives.

The goal of the CORONA database isn’t to find a wonder drug per se, but to help design better clinical trials that can establish a real cause-and-effect relationship between a drug agent and an individual’s survival.

In the war against the coronavirus, Fajgenbaum hopes CORONA aims to help light the way so the heavy artillery on the front lines can better know what to shoot at Covid-19.

“It’s hard to fight a war if you’re not keeping track of what weapons are being used against the enemy,” he said.


Shown here is one of the researchers’ computer screens as they review Covid-19 treatment data while on a video call. The left side shows a spreadsheet where they tabulate data from the studies. The right side shows the study they’re currently analyzing.

They’re collaborating with FDA analysts

Fajgenbaum’s CORONA database dovetails with ongoing work at the US Food and Drug Administration. For years, the agency has been developing an app called CURE ID, a platform designed to help health care providers capture novel uses of already approved drugs.

The app launched in December with two goals in mind: The first was to help advise physicians searching for new treatment ideas, prescription guidelines and emergency use advisories for drugs across hundreds of diseases. The agency’s second aim was to build a structure by which health providers in the trenches could quickly input anonymized information about their patients so that other doctors around the world could quickly see whether they had been successful using an off-label drug.

The app was ready just in time for the pandemic, and Fajgenbaum gave the keynote speech at its launch.

“It’s really been a terrific collaboration,” said a health policy analyst with the FDA. “His life follows very much the model we hope to use.”

Now that he and his team are working on the coronavirus, the urgency of their partnership has strengthened.

“Nobody wants to go to a database with no data in it,” the analyst said. “Rather than reinventing the wheel, he was kind enough to provide all his data.”

And while the CORONA database project is primarily intended to aid researchers, it’s tapping into major currents in health economics that explain weak points in the way the public and private sector develop therapies together.

“Covid-19 illustrates a market failure in how we build vaccines,” said Amitabh Chandra, a health economist with joint appointments as a professor at the Harvard Kennedy School and Harvard Business School. “We haven’t given firms the correct incentives to make vaccines before a pandemic. Vaccines are very hard to test before the pandemic hits.”

There aren’t old vaccines sitting on a shelf waiting to be dusted off to save the world from the coronavirus. But there are hundreds of FDA-approved drugs at your local pharmacy that can save lives immediately.

When teaching classes, Chandra uses a 2017 New York Times story profiling Fajgenbaum to illustrate the value of drug repurposing and motivate his students to think boldly about how to create economic incentives to cure diseases, particularly when a “invisible medicine” might be right under your nose.

“There’s no substitute for a good story to get people motivated,” he said.
Many drugs are beginning to stand out.

The combination of antivirals lopinavir and ritonavir is the Covid-19 treatment protocol with the most number of studies published so far. As of mid-June, the team had looked at papers on that drug pairing involving more than 4,500 patients.

Next, corticosteroids have shown particular promise, making appearances in studies with another 4,000 patients. At the cellular level, antivirals work for a variety of reasons, each with its own specialty in attacking the virus at different points in its life cycle. Corticosteroids are different, however.

“Steroids tend to act the same, with replicating cortisol,” Fajgenbaum said.

He feels particularly elated about a recent United Kingdom-based study on the steroid dexamethasone. The study garnered headlines for its result showing that a low-dose 10-day regimen of the drug could reduce the risk of death by a third among hospitalized patients requiring ventilation.

In their spreadsheets, the numbers around dexamethasone were like a beacon.
“We built CORONA to help uncover something like dexamethasone,” he said. “It’s a cheap repurposed drug that’s been around for 60 years. This is what it’s all about.”

Studies need rigor

Because Covid-19 is so new, many of the studies are observational or anecdotal. These types of studies obviously matter as scientists are building a foundation of knowledge.

But the best insights come from running double-blind placebo-controlled studies. One shortfall is that many of the published studies just don’t have the level of rigor to inform larger-scale scientific decision-making.

“There are a lot of biases in these observational studies,” Fajgenbaum said.
One drug, the anti-malarial drug hydroxychloroquine, has famously received a lot of boosterism from US President Donald Trump. But in the published studies available for Fajgenbaum’s team to review, the drug hasn’t outperformed others.

Two French studies on hydroxychloroquine drew red flags for the University of Pennsylvania-based team because of the clinical end point the researchers chose: the time when the coronavirus cleared the body. It can be problematic to base an argument for a drug’s success only on that particular metric, because it leaves out crucial details from a person’s longer-term experience following infection.

“‘Virally cured’ is a challenging term,” Fajgenbaum said. “We don’t know if they’re discharged how they fared after leaving the hospital.”

On top of that, the reviewers were skeptical because the virus took a long time to leave the patients’ bodies, which they refer to as “a high time to viral clearance.”

That indicator that could suggest the drug was slow to take effect, or that other factors, including the patient’s own immune system, played a larger role in expelling the pathogen.

Know how to sort through the data

With dozens of people working full time to sort through thousands of studies, it’s obviously impossible for a single frontline health provider to keep abreast of all there is to know about Covid-19 while also treating patients at the same time.

It’s even harder for the average person following the story in the news, especially if you’re not equipped with a graduate degree in statistical analysis.

“Covid threw the world in flux,” said Sheila Pierson, associate director for clinical research at the CSTL. A biostatistician originally hired to study Castleman disease, she’s accepted the new mission along with her colleagues.

“There’s a lot of great science being done,” she explained. With that pace of innovation, it’s incredibly difficult for the average person to stay up to date, so the CORONA database helps everyone with a little extra scientific literacy amid headlines about new treatments that induce a form of intellectual whiplash.

“You should rely on multiple news sources,” Pierson said, in order to sort through what may appear to be conflated messages about whether a certain drug works or not for a certain group of people.

“It’s difficult when you’re only looking at one person’s view of a drug,” she said. “Look for a different write-up and a different view.”

He’s repeating the same methods that saved his life

As of June 27, Fajgenbaum has lived free of Castleman’s cytokine storms for 77.72 months. His last Castleman relapse ended on January 5, 2014. He’s a living experiment, and in his personal accounting he won’t round up to the next full month. Each new day is a precious moment with a daughter he feared he’d never meet.

The doctor and researcher remains immune compromised and won’t take risks with the coronavirus.
He hasn’t set foot in a building other than his home since March 13. And his life still relies on siltuximab and chemotherapy infusions administered monthly through a chest port.

“I’m reminded every time I touch the port in my chest of the cytokine storms I had,” he said. “I want so badly to solve (Covid-19) the way I did with Castleman. I have the same sense of urgency.”

Castleman disease nearly killed Fajgenbaum five times in his 20s while he was working his way through University of Pennsylvania’s Perelman School of Medicine and then earning an MBA at the University of Pennsylvania’s Wharton School.

Each time, the deadly disease triggered cytokine storms that led to multiple organ failure.

But the young man created a global organization to rally doctors, scientists and patients toward finding a cure. With intense study and brilliant partners, he zeroed in on an already available immunosupressant that could be repurposed to save his life.

Last year he published his memoir, “Chasing My Cure,” detailing a journey in which at one point a priest was brought to his hospital room to give his last rites.

Fajgenbaum’s story reads likes the teaser for a hit Netflix series. But if it were a show, all of that is really just season one. Because, spoiler alert — then a global pandemic hit.

A year ago you might have thought what the writers threw at him in a second season might be a bit unrealistic. But this project is the obvious next step.

“I see myself bringing our experiences with Castleman now over to the global fight against corona,” he said.

https://www.cnn.com/2020/06/27/health/coronavirus-treatment-fajgenbaum-drug-review-scn-wellness/index.html


Human cell types within corresponding organs that express the genes for both ACE2 and CTSL (green dot) or both ACE2 and TMPRSS2 (orange dot).

by Chris Baraniuk

When the SARS-CoV-2 virus enters the human body, it breaks into cells with the help of two proteins that it finds there, ACE2 and TMPRSS2. While there has been much discussion of viral infection in gut and lung cells, researchers have dug into massive gene expression datasets to show that other potential target cells also producing ACE2 and TMPRSS2 are scattered throughout the body—including in the heart, bladder, pancreas, kidney, and nose. There are even some in the eye and brain.

The results, published in a preprint on bioRxiv April 21, show that such cells are strikingly abundant. Many are epithelial cells, which line the outer surface of organs. The new findings add to an emerging picture of SARS-CoV-2 as a virus that can target cells in many places in the human body, rather than being focused on a particular organ or part of the respiratory tract.

Cardiologist Frank Ruschitzka at the University Hospital of Zürich and colleagues separately published a letter in The Lancet April 17 in which they described how virus particles had been found in the vascular endothelium, a thin layer of cells lining blood vessels in various organs of the body, for instance.

“This is not just a virus pneumonia,” Ruschitzka, who was not involved in the latest study, tells The Scientist, referring to COVID-19. “This is a disease like we have never seen before—it is not an influenza, it hits the vessels all over, it hits the heart as well.”

To uncover the locations of cells bearing ACE2 and TMPRSS2, the preprint researchers turned to the Human Cell Atlas, a project that has allowed scientists to pool together data on human cells since 2016.

By scouring single-cell sequencing records of around 1.2 million individual cells from human tissue samples, the team was able to find out which of those cells produce both ACE2 and TMPRSS2, and note their locations in the body. The analysis used 16 unpublished datasets of lung and airway cells and 91 published datasets spanning a range of human organs.

Coauthor Christoph Muus, a graduate student at Harvard University and the Broad Institute, explains that while the data show cells in many locations in the body produce SARS-CoV-2 receptors, it’s not certain that the virus can infect all of those tissues.

“Expressing the receptor is a necessary condition but not necessarily a sufficient condition,” he says. For example, potential target cells were found in the testes, but scientists still don’t know if SARS-CoV-2 infects and replicates in that part of the body.

Jeremy Kamil, a virologist at Louisiana State University Health Shreveport, says the preprint provides important details about the human body that may help scientists understand how SARS-CoV-2 infects hosts. By finding viral protein fragments in tissue samples from patients who died because of COVID-19, scientists might be able to firm up which organs are genuine sites of infection, he adds.

“I’d say this paper gives people a roadmap at where you might want to look in the body to understand where this virus is going,” he says.

One limitation of the work is that relatively little metadata about the people who donated tissue samples were available for the various datasets, though information about age and gender were included in many. The researchers don’t know, for example, whether there was an ethnicity bias in the data, whether patients had pre-existing conditions, or whether they were taking any medications. All of these things could affect gene expression in particular cells.

Smoking status was available for a subset of the data, and the team used this to show that smoking is correlated with a greater expression of the ACE2 gene in the upper airway, but lower expression in certain lung cells. Further research is needed to understand whether this affects smokers’ susceptibility to COVID-19. Data from China suggest that smokers are 14 times more likely to develop a severe form of the disease.

Some researchers from the same group using similar data have also recently published papers in Cell and Nature. In those cases, the researchers focused on certain groups of cells. The study reported in Nature examined cells potentially involved in viral transmission and found that nasal epithelial cells, in particular, were associated with expression of ACE2 and TMPRSS2. The authors report that the virus might exploit cells that secrete fluids in the nasal passage, which might help it spread from one person to another in droplets released, say, when someone sneezes.

The Cell study, meanwhile, also found ACE2 and TMPRSS2 transcripts in nasal, gut, and lung cells but the researchers also found that the protein interferon activated ACE2 expression in vitro. The human body uses interferon to fight infections, so it is not clear whether the protein is of overall benefit or detriment to COVID-19 patients.

The use of so many different data sources backs up the validity of the preprint authors’ findings, says Marta Gaglia, a molecular biologist at Tufts University. She agrees with the researchers that discovering ACE2- and TMPRSS2-producing cells in various places around the body does not prove the virus can always infect such cells.

“I think the reality is that most of the problems come from the lung,” she adds. Plus, while doctors treating COVID-19 patients may detect problems in multiple organs, those issues might not necessarily be caused directly by SARS-CoV-2 infection, says Gaglia. A problematic immune system response, for instance, could damage certain tissues in the body as an indirect consequence of viral infection.

https://www.the-scientist.com/news-opinion/receptors-for-sars-cov-2-present-in-wide-variety-of-human-cells-67496?utm_campaign=TS_DAILY%20NEWSLETTER_2020&utm_source=hs_email&utm_medium=email&utm_content=87213170&_hsenc=p2ANqtz-_vGzY0JSZbqON-CbrWnU2wp22vNPAa-zcPDPoSZR69MA0qXhi3ukYIXekJJKZ_A_GfMi8lV1cuO5y2DnnkhV-rdYFrPQ&_hsmi=87213170


The unprecedented explosion of video calling in response to the pandemic has launched an unofficial social experiment.

BY JULIA SKLAR

JODI EICHLER-LEVINE FINISHED teaching a class over Zoom on April 15, and she immediately fell asleep in the guest bedroom doubling as her office. The religion studies professor at Lehigh University in Pennsylvania says that while teaching is always exhausting, she has never “conked out” like that before.

Until recently, Eichler-Levine was leading live classes full of people whose emotions she could easily gauge, even as they navigated difficult topics—such as slavery and the Holocaust—that demand a high level of conversational nuance and empathy. Now, like countless people around the world, the COVID-19 pandemic has thrust her life into a virtual space. In addition to teaching remotely, she’s been attending a weekly department happy hour, an arts-and-crafts night with friends, and a Passover seder—all over the videoconferencing app Zoom. The experience is taking a toll.

“It’s almost like you’re emoting more because you’re just a little box on a screen,” Eichler-Levine says. “I’m just so tired.”

So many people are reporting similar experiences that it’s earned its own slang term, Zoom fatigue, though this exhaustion also applies if you’re using Google Hangouts, Skype, FaceTime, or any other video-calling interface. The unprecedented explosion of their use in response to the pandemic has launched an unofficial social experiment, showing at a population scale what’s always been true: virtual interactions can be extremely hard on the brain.

“There’s a lot of research that shows we actually really struggle with this,” says Andrew Franklin, an assistant professor of cyberpsychology at Virginia’s Norfolk State University. He thinks people may be surprised at how difficult they’re finding video calls given that the medium seems neatly confined to a small screen and presents few obvious distractions.

Zoom gloom

Humans communicate even when they’re quiet. During an in-person conversation, the brain focuses partly on the words being spoken, but it also derives additional meaning from dozens of non-verbal cues, such as whether someone is facing you or slightly turned away, if they’re fidgeting while you talk, or if they inhale quickly in preparation to interrupt.

These cues help paint a holistic picture of what is being conveyed and what’s expected in response from the listener. Since humans evolved as social animals, perceiving these cues comes naturally to most of us, takes little conscious effort to parse, and can lay the groundwork for emotional intimacy.

However, a typical video call impairs these ingrained abilities, and requires sustained and intense attention to words instead. If a person is framed only from the shoulders up, the possibility of viewing hand gestures or other body language is eliminated. If the video quality is poor, any hope of gleaning something from minute facial expressions is dashed.

“For somebody who’s really dependent on those non-verbal cues, it can be a big drain not to have them,” Franklin says. Prolonged eye contact has become the strongest facial cue readily available, and it can feel threatening or overly intimate if held too long.

Multi-person screens magnify this exhausting problem. Gallery view—where all meeting participants appear Brady Bunch-style—challenges the brain’s central vision, forcing it to decode so many people at once that no one comes through meaningfully, not even the speaker.

“We’re engaged in numerous activities, but never fully devoting ourselves to focus on anything in particular,” says Franklin. Psychologists call this continuous partial attention, and it applies as much to virtual environments as it does to real ones. Think of how hard it would be to cook and read at the same time. That’s the kind of multi-tasking your brain is trying, and often failing, to navigate in a group video chat.

This leads to problems in which group video chats become less collaborative and more like siloed panels, in which only two people at a time talk while the rest listen. Because each participant is using one audio stream and is aware of all the other voices, parallel conversations are impossible. If you view a single speaker at a time, you can’t recognize how non-active participants are behaving—something you would normally pick up with peripheral vision.

For some people, the prolonged split in attention creates a perplexing sense of being drained while having accomplished nothing. The brain becomes overwhelmed by unfamiliar excess stimuli while being hyper-focused on searching for non-verbal cues that it can’t find.

That’s why a traditional phone call may be less taxing on the brain, Franklin says, because it delivers on a small promise: to convey only a voice.

Zoom boon

By contrast, the sudden shift to video calls has been a boon for people who have neurological difficulty with in-person exchanges, such as those with autism who can become overwhelmed by multiple people talking.

John Upton, an editor at the New Jersey-based news outlet Climate Central, recently found out he is autistic. Late last year, he was struggling with the mental load of attending packed conferences, engaging during in-person meetings, and navigating the small-talk that’s common in work places. He says these experiences caused “an ambiguous tension, a form of anxiety.”

As a result, he suffered a bout of autistic burnout and struggled to process complicated information—which he says is normally his strength—leading to feelings of helplessness and futility. To combat the issue, he began transitioning to working mostly from home and stacking all in-person meetings on Thursdays, to get them out of the way.

Now that the pandemic has pushed his coworkers to be remote as well, he has observed their video calls lead to fewer people talking and less filler conversation at the beginning and end of each meeting. Upton says his sense of tension and anxiety has been reduced to the point of being negligible.

This outcome is supported by research, says the University of Québec Outaouais’s Claude Normand, who studies how people with developmental and intellectual disabilities socialize online. People with autism tend to have difficulty understanding when it’s their turn to speak in live conversations, she notes. That’s why the frequent lag between speakers on video calls may actually help some autistic people. “When you’re Zooming online, it’s clear whose turn it is to talk,” Normand says.

However, other people on the autism spectrum may still struggle with video chatting, as it can exacerbate sensory triggers such as loud noise and bright lights, she adds.

On the whole, video chatting has allowed human connections to flourish in ways that would have been impossible just a few years ago. These tools enable us to maintain long-distance relationships, connect workrooms remotely, and even now, in spite of the mental exhaustion they can generate, foster some sense of togetherness during a pandemic.

It’s even possible Zoom fatigue will abate once people learn to navigate the mental tangle video chatting can cause. If you’re feeling self-conscious or overstimulated, Normand recommends you turn off your camera. Save your energy for when you absolutely want to perceive the few non-verbal cues that do come through, such as during the taxing chats with people you don’t know very well, or for when you want the warm fuzzies you get from seeing someone you love. Or if it’s a work meeting that can be done by phone, try walking at the same time.

“Walking meetings are known to improve creativity, and probably reduce stress as well,” Normand says.

https://www.nationalgeographic.com/science/2020/04/coronavirus-zoom-fatigue-is-taxing-the-brain-here-is-why-that-happens/

by Emma Yasinski

Paul Matewele, a microbiologist who identified pathogenic bacteria on surfaces that humans contact everyday, died as a result of COVID-19 on April 7 at the age of 62.

Matewele was a senior lecturer at London Metropolitan University for 30 years and is best known for his work characterizing potentially pathogenic microbes that people are likely to come in contact with in their homes and public places, according to Úna Fairbrother, an interim head of the School of Human Sciences at London Metropolitan University.

Matewele was born in Zimbabwe in 1958 and earned a master’s degree in biochemistry from St. Andrews University and a PhD in microbiology from Southampton University.

Partially inspired by the growing crisis of antibiotic resistance, Matewele conducted studies identifying sometimes-deadly microbes living on handbags, McDonald’s touch screens, reusable water bottles, makeup, vehicle air conditioners, drinks served in cinemas, London transport systems, and coins. His work on the London transportation system led to a deep cleaning of 50 stations in the London Underground in June 2017.

But among colleagues, he was best known for the time he spent lecturing and tutoring thousands of students. “Paul was a warm, kind, intelligent and conscientious man. He was dedicated to his students and a brilliant colleague to have,” Fairbrother tells The Scientist in an email. “He was a genuinely happy, open person and will be much missed from our team on a personal and professional level.”

Several of Matewele’s students and colleagues shared thoughts and memories in a tribute on the university’s webpage describing him as a “dedicated teacher,” “a kind soul,” and someone who “never stopped smiling.”

Sean Frost, a former colleague of Matawele who is currently a lecturer at the University of Hull, writes on the university page that Matewele “took on the biggest challenges and was never afraid to fight for what he believed in, McDonalds being particularly memorable. Even up until March he was broadcasting warnings about risk of infection from cash, Paul always took the side of the little guy, be it colleagues, students or society. He was a fine example of what an academic should aspire to become.”

Matawele is survived by his 18-year-old son, William.

https://www.the-scientist.com/news-opinion/microbiologist-who-studied-deadly-bacteria-in-public-places-dies-67452?utm_campaign=TS_DAILY%20NEWSLETTER_2020&utm_source=hs_email&utm_medium=email&utm_content=86856096&_hsenc=p2ANqtz-8BKRYRGs_fo90ZncO_fmihHmxcb7igfgKB79gkfdKckRdyLVHnViIWWELwSyNw7QIkAcI47O7ksk1iFQ0kJDaX39xITA&_hsmi=86856096

It’s Easter Sunday, just after Passover, just after another exhausting13 hour shift. I can’t watch the news. I’m too busy and too frustrated by all the misinformation. Forgive me, but I need to debunk a few viral myths.

Myth #1: COVID-19 is a disease of the old and sick

This cannot be further from the truth. As a critical care physician, I’m caring for the sickest of the sick. I know the data. What little good data there is shows that 80% of ICU patients are under 65 (in a Wuhan study) or that 40% in ICU were under 60 (in an Italian study). The highest death age group was 60-69. The third highest was 50-59. The most common co-morbid conditions were high blood pressure, diabetes and obesity. These are not weird immune-related illnesses, they’re common, and this hits close to home. I’m 53, I have high blood pressure, diabetes and, like millions of Americans, I’m a little obese. Our stats? 60% of our intubated patients are under 65. Most of my ICU patients have never been sick enough to be hospitalized before this. Sure, many who die are old and have other illnesses, but the popular narrative almost says if you’re not in a nursing home you’re safe. Nothing can be further from the truth. It’s a myth.

Myth number #2: The main concern is a lack of PPE and ventilators

Partially false. Sure, some NYC and UK caregivers have had to use cooking aprons, garbage bags, and other scraps to protect themselves, but many hospitals have all the PPE they need. Luckily, my hospital has been able keep up with all our PPE needs. But many unanticipated shortages go unreported: COVID test swabs, dialysis machines and dialysis fluid needed to keep people alive (COVID causes kidney failure), sedative medications, and we need more oxygen, we’re using so much.

But most of all, we need more amazing people. Especially nurses and respiratory therapists, because many are now sick and some have died. Over 100 doctors have died in Italy. Doctors, therapists, pharmacists, students, and others now have a new career as nursing assistants. No-one is a specialist anymore, we are all COVID care providers. Thank you to the many volunteer doctors and nurses from all across the US that have come to NYC to help. Recovery for patients can take weeks to months, so we’ll need your help and sacrifice for a while yet.

Myth #3: Hydroxychoriquine is a “game changer” and it’s safe.

This potentially false idea was launched on the back of a very small trial from France. I’ve read the paper and it has major flaws. Three larger and more recent trials were negative but they don’t get press. These “game changer” drugs have dangerous side-effects. A recent trial in Brazil was stopped early for fear that high-dose chloroquine was killing people. Other drugs, however, show promise. Watch this space but no “game changers” yet.

Myth #4: Social distancing is our only option and it’s easy to do

This is also untrue. My home, NYC, is one of the most densely populated cities in the world. Many of my patients are poor and immigrated here. They live in small apartments with large families. Social distancing is impossible for many parts of NYC. And in the US more than 10% of the work force is unemployed. Sure, we’re finally flattening the curve, but as a Korean-American, I am proud to say that South Korea did it better and they didn’t shut down their economy. They tested, tested, tested, tracked, and isolated people and provided a mobile app, food, masks, and a thermometer to track their fever. This was done for visitors as well as citizens. The US hasn’t tested widely or efficiently enough. And we need to talk about the painful economic and human impacts of social distancing. Banning all hospital visitors means many terrified patients dying lonely deaths. The loss of human dignity is unimaginable.

Myth #5: We can blame China for the current US pandemic

This is false. Recent research shows that our outbreak in NYC came from Europe. And how helpful are country labels anyway? The 1918 Spanish Flu apparently didn’t originate in Spain, so should we rename it? When it comes to infectious diseases, borders mean nothing in our global economic village, but anti-Asian sentiment has spiked all over the world. Just read the online hate speech about the “KungFlu” and the “WuhanVirus”. As an Asian American, who is doing as much as I can, this is very distressing.
Andrew Yang wrote “We need to step up, help our neighbors, donate … and do everything in our power to accelerate the end of this crisis.” This is what my wife and I and so many others are doing. I work 12-15 hours days alongside residents, doctors, nurses, pharmacists and others. (BTW, many of these heroes are Asian-American.) We’re active in our local church, and my wife has a Facebook group that donates tens of thousands of dollars to food and supplies for front-line workers. Daily, she buys food from struggling restaurants, delivers it to the hospital, and I distribute it in between seeing my patients. This has been our life for months and will be our future for a while.

Does it really matter if the virus is from China, Europe or Mars? Our response would have been the same: to save as many lives as we can.

Myth number #6: This is all overblown, COVID is just like the Flu

I’m just shocked by this one. The infectivity of COVID 19 is three times that of the flu, and it is 40 times more deadly (Dr. Fauci says “10 times”). On Good Friday in NYC, 783 patients died; that’s one death every 2 minutes. In the US, it was one death every 42 seconds. Brace yourself. This is nothing like the flu. If you don’t believe me, just walk into any emergency room in New York, Detroit, Miami, LA or New Orleans.

On a final and personal note, I’m blown away by the response of my residents, my colleagues, the people around me, and all NYC hospital staff. Never have I been more proud to be a health care worker and a residency director. I’m impressed by the sacrifice and commitment of all my residents. I’m in awe of their hard work. These are the finest people on earth. I am humbled by their sacrifice and courage to go above and beyond the call of duty. Oddly, it took a pandemic to bring us this level of mass cooperation. But it’s also frightening. I have practiced critical care medicine for more than 25 years and never have I been so challenged, saddened and emotional. Almost every hour of every shift, someone needs intensive care. I’m very used to comforting patients and their families to prepare for death. I used to do this for someone weekly; , now it’s hourly. Death has become very common: every shift, every ward, and in every emergency room. It feels like a bomb went off somewhere and the whole of New York is slowly suffocating.
The 7pm cheering for health care workers moves me. Previously, at parties, I’d say “I work in an ICU and I ventilate people”. That was a big conversation killer. Now, I feel like a rock star or a military veteran. Who knows? Maybe one day I’ll get to priority board an airplane. But seriously; this experience will lead to future PTSD, pain, scars, and tears, for me and so many residents and health care workers. For now, however, we really need your prayers and support.

I hope this demystifies a few things. Thanks for reading. #columbiamedicine #columbiastrong


Across the globe, wildlife is exploring empty places usually occupied by people.

As humans are remaining indoors in response to the coronavirus pandemic, it appears that wildlife around the world took notice of our absence. There seems to be a never-ending list of animals becoming emboldened during this time to explore areas that are typically heavily populated: Buffalo have taken to the deserted highways in India. Mountain lions have rested in trees in Boulder, Colorado. Wild boar walk the streets of Barcelona while peacocks strut along open streets in Brazil.

Rats in New York City have somehow become even more confident in their quest for food. And a groundhog appeared to stare down two dogs watching through a window while eating a piece of pizza, which probably doesn’t have anything to do with the lockdown, but was a welcome distraction on social media nonetheless.

The Washington Post reports that a tribe of goats overtook the streets of Wales. Video taken by resident Andrew Stuart shows the animals nonchalantly roaming the empty streets and helping themselves to a meal of hedges and flower gardens.

According to SFGate, an employee from Yosemite National Park claims that since the park closed to the public in late March, the sightings of large animals including bears, bobcats, and coyotes have gone up fourfold.

“It’s not like [bears] aren’t usually here,” Yosemite employee Dane Peterson tells SFGate, “it’s that they usually hang back at the edges, or move in the shadows.”

In Mexico, crocodiles that generally stay hidden in lagoons near the beaches in La Ventanilla, Oaxaca, have been coming out in the open since the beaches were closed to the public about two weeks ago, Mexico News Daily reports.

Endangered sea turtles have also taken advantage of empty beaches to nest in Brazil and Florida. It’s too early to tell how lockdown measures will affect sea turtle numbers when it is time for the eggs to hatch. Decreased traffic could create less artificial light to confuse the hatchlings about which direction to go, Shanon Gann, the program manager at Brevard Zoo Sea Turtle Healing Center in Florida, tells weather.com.

A mixed bag for animals that depend on humans

In urban areas where wildlife is, for better or worse, dependent on human activity, the lockdown brings new challenges. The New York Times describes scenes in Thailand, where macaques have come to rely on humans for food. Their populations have become so dense in these areas because of that food supply that people staying home has quickly created a scarcity of resources, leading to aggressive behavior.

The same goes for duck ponds, ecologist Becky Thomas of Royal Holloway in London writes for The Conversation. Although feeding bread to ducks is harmful to their health and the water around them, there will be an adjustment as they compete for healthier resources.

Thomas notes that decreased traffic will lead to less hedgehog roadkill as well as reduced noise pollution that negatively affects the ability of bats, birds, and other animals to communicate.

The lack of human presence hasn’t benefited all animals, as the Times reports, particularly animals in African nature preserves. With fewer tourists around, poachers are killing rhinos with an increased frequency in Botswana and South Africa.

“We’re in a situation of zero income, and our expenses are actually going up all the time just trying to fight off the poachers and protect the reserve,” Lynne MacTavish, operations manager at Mankwe Wildlife Reserve in South Africa, tells the Times. “To say it’s desperate is an understatement. We’re really in crisis here.”

Some of the earliest widely shared reports of wildlife emerging in populated areas turned out to be false, according to National Geographic’s debunking of some of the more common untruths. One such tale says baby elephants in China got drunk on corn wine and passed out in a tea field, which might be very relatable during these times, but never happened. The absence of boats in the canals of Venice brought claims of dolphins appearing for the first time in decades, but the images were from the island of Sardinia, nearly 500 miles away.

There may not be dolphins in Venice, but the waters have gotten astonishingly clear, as the lack of gondolas and other boats on the water haven’t been stirring up sediment, CNBC reports.

Right now, it isn’t clear what the long-term effects of this lockdown will be on nature, primarily because this is occurring when many species in the Northern Hemisphere are mating, giving birth, or coming out of hibernation. Air pollution in some areas has been cut in half since the lockdowns began, Forbes reports, due to the lack of emissions from vehicles and factories. Some cities notorious for smoggy skies, including Los Angeles and Beijing, are enjoying some of the cleanest air they’ve experienced in decades. While the tolls of air pollution on human health are widely known, animals are also at risk, according to the National Wildlife Refuge System.

As many are still sheltering-in-places as we approach the 50th annual Earth Day, this resurgence of wildlife is giving some cause for hope that this evidence will ultimately lead to better policies to protect the environment and create a new normal.

“I am hopeful,” anthropologist Jane Goodall tells the Post. “I am. I lived through World War II. By the time you get to 86, you realize that we can overcome these things. One day we will be better people, more responsible in our attitudes toward nature.”

https://www.the-scientist.com/news-opinion/with-humans-indoors-animals-go-wild-67434?utm_campaign=TS_DAILY%20NEWSLETTER_2020&utm_source=hs_email&utm_medium=email&utm_content=86538478&_hsenc=p2ANqtz-92e5YchE_c5eEZJOR2VWChyXs-TUYFALDBiX0cEwNWRvtMhsuRr4MWSGBf0DCvU1hKkYi4eEAJ3QErLAitWrBijvumwg&_hsmi=86538478


Second Breath will help save lives during coronavirus pandemic

It’s called “Second Breath,” and this piece of equipment will save lives.

“Without this ventilator there are a lot of folks who might not have a chance at a breath,” said Dr. Mada Helou, from University Hospitals.

Three Cleveland organizations put their innovative skills, knowledge and can-do attitude together to create and manufacturer a breathing pump that will alleviate some of the demand for ventilators, all across the country.

“We like to respond to things, and more importantly the team likes to respond. There were eight engineers that developed this and these guys wanted to do something and they came to me,” said Dan T. Moore, president and CEO, Dan T. Moore Co.

It collaborated with several other organizations and in three weeks, designed “Second Breath.”

“Coronavirus’ main target is the lungs. It effects many organs, but it has a profound effect on our ability to hold oxygen within our blood,” said Dr. Helou.

Experts said an average ventilator costs anywhere from $20,000 and up to $100,000. Second Breath costs about $6,000.

Dan T. Moore Co. has made about 36 ventilators and they’re ready to ship out around the world. Engineers told 19 News they can design about a hundred ventilators a day.

The team tells 19 News they are proud.

“I think great innovation comes under pressure and when the COVID-19 surge showed up folks thought you know what, we need to respond to this quickly,” said Dr. Helou. “Everything about this says Cleveland. It speaks helping people and it speaks collaboration,” she said. “Cleveland, you’ve done this!”

https://www.fox19.com/2020/04/16/ohio-company-invents-second-breath-ventilator-that-will-save-lives-during-coronavirus-pandemic/


A patient is moved out of Gateway Care and Rehabilitation Center, a skilled nursing facility in Hayward, Calif., on Thursday.

People with severe COVID-19 may experience neurological symptoms, including confusion, delirium and muscle pain, and could be at higher risk for a stroke, a new study out of Wuhan, China has suggested.

Nearly 40 percent of people with the disease caused by the new coronavirus suffered brain-related complications, according to findings published Friday in JAMA Neurology.

Among those with serious infection as a result of the virus, nearly 6 percent experienced a stroke or stenosis, roughly 15 percent had dementia-like symptoms and roughly 20 percent reported severe muscle pain, researchers in China reported.

“This study indicates that neurological complications are relatively common in people who have COVID-19,” S. Andrew Josephson, professor and chair of the Department of Neurology at the University of California, San Francisco and editor-in-chief of JAMA Neurology, told UPI. Josephson also co-authored a related commentary on the study findings.

“However, the majority of those complications are are also relatively common in people with severe pneumonia and viral infections in hospital intensive care units,” he added.

That includes symptoms such as muscle pain and “confusion or difficulty thinking,” according to Josephson, although he emphasizes that if these neurological issues develop in people who know they have COVID-19 — or have symptoms of the disease and are among those at high risk for serious illness — they should be considered a “red flag like shortness of breath,” he said.

“Somebody who has COVID-19 and is at home and experiences difficulty thinking or confusion or anything that indicates a possible stroke, that is a sign they should come into the hospital for additional care,” Josephson continued. “But a symptom like muscle pain is common in viral infections. People don’t need to come into hospital with that.”

To date, nearly 1.7 million people worldwide have been infected with COVID-19, and nearly 100,000 have died from the disease. Although numbers vary by country and region, it is believed that approximately 20 percent of people infected by the new coronavirus become ill enough to require hospital care, and roughly 5 percent experience life-threatening symptoms, including pneumonia.

Those at highest risk for serious illness are believed to be the elderly, as are people with a history of diabetes, high blood pressure and heart disease. Of course these same people are also at increased risk for cerebrovascular diseases like stroke and stenosis, Josephson noted.

The new study looked at 214 patients with the disease at three Wuhan hospitals, all of whom were hospitalized between Jan. 16 and Feb. 19.

Of the 214 patients, who had mean age of 53, 87 were men and 126, or 59 percent, had severe infection based on respiratory status — with shortness of breath caused by a severe lower respiratory tract infection, like pneumonia.

As in prior studies, those with serious illness were older, had more underlying conditions — particularly high blood pressure — and had fewer typical symptoms of COVID-19, like fever and cough, when compared to patients with mild to moderate infection.

Additionally, 6 percent of patients experienced “taste impairment” and 5 percent had “smell impairment.” What causes people with the virus to experience these neurological complications remains unclear, according to Josephson. Because of the known heart-related complications associated with the virus, it’s possible they are the result of blood clots emanating from the heart, he added.

“As with all of the research coming out about the virus, this study shows we still have a lot more to learn,” Josephson said. “The bottom line is that people should be aware of these neurological symptoms, and seek medical attention if they need it.”

https://www.upi.com/Health_News/2020/04/10/40-of-people-with-severe-COVID-19-experience-neurological-complications/2491586526495/?ur3=1

By Olivia Konotey-Ahulu

A vaccine against the coronavirus could be ready by September, according to a scientist leading one of Britain’s most advanced teams.

Sarah Gilbert, professor of vaccinology at Oxford University, told The Times on Saturday that she is “80% confident” the vaccine would work, and could be ready by September. Experts have warned the public that vaccines typically take years to develop, and one for the coronavirus could take between 12 to 18 months at best.

In the case of the Oxford team, however, “it’s not just a hunch, and as every week goes by we have more data to look at,” Gilbert told the London newspaper.

Gilbert’s team is one of dozens worldwide working on a vaccine and is the most advanced in Britain, she told the Times. As the country looks set to begin its fourth week under lockdown, a vaccine could be fundamental in easing the measures and returning to normal life. Gilbert said human trials are due to start in the next two weeks.

Her remarks came as the death toll from the virus pushed past 100,000 globally. On Friday, the U.K. reported 980 fatalities, taking the total count from the virus to 8,958, and the government has repeatedly pleaded with the public to obey lockdown rules during the long Easter holiday weekend. As Prime Minister Boris Johnson begins his recovery after a spell in intensive care, Patrick Vallance, the government’s chief scientific adviser, warned he expects the number of deaths to increase for “a few weeks” yet.

Manufacturing the millions of vaccine doses necessary could take months. Gilbert said she’s in discussions with the British government about funding, and starting production before the final results are in, allowing the public to access the vaccine immediately if it proves to work. She said success by the autumn was “just about possible if everything goes perfectly.”

https://www.bloomberg.com/news/articles/2020-04-11/coronavirus-vaccine-could-be-ready-in-six-months-times