Trump abruptly ends briefing after being pressed over retweeting misinformation

By Kevin Liptak, CNN
Updated 8:02 PM ET, Tue July 28, 2020


Trump walks out of briefing after CNN question

(CNN)Even amid an attempt by President Donald Trump's aides to shift his focus back to coronavirus, he continues to hear from a wide range of associates -- including the CEO of a far-right television network -- who are undermining the administration's health experts and questioning their approach to the pandemic, people familiar with the conversations say.

Trump resumed his daily news briefings on Tuesday afternoon, where he again touted advancements on vaccines and treatments for the virus. After largely ignoring the pandemic for weeks and denying its severity, the White House revived the briefings last week to demonstrate presidential leadership.

But the approach has hit early stumbling blocks.

When Trump was pressed by CNN's Kaitlan Collins about his words of support for a doctor who downplayed masks and suggested alien DNA was used in medical treatments, he cut the briefing short and stormed out.

It was a sign that despite the efforts of his aides to recalibrate his approach, his own desire to improve his standing and the pandemic raging throughout the country, Trump is still trapped in some of the self-destructive tendencies that have brought him low.

While the President and Dr. Anthony Fauci are speaking again after going more than a month without meeting, Trump continues to hear from outside allies and even some inside the administration who have offered him competing advice and sometimes bad information, worrying some of his advisers who had once hoped to turn a page in the coronavirus response.

Trump also continues to hear steady criticism of Fauci, who has resumed making television appearances after weeks off the national airwaves -- earning him more irritation from the President, according to the people familiar.

Trump shatters his own show of responsibility on the pandemic

Trump declared his relationship with Fauci is "very good" on Tuesday, but wondered why the doctor's approval rating is so high when his is so low.
"He's got this high approval rating. So why don't I have a high approval rating with respect -- and the administration -- with respect to the virus?" the President asked. "We should have it very high."
"It can only be my personality, that's all," he concluded.
The competing voices spilled into public view when Trump retweeted a message late Monday critical of Fauci that claimed the infectious disease expert had "misled the American public on many issues."
Fauci appeared hours later on ABC to say he would continue doing his job, despite the President's attacks.
A series of events earlier on Monday illustrated the dueling stream of voices influencing Trump as the outbreak continues to rage across the nation.
Midday, Fauci and others gathered in the Oval Office to update Trump on the 30,000-person Phase 3 trial launched by Moderna. Trump later told reporters it was a "great meeting" and participants walked away believing the President was sincere in his efforts to convey more leadership on the outbreak.
"We had a lot of our wonderful doctors and researchers with me," Trump said. "I think the meeting went really well."
While the meeting focused almost exclusively on the vaccine trial, and not on Trump's response to the virus more broadly, it seemed to participants like the President was engaged -- unlike some previous meetings that became derailed with unrelated topics and complaints.
But as the day progressed, Trump heard from several others who reinforced a different message than the one being offered by the administration's health experts. His hawkish trade adviser Peter Navarro -- who recently published an op-ed in USA Today trashing Fauci without running it past the White House but was never formally reprimanded -- traveled alongside Trump to North Carolina, where the President broke with health experts by calling on governors to reopen.
"I really do believe a lot of the governors should be opening up states that they're not opening," Trump said, countering the advice being offered by Fauci and Dr. Deborah Birx for states to rethink how they are lifting restrictions.
The same day, Trump spoke with Robert Herring, the chief executive of far-right OANN, about an unproven anti-malarial that Trump has long touted and even took himself, despite a lack of clear evidence on its efficacy in preventing or treating Covid.
"Yesterday, I had a chance to talk to President Trump about hydroxychloroquine," Herring later wrote on Twitter. "I gave him a list of doctors we have interviewed. I know he wants to help & put people back to work. Hope he talks to real doctors & not Dr. 'Farci.' "
Trump has cited OANN as a new favorite television channel after becoming frustrated with Fox News' willingness to interview Democrats. The channel, which is not distributed widely, often peddles wild conspiracies and false information.
By Monday evening, Trump had taken the hydroxychloroquine message public, retweeting a series of videos that were later removed by Twitter for containing false and misleading information about mask-wearing and the unproven drug.
Trump defended the video and the doctor it featured on Tuesday: "There was a woman who was spectacular in her statements about it and she's had tremendous success with it. And they took her voice off," he said.
But he seemed to back off when pressed about the statements made in the video itself, including that "you don't need masks" and the doctor's past statements about alien DNA used in medical treatments.
"I thought her voice was an important voice, but I know nothing about her," Trump said before abruptly departing the briefing room.
Fauci said on ABC he agrees with the Food and Drug Administration that "the overwhelming prevailing clinical trials that have looked at the efficacy of hydroxychloroquine have indicated that it is not effective in coronavirus disease."
The mild rebuke from Fauci caused some Trump advisers to shake their heads, fearing another round of headlines pitting Trump against the well-respected disease expert.
Last week, Trump said Fauci was a "nice guy" in an interview before his interviewer, Dave Portnoy of Barstool Sports, said the doctor was "on my ax list because every time he talks and says the country should stay inside, my stocks tank."
"Well, he'd like to see it closed up for a couple of years, but that's OK because I'm President, so I say, 'Well, I appreciate your opinion. Now give me another opinion, somebody please,' " Trump responded.
Meanwhile, Navarro has sustained his attacks on Fauci, saying he doesn't regret his unsanctioned op-ed and dinging the doctor for his wild first pitch last week at Nationals Park.
Asked by reporters at the White House on Tuesday about the continued attacks on Fauci, Navarro stormed away.

This story and headline have been updated with further news developments.

Brazil's Bolsonaro says he has 'mold' in his lungs as his wife tests positive for Covid-19

By Rodrigo Pedroso and Amy Woodyatt, CNN
Fri July 31, 2020


Bolsonaro traveling despite complaining of 'mold' in his lungs

Sao Paulo, Brazil (CNN)Brazil's President Jair Bolsonaro said on Thursday he felt weak and might have "mold in the lung" having spent weeks in isolation after catching Covid-19.
In his first Facebook live video since recovering from Covid-19, Bolsonaro said: "I've just taken a blood exam. I was a bit weak yesterday. They have also found a bit of an infection. I'm taking antibiotics now. It must have been those 20 days inside the house, we catch other things. I've caught mold, mold in my lungs. It must be that."

The President spent nearly 20 days in semi-isolation, after testing positive for the virus on July 7 and on subsequent occasions. On July 25, he announced via Twitter that he had tested negative.

His wife, Michelle Bolsonaro, has also tested positive for Covid-19, according to a statement from the President's press office.




Brazil's first lady Michelle Bolsonaro tested positive for Covid-19, according to an official statement released Thursday.

The first lady, who was last seen in public on Wednesday afternoon when she attended an official event in Brasilia with her husband, "is in good health and will follow all established protocols," the statement said.

Inside Brazil's cult of hydroxychloroquine

"The first lady is being accompanied by the medical team of the Presidency of the Republic," the statement adds.

In his Thursday address, the President also thanked God and hydroxychloroquine for his health.I'm healed from Covid. I have antibodies, no problems. In my particular case, I first thank God, and secondly, the medication prescribed by the presidential doctor: hydroxychloroquine," Bolsonaro said.

"The following day, I was already OK. If it was a coincidence or not, I don't know. But it works," the president added.

Numerous studies have shown that the drug -- also touted by US President Donald Trump -- is ineffective against Covid-19, and may even be harmful.

Brazil is second only to the United States in numbers of coronavirus infections and deaths. But Bolsonaro has downplayed the virus for months, and often appears in public and at rallies without a face mask, even hugging supporters.

The President made an appearance on horseback Thursday during a visit to Piaui State, where he was greeted by supporters, some of whom were not wearing masks.
In a video posted to Bolsonaro's official Facebook page, the President is seen on a horse, given to him as he arrived at Sao Raimundo Notato airport. Bolsonaro initially wore a mask, but removed it while celebrating with supporters.

The visit was intended to improve Bolsonaro´s political relations with regional authorities, and to inaugurate a water system in Campo Alegre de Lourdes, a small town in the northeast state of Bahia, a region known for severe droughts.

Rodrigo Pedroso reported from Sao Paulo, Amy Woodyatt wrote in London.

JULY 31, 2020
Bacterial, fungal coinfection uncommon in COVID-19 patients


(HealthDay)—Bacterial and fungal infections are uncommon in hospitalized COVID-19 patients, but coinfection is associated with high mortality and antibiotic use is widespread, according to a study published in the July issue of Infection Control & Hospital Epidemiology.

Priya Nori, M.D., from the Albert Einstein College of Medicine in Bronx, New York, and colleagues conducted a retrospective observational study of COVID-19 patients admitted between March 1, 2020, and April 18, 2020, to characterize the microbiology of bacterial and fungal coinfections during the pandemic surge.

The researchers identified bacterial or fungal coinfections in 152 of 4,267 COVID-19 patients (3.6 percent); mortality was 57 percent, while 16 percent of patients were discharged and 28 percent were still admitted at the time of analysis. Seventy-four percent of patients received mechanical ventilation. Overall, 91 (60 percent), 82 (54 percent), and 21 (14 percent) patients had positive respiratory cultures, positive blood cultures, and both positive blood and respiratory cultures, respectively. Nine percent of patients (13 patient) had polymicrobial cultures. Seventy-nine percent of patients had antibiotic exposure in the 30 days before positive microbiology. Ninety-eight percent of the study patients received antibiotics at any point during COVID-19 hospitalization; 107 patients (70 percent) received more than three antibiotic classes. Of 5,853 COVID-19 patients admitted between March 1 and May 31, 2020, 71 percent received at least one antibiotic dose.

"The pandemic has highlighted the need for close collaboration between stewardship and infection prevention programs to monitor for nosocomial infections, excess antibiotic use and multidrug resistance," the authors write.


Explore further Patients aged 60 to 69 most often hospitalized with COVID-19

More information: Abstract/Full Text (subscription or payment may be required)

Copyright © 2020 HealthDay. All rights reserved.

To distinguish contexts, animals think probabilistically, study suggests
by Massachusetts Institute of Technology

A maze in the Wilson lab at MIT. A rodent must infer that this is a different context than, say, a maze that used different shape cues or one that had an additional arm. A new study suggests they weigh probabilities in doing so. Credit: Peter Goldberg

Among the many things rodents have taught neuroscientists is that in a region called the hippocampus, the brain creates a new map for every unique spatial context—for instance, a different room or maze. But scientists have so far struggled to learn how animals decides when a context is novel enough to merit creating, or at least revising, these mental maps. In a study in eLife, MIT and Harvard researchers propose a new understanding: The process of "remapping" can be mathematically modeled as a feat of probabilistic reasoning by the rodents.

The approach offers scientists a new way to interpret many experiments that depend on measuring remapping to investigate learning and memory. Remapping is integral to that pursuit, because animals (and people) associate learning closely with context, and hippocampal maps indicate which context an animal believes itself to be in.

"People have previously asked 'What changes in the environment cause the hippocampus to create a new map?' but there haven't been any clear answers," said lead author Honi Sanders. "It depends on all sorts of factors, which means that how the animals define context has been shrouded in mystery."

Sanders is a postdoc in the lab of co-author Matthew Wilson, Sherman Fairchild Professor in The Picower Institute for Learning and Memory and the departments of Biology and Brain and Cognitive Sciences at MIT. He is also a member of the Center for Brains, Minds and Machines. The pair collaborated with Samuel Gershman, a professor of psychology at Harvard on the study.

Fundamentally a problem with remapping that has frequently led labs to report conflicting, confusing, or surprising results, is that scientists cannot simply assure their rats that they have moved from experimental Context A to Context B, or that they are still in Context A, even if some ambient condition, like temperature or odor, has inadvertently changed. It is up to the rat to explore and infer that conditions like the maze shape, or smell, or lighting, or the position of obstacles, and rewards, or the task they must perform, have or have not changed enough to trigger a full or partial remapping.

So rather than trying to understand remapping measurements based on what the experimental design is supposed to induce, Sanders, Wilson and Gershman argue that scientists should predict remapping by mathematically accounting for the rat's reasoning using Bayesian statistics, which quantify the process of starting with an uncertain assumption and then updating it as new information emerges.

"You never experience exactly the same situation twice. The second time is always slightly different," Sanders said. "You need to answer the question: 'Is this difference just the result of normal variation in this context or is this difference actually a different context?' The first time you experience the difference you can't be sure, but after you've experienced the context many times and get a sense of what variation is normal and what variation is not, you can pick up immediately when something is out of line."


The trio call their approach "hidden state inference" because to the animal, the possible change of context is a hidden state that must be inferred.

In the study the authors describe several cases in which hidden state inference can help explain the remapping, or the lack of it, observed in prior studies.

For instance, in many studies it's been difficult to predict how changing some of cues that a rodent navigates by in a maze (e.g. a light or a buzzer) will influence whether it makes a completely new map or partially remaps the current one and by how much. Mostly the data has showed there isn't an obvious "one-to-one" relationship of cue change and remapping. But the new model predicts how as more cues change, a rodent can transition from becoming uncertain about whether an environment is novel (and therefore partially remapping) to becoming sure enough of that to fully remap.

In another, the model offers a new prediction to resolve a remapping ambiguity that has arisen when scientists have incrementally "morphed" the shape of rodent enclosures. Multiple labs, for instance, found different results when they familiarized rats with square and round environments and then tried to measure how and whether they remap when placed in intermediate shapes, such as an octagon. Some labs saw complete remapping while others observed only partial remapping. The new model predicts how that could be true: rats exposed to the intermediate environment after longer training would be more likely to fully remap than those exposed to the intermediate shape earlier in training, because with more experience they would be more sure of their original environments and therefore more certain that the intermediate one was a real change.

The math of the model even includes a variable that can account for differences between individual animals. Sanders is looking at whether rethinking old results in this way could allow researchers to understand why different rodents respond so variably to similar experiments.

Ultimately, Sanders said, he hopes the study will help fellow remapping researchers adopt a new way of thinking about surprising results—by considering the challenge their experiments pose to their subjects.

"Animals are not given direct access to context identities, but have to infer them," he said. "Probabilistic approaches capture the way that uncertainty plays a role when inference occurs. If we correctly characterize the problem the animal is facing, we can make sense of differing results in different situations because the differences should stem from a common cause: the way that hidden state inference works."


Explore furtherBrain network mechanism causing spatial memory impairment revealed

More information: Honi Sanders et al, Hippocampal remapping as hidden state inference, eLife (2020). DOI: 10.7554/eLife.51140

Journal information: eLife

Provided by Massachusetts Institute of Technology
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Report linking 5G to COVID-19 swiftly debunked

by Peter Grad , Medical Xpress

Credit: CC0 Public Domain

"This paper made my jaw drop."

"It is just a wacko hypothesis."

"This article isn't so much a scientific paper as a representation of what a moron thinks a scientific paper is."

"You haven't seen the stupidest published SARS-CoV-2 take yet [until you read this]. I PROMISE you."

The reception given to a recently published report claiming 5G transmissions could trigger human cells to create coronavirus has been less than stellar.

A team of researchers published a paper in PubMed, a free biomedical database, that suggested 5G millimeter waves "are similar to shapes of hexagonal and pentagonal bases of their DNA source" that "produce holes in liquids with the nucleus." Their conclusion: "These bases could join to each other and form virus-like structures such as coronavirus."

Despite the impressive-sounding credentials of the group—members of the Guglielmo Marconi University, Central Michigan University and First Moscow State Medical University—the paper drew swift condemnation for its wild conclusions and failure to support any of its research.
Elisabeth Bik, a former Stanford science consultant who specializes in science ethics, said that despite the paper's claims, there is nothing in the report that proves them. "It is absolute nonsense," she said.

Bik said the group is known for publishing fantastic and unsupported hypotheses. She cited previous questionable research by the group proposing wild theses such as that the chemical structure of DNA differs between males and females (it doesn't) and that "infecting a pregnant woman with male or female influenza viruses" can determine the gender of a fetus.
She termed their latest effort "a wacko hypothesis."

An incensed Bik said, "I invite everyone to rip this piece apart, and to urge NCBI [PubMed's parent company] to ban this journal to the far end of predatory territory."

Joel Hruska of ExtremeTech says the researchers "blatantly misrepresented the actual bands that mmWave 5G deployments use" and ridiculed the notion asserted by the authors that any radio wave could help a virus colonize the human body. He noted that one of the article's authors recently published a highly questionable paper claiming COVID-19 could be treated with a psoriasis medication based on results from a single asymptomatic patient.

"None of these authors has the standing or authority to speak to the causes of COVID-19, and the fact that this paper has appeared in the PubMed database or been linked by the NIH is evidence of serious methodological flaws in the approval process," Hruska said. "This isn't science. It's what people who don't actually practice the scientific method appear to think it looks like."

After an outpouring of criticism over the article, PubMed removed the controversial report from its database.

The release of such a sham report is troubling, especially now. It serves to fuel a growing movement among "low-information" citizens, a term increasingly used to describe people who cannot distinguish between legitimate news sources and utterly preposterous conspiracy sites populating the fringes of the internet. Such sites cast doubts on legitimate research and established facts, and spread malicious distortions of news events, science and health and create needless fear and doubt.

Furthermore, by littering the global consciousness with yet more phony science, it makes it more challenging for the public to distinguish between propaganda and genuine research highlighting potentially risky developments in an era witnessing rapid growth of low-frequency electromagnetic wave transmission.

5G will usher in a revolution in telecommunications. It promises lightning-fast internet connection speeds—up to 50 times current rates—far broader coverage, lower power consumption and greater integration among smart devices.

But the fact remains that there are no studies confirming the massive network required to set up 5G infrastructure will not affect health. There are currently 200,000 cellular towers supporting 4G LTE communications; 5G may well require millions of towers.

Most current safety regulations governing EMF exposure are based on research from the 1980s. But more than 500 studies since then, according to Scientific American, point to at least possible harmful effects of radiation. None is conclusive, but none completely exonerates RF waves, either.

As Leeka Kheifets, an epidemiology professor at UCLA, told the Los Angeles Times about EMF, "I don't think it's clear that there are health risks, but it's also not clear that there are no health risks."

The International Agency for Research on Cancer in 2011 declared radio frequency radiation a possible human carcinogen. Scientific American last fall called for a moratorium on 5G deployment and funding for more thorough research. And a group of 250 scientists recently urged the United Nations and World Health Organization to issue tougher guidelines on EMF to protect consumers' health.

We have sadly learned that the institutions responsible for products once deemed safe but later found to be harmful are not usually the ones to raise the first alarms. Cigarettes, food dyes, preservatives, pharmaceuticals, fracking operations, pesticides—it was only through diligent scientific probing and publicity by public interest groups that risks posed by products once deemed safe were ultimately exposed and the products or activity banned, modified or restricted.

The reckless publication of an absurd study serves to remind that wild claims of danger must be treated with reasoned skepticism, but so must unsupported assurances of benefits and safety by those who stand to profit from new, untested technologies.


Explore furtherRetractions and controversies over coronavirus research show that the process of science is working as it should
More information: WITHDRAWN: 5G Technology and induction of coronavirus in skin cells, pubmed.ncbi.nlm.nih.gov/32668870/

© 2020 Science X Network
1440 shares

CDC reports the rich sleep better at night

by Bob Yirka , Medical Xpress

Credit: Pixabay/CC0 Public Domain

The U.S. Centers for Disease Control and Prevention has conducted a sleep study and found that rich people, on average, sleep longer at night than poor people. According to a report by CNN, researchers at the agency sent surveys to people in the United States over the years 2011 to 2014 inquiring about their sleep habits and have now made their results public.


The results showed that out of 140,000 adults who filled out and returned the surveys, 55% who reported living at or near the poverty line were able to get the recommended seven to eight hours of sleep at night. In contrast, for those living 400% above the poverty line, 66.6% reported getting a full night's sleep. The poverty line in the U.S. varies by income compared to family size. For a single person, it falls at $11,670 a year, while for a family of four, the number is $23,850.

The researchers did not dig deeper to discover why rich people sleep more, but some in the sleep field have suggested it is likely linked to the number of hours people have to work, or even the number of jobs. They also note that rich people have more help with childcare and other assistance with daily matters, such as cooking, cleaning and taking care of themselves. Rich people also tend to live in accommodations that are more receptive to sleep, such as quiet neighborhoods and private comfortable beds. The researchers also did not look into the impact of sleep differences between rich and poor on the country or the impact of chronic sleep deprivation on people living in sometimes desperate conditions. Also not mentioned was the impact the pandemic is having on the sleep patterns of people of both classes.

Prior research has shown that chronic shortages of sleep can lead to many health problems, from high blood pressure to depression, obesity and diabetes. When combined with overall stress, it has been found to be a contributor to heart disease, cancer risk, a reduction in quality of life and a greater chance of dying.


Explore further

Ethnically diverse mothers, children living in poverty at risk for sleep problems

Virus effects to last decades, WHO says six months on

Credit: CC0 Public Domain

The WHO said Friday that coronavirus pandemic effects would be felt for decades as its emergency committee assessed the situation six months after sounding its top alarm over the outbreak.

The novel coronavirus has killed nearly 675,000 people and infected at least 17.3 million since it emerged in China last December, according to a tally from official sources compiled by AFP.

The World Health Organization's emergency committee, comprising 18 members and 12 advisers, is meeting for the fourth time over the COVID-19 crisis.

"It's sobering to think that six months ago, when you recommended I declare a public health emergency of international concern (PHEIC), there were less than 100 cases and no deaths outside China." WHO chief Tedros Adhanom Ghebreyesus said as the meeting began.

"The pandemic is a once-in-a-century health crisis, the effects of which will be felt for decades to come."

The committee can propose new recommendations or amend existing ones.

However, there is little doubt that the WHO will maintain the pandemic's status as a PHEIC—its highest level of alarm—first declared on January 30.

The WHO has been sharply criticised for the length of time it took to declare an international emergency.

The United States, which accused the organisation of being too close to China, officially began its withdrawal from the organisation in July.

The agency has also been criticised for recommendations deemed late or contradictory, in particular on wearing masks, or the modes of transmission of the virus.

Questions unanswered

"Many scientific questions have been resolved; many remain to be answered," Tedros said.

"Early results from serology studies are painting a consistent picture: most of the world's people remain susceptible to this virus, even in areas that have experienced severe outbreaks.

"Many countries that believed they were past the worst are now grappling with new outbreaks. Some that were less affected in the earliest weeks are now seeing escalating numbers of cases and deaths. And some that had large outbreaks have brought them under control."

The highly restrictive lockdowns enforced to deal with the pandemic earlier this year caused economic turmoil and an effective vaccine may be the only long-term solution to the highly contagious respiratory disease.

"Although vaccine development is happening at record speed, we must learn to live with this virus, and we must fight it with the tools we have," said Tedros.
© 2020 AFP


JUL 30, 2020
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STRANGERS ON A TRAIN

Study reveals COVID-19 transmission rate on trainsby University of Southampton JULY 31,2020

Attack rate of COVID-19 per different seats and co-travel time on a high-speed train Credit: University of Southampton

A study by scientists from the University of Southampton has examined the chances of catching COVID-19 in a train carriage carrying an infectious person.

Based on high-speed routes in China, researchers from WorldPop found that for train passengers sitting within three rows (widthwise) and five columns (lengthwise) of an infected person (index patient) between zero and ten percent (10.3) caught the disease. The average rate of transmission for these 'close contact' travelers was 0.32 percent.

The study, in collaboration with the Chinese Academy of Sciences, China Academy of Electronics and Information Technology, and Chinese Centre for Disease Control and Prevention, also showed that passengers traveling in seats directly adjacent to an index patient suffered the highest level of transmission, with an average of 3.5 percent contracting the disease. For those sitting on the same row, the figure was 1.5 percent.

The 'attack rate' for each seat—the number of passengers in a given seat diagnosed with COVID-19, divided by the total number of passengers traveling in the same seat—increased by 0.15 percent for every hour that a person traveled with an index patient. For those in adjacent seats, this rate of increase was higher at 1.3 percent per hour.

Interestingly, the researchers found that only 0.075 percent of people who used a seat previously occupied by an index patient went on to contract the disease.

Details are published in the journal Clinical Infectious Diseases.

The WorldPop team, experts in population mapping, used sophisticated modeling to analyze anonymised itinerary and infection data relating to train passengers on China's high-speed G train network. This included those who had COVID-19 at the time of travel and their close contacts (who showed symptoms within 14 days of travel). The data, covering a period between 19 December 2019 and 6 March 2020, included 2,334 index patients and 72,093 close contacts. Their travel times ranged from between less than an hour to eight hours.

Lead investigator, Dr. Shengjie Lai, comments, "Our study shows that although there is an increased risk of COVID-19 transmission on trains, a person's seat location and travel time in relation to an infectious person can make a big difference as to whether it is passed on. The findings suggest that during the COVID-19 epidemic it is important to reduce the density of passengers and promote personal hygiene measures, the use of face coverings and possibly carry-out temperature checks before boarding."

The researchers conclude that given the attack rates estimated for passengers in the same row as an index patient, a safe social distance of more than one meter is required for one hour spent traveling together. After two hours of contact, they consider a distance of less than 2.5 meters may be insufficient to prevent transmission.

Director of WorldPop, Professor Andy Tatem adds: "Our research is the first to quantify the individual risk of COVID-19 transmission on public transport based on data from epidemiological investigations of disease cases and their close contacts on high-speed trains.

"It shows that the transmission risk not only relates to the distance from an infected person, but also the time in their presence. We hope it can help to inform authorities globally about measures needed to guard against the virus and in-turn help to reduce its spread."


Explore further Follow the latest news on the coronavirus (COVID-19) outbreak

More information: Maogui Hu et al. The risk of COVID-19 transmission in train passengers: an epidemiological and modelling study, Clinical Infectious Diseases (2020).

DOI: 10.1093/cid/ciaa1057

Journal information: Clinical Infectious Diseases


Provided by University of Southampton

We thought COVID-19 was just a respiratory virus—we were wrong

by Ariel Bleicher, Katherine Conrad, 

University of California, San Francisco JULY 31,2020

Credit: Anna and Elena Balbusso

In late January, when hospitals in the United States confirmed the presence of the novel coronavirus, health workers knew to watch for precisely three symptoms: fever, cough, and shortness of breath. But as the number of infections climbed, the symptom list began to grow.

Some patients lost their sense of smell and taste. Some had nausea or diarrhea. Some had arrhythmias or even heart attacks. Some had damaged kidneys or livers. Some had headaches, blood clots, rashes, swelling, or strokes. Many had no symptoms at all.

By June, clinicians were swapping journal papers, news stories, and tweets describing more than three dozen ways that COVID-19, the disease the coronavirus causes, appears to manifest itself. Now researchers at UC San Francisco and around the world have begun taking a closer look at this dizzying array of symptoms to get at the disease's root causes. They are learning from people inside the hospital and out; people on the brink of death and only mildly sick; people newly exposed and recovered; people young and old, Black, brown, and white. And they are beginning to piece together the story of a virus unlike any known before.

How infection sets in

Viruses lead a curious purgatorial existence of being neither fully alive nor dead. Enveloped in a protein cloak, a virus consists almost entirely of genetic material—DNA or RNA, the blueprints for all of life. But it can't reproduce on its own. To survive, it must break into a cell and co-opt the cell's gene-copying machinery.

The novel coronavirus, an RNA virus named SARS-CoV-2, has become notorious for its skill at breaking and entering human cells. Its tools of choice are the protein spikes protruding from its surface—a feature that distinguishes all coronaviruses. The spikes of SARS-CoV-2 are the crème de la crème: By the luck of the evolutionary draw, they are able to easily grab hold of protein gates on human cells known as ACE2 receptors and, like jackknives, pry these gates open.

"You can think of an ACE2 receptor like a docking site," says Faranak Fattahi, Ph.D., a UCSF Sandler Fellow. When the coronavirus pandemic hit San Francisco, Fattahi repurposed her laboratory to study this key receptor, which normally plays a role in regulating blood pressure. "When the virus lands on it," she says, "it initiates a molecular process that brings the virus inside the cell."


If you're exposed to SARS-CoV-2—say, from a cough or sneeze—the virus will likely first encounter ACE2 receptors on cells in your nose or throat. But these receptors also populate your heart, gut, and other organs. Fattahi's team has found evidence suggesting that male sex hormones such as testosterone may increase the number of ACE2 receptors that cells produce, which could help explain why SARS-CoV-2 seems to wreak greater havoc on men than on women and why kids rarely get sick. "The fewer ACE2 receptors, the less risk of infection—that's the idea," she says, adding that this hypothesis for the disease's gender gap is only one of several.

Once inside a few initial host cells, the virus sets them to work churning out copies of itself. Within hours, thousands of new virus particles begin bursting forth, ready to infect more cells. Although SARS-CoV-2 is less deadly than the original SARS virus, which emerged in 2002, it replicates more rapidly. Also unlike SARS, which primarily infects the lungs, SARS-CoV-2 replicates throughout the airway, including in the nose and throat, making it highly contagious—like the common cold.

However, infection with SARS-CoV-2 usually doesn't feel like a cold. Fewer than 20 percent of infected people who eventually show up at a hospital report having had a sore throat or runny nose. During the first few days of being infected, you're more likely to have a fever, dry cough or, peculiarly, lose your sense of smell or taste.

Most likely, though, you won't feel sick at all. When UCSF researchers tested people for SARS-CoV-2 in San Francisco's Mission District, 53 percent of those infected never had any symptoms. "That's much higher than expected," says Monica Gandhi, M.D., MPH, a UCSF professor of medicine with expertise in HIV. Surveys of outbreaks in nursing homes and prisons show similar or even higher numbers. "If we did a mass testing campaign on 300 million Americans right now, I think the rate of asymptomatic infection would be somewhere between 50 percent and 80 percent of cases," Gandhi says. Millions of people may be spreading the virus without knowing it, she points out, making asymptomatic transmission the Achilles' heel of efforts to control the pandemic—and highlighting the importance of universal masking.

Spikes on the virus’s surface act like jackknives to break and enter human cells. Credit: UCSF

"The majority of people who have COVID-19 are out in the community, and they are either asymptomatic or only mildly ill," says Sulggi Lee, M.D., Ph.D., a UCSF assistant professor of medicine. When the coronavirus pandemic hit San Francisco in early March, Lee conceived a study to investigate why. She scrambled to assemble a team and procure funding and equipment. She borrowed a colleague's mobile clinic—a van outfitted with an exam table and a phlebotomy chair—so that her team could drive around the city, collecting samples from infected people. Lee hopes data from the study, called CHIRP (COVID-19 Host Immune Response Pathogenesis), will show how people's immune systems respond as SARS-CoV-2 starts to gain a foothold in their bodies.

"A lot is riding on that initial response," she says. If Lee and her collaborators can figure out the biological processes that allow some infected people to stay relatively well, they can perhaps use that knowledge to prevent others from falling severely ill.

Battling in the lungs

True to its name, SARS-CoV-2 (which stands for severe acute respiratory syndrome coronavirus 2) is first and foremost a bad respiratory virus. If your immune system doesn't defeat it at its landing site in your nose or throat, it will advance down your windpipe, infiltrating the cells lining your lungs' branching air tubes. At the tubes' ends, tiny air sacs called alveoli pass oxygen to your blood. As the virus multiplies, the alveoli may fill with fluid, shutting down this critical gas exchange. Your blood-oxygen level may drop and, typically about six days into an infection, you may start feeling short of breath.

What causes this mayhem? "Some of it is definitely caused by the virus itself," says Michael Matthay, M.D., a UCSF professor of medicine who has studied acute respiratory diseases for more than 30 years. Inevitably, a fast-replicating virus will kill or injure many of the lung cells it infects; the more cells it infects, the more ruin it will leave in its wake.

But SARS-CoV-2 doesn't appear to be a savage destroyer of cells. Although it's too early to know for sure, the virus's fatality rate seems to be roughly 10 times that of the flu. "You would think that's because it's just a killing machine," says Max Krummel, Ph.D., UCSF's Smith Professor of Experimental Pathology and chair of the Bakar ImmunoX initiative. So far, however, the science suggests otherwise.

"One of the weirder things about this new coronavirus is it doesn't seem to be incredibly cytopathic, by which we mean cell-killing," Krummel says. "Flu is really cytopathic; if you add it to human cells in a petri dish, the cells burst within 18 hours." But when UCSF researchers subjected human cells to SARS-CoV-2, many of the infected cells never perished. "It's pretty compelling data that maybe we're not dealing with a hugely aggressive virus," Krummel says.

The bigger provocation, he suspects, may be your own immune system. Like any pathogen, SARS-CoV-2 will trigger an immune attack within minutes of entering your body. This counterstrike is extraordinarily complex, involving many tactics, cells, and molecules. In a UCSF study called COMET (COVID-19 Multi-Phenotyping for Effective Therapies), Krummel and other scientists have been observing this immune warfare in more than 30 people admitted to UCSF hospitals with COVID-19 and other respiratory infections. "What we're doing is looking at patients' blood, their genes, and the secretions from their noses and lungs, and we're asking, 'What's your army? What's your response strategy?'"

An early analysis of COMET data, Krummel says, suggests that the immune systems of many hospitalized patients mobilize differently—and more aggressively—against SARS-CoV-2 than against influenza viruses, which cause the flu. Their lungs are ravaged, these data suggest, not by the virus alone but by the detritus of an immunological battle gone awry. This rogue immune response could explain why, around day 11 of a COVID-19 infection, patients often develop a severe pneumonia known as acute respiratory distress syndrome, or ARDS.

Ultimately, COMET seeks to find COVID-19 therapies that can rein in an overeager immune system in order to prevent or treat ARDS. But that feat won't be easy, says Carolyn Calfee, M.D., MAS '09, an ARDS expert, UCSF professor of medicine, and co-leader of the study. Too much or the wrong kind of intervention, she explains, could cripple a person's immune system to the point where it can't clear an infection. "It's a fine line between therapeutic and deleterious," Calfee says. "We're trying to find that balance."

Typically, people who die from COVID-19 ARDS die around day 19. Reported rates of mortality have varied widely, with the highest rates being where the pandemic has hit hardest, overwhelming hospital resources and staff. At UCSF hospitals—likely due to the city's early shelter-in-place orders, which prevented an initial surge of COVID-19 cases—so far only 10 of 85 critically ill patients have died.

SARS-CoV-2 replicates throughout the airway, making it highly contagious, like the common cold. Credit: Anna and Elena Balbusso/UCSF

"The good news is that we've been doing clinical trials of best-care practices for ARDS since 1998," Matthay says. Thanks to research by him and others, for example, clinicians have long known which ventilator settings result in the fewest deaths and how to flip patients onto their stomachs—a technique known as proning—to best help them breathe. If public health measures can keep hospital admissions low so that frontline providers can make good use of the skills and knowledge they already have, we may find that we have less to fear from SARS-CoV-2 than we thought.

On the other hand, the virus behaves in ways that are still mysterious.

Heart failure

In April, Susan Parson, M.D., a Bay Area medical examiner, made a startling discovery. For nearly two months, officials had believed that the first people in the U.S. to die from COVID-19 had died of respiratory failure in Washington state in late February. At the time, the U.S. Centers for Disease Control and Prevention limited testing to people who had respiratory symptoms and had recently traveled to China or otherwise been exposed to the virus. Those restrictions, however, turned out to be misguided.

As a medical examiner for California's Santa Clara County, Parson had done a routine autopsy on a 57-year-old woman named Patricia Dowd, who had died suddenly at home on February 6. In Dowd's tissues, Parson found the cause of her death: SARS-CoV-2. But the virus hadn't wrecked Dowd's lungs. In fact, she had only mild pneumonia. Instead, SARS-CoV-2 had ruptured her heart.

Meanwhile, epidemiologists began learning that preexisting heart disease and related conditions put people at greater risk of suffering and dying from COVID-19. "We're finding that many patients who have more severe forms of the illness are obese, they are diabetic, they are hypertensive," says cardiologist Nisha Parikh, M.D., a UCSF associate professor who specializes in population health research. Such risk factors, she says, are unusual. "They're not ones that really stood out in prior epidemics."

Clinicians, too, were seeing surprising numbers of COVID-19 patients develop heart problems—muscle weakness, inflammation, arrhythmias, even heart attacks. "We're not used to respiratory viruses having such dire consequences on the heart in such apparently high numbers," says cardiologist Gregory Marcus, M.D., MAS '08, UCSF's Endowed Professor of Atrial Fibrillation Research. Many patients whose hearts acted up also had failing lungs. But others had no other symptoms or, like Dowd, only mild ones.

Since March, Marcus has co-led one of the largest community surveys to better understand the spread of SARS-CoV-2 and its myriad effects. The study, dubbed COVID-19 Citizen Science, has so far enrolled more than 27,000 people; anyone with a smartphone can participate. Marcus plans to also start collecting data from wearable devices, including Fitbits and Zio patches, which wirelessly monitor heart rhythms. "There may be large numbers of people who are suffering from cardiovascular effects of COVID-19 in the absence of other symptoms," Marcus says. "I'm worried we're missing those cases."

It stands to reason that SARS-CoV-2 affects the heart. After all, heart cells are flush with ACE2 receptors, the virus's vital port of entry. And, indeed, laboratory experiments suggest that the virus can enter and replicate in cultured human heart cells, says Bruce Conklin, M.D., a professor of medicine and an expert in heart-disease genetics at UCSF and the Gladstone Institutes.

But Conklin doesn't think SARS-CoV-2 necessarily kills heart cells outright. Rather, in the process of copying itself, the virus steals pieces of the genetic instructions that tell the heart cells how to do their job. "It's hauling away and hijacking stuff that's necessary for the heart to beat," he says. He is currently testing this hypothesis using human heart cells grown in cup-sized vessels in the lab of Todd McDevitt, Ph.D., a bioengineer at UCSF and the Gladstone Institutes.

It's also possible, however, that an infected person's own immune system may do the majority of the damage in the heart, as it appears to do in the lungs. "The heart probably gets infected by a lot of other viruses, and they don't have a lethal effect," Conklin says. "What makes this one different?"
From Head to “COVID Toes”: People with COVID-19 exhibit from none to many of these symptoms. Some symptoms (such as fever, cough, and loss of smell) are common, while others (such as sore throat, pink eye, and stroke) are rare. Credit: Illustration: Stephanie Koch. Concept: Jennifer Babik, M.D., Ph.D.

Stranger things

Toward the end of March, as San Francisco began to warm up, Sonia got cold feet. She put on wool socks and turned up her heater. Still, her feet felt frozen. Three days later, her soles turned splotchy purple. Red dots appeared on her toes. At night, her cold feet itched and burned. Walking hurt. And she was exhausted, napping through afternoon Zoom meetings. "It was so bizarre," says Sonia, a San Francisco resident. A week later, her symptoms were gone.

"Yes, COVID," wrote Lindy Fox, M.D., a UCSF professor of dermatology, replying to an email describing Sonia's case. Sonia wasn't surprised. Anyone, like her, who's been following news of the pandemic has probably heard about "COVID toes," a painful or itchy skin rash that sometimes pops up in young adults with otherwise mild or asymptomatic cases of COVID-19. "It looks like what we call pernio, or chilblains," Fox says, "which is a pretty common phenomenon when somebody goes out in cold weather—they start to get purple or pink bumps on their fingers or toes."

Many people with rashes like Sonia's don't test positive for COVID-19, Fox says, which has made some clinicians skeptical of the connection; when patients have both, it's just a coincidence, they believe. But Fox doesn't think so. For one thing, "the time of year is wrong," she says. "Pernio usually shows up in the dead of winter." Even more compelling, dermatologists around the world are "getting crazy numbers of calls about it," Fox says. "In the last three weeks, I've had somewhere between 10 and 12 patients.

Normally, I have four a year."

And it's not just dermatologists who are adding their observations to COVID-19's ever-expanding symptom list. Gut specialists are finding that 20 percent to 40 percent of people with the disease experience diarrhea, nausea, or vomiting before other symptoms, says gastroenterologist Michael Kattah, M.D., Ph.D., a UCSF assistant professor. If you swallow virus particles, he says, there's a good chance they will infect cells lining your stomach, small intestine, or colon. As in the lungs and heart, these cells are studded with vulnerable ACE2 portals.

Especially disconcerting, Kattah says, is how long the virus seems to persist in the gut. About 50 percent of patients with COVID-19 have virus particles in their stools, often for weeks after their nose swabs test negative, he points out. Laboratory studies show that these particles are often still alive and can infect cells in a petri dish. Whether fecal transmission occurs between people, however, is an open question. If the answer is yes, people recovering from COVID-19 may need to stay quarantined even after they feel well, and the rest of us will need to be as meticulous about bathroom hygiene as we've become about handwashing and mask-wearing.

Other specialists are also raising flags. Neurologists worry about reports of COVID-19 patients with headaches, "brain fog," loss of the sense of smell, dizziness, delirium, and, in rare cases, stroke. Nephrologists worry about kidney stress and failure. Hepatologists worry about liver injuries. Ophthalmologists worry about pink eye. Pediatricians, meanwhile, worry about a peculiar COVID-related inflammatory syndrome that's showing up in kids and young adults.

Researchers are still sorting out the causes for this constellation of effects. If you come down with a particular symptom, is it because the virus is attacking your cells? Because your immune system is overreacting? Or just because you're very sick? In any severe illness, for example, the kidneys must work extra hard to filter waste and control nutrients and fluid; if overtaxed, they may begin to fail. Similarly, cognitive problems can result from increased blood toxins due to stressed kidneys or from low oxygen due to respiratory distress. "There's a lot of smoke," says Michael Wilson, M.D. '07, MAS '16, the Rachleff Distinguished Professor at UCSF's Weill Institute for Neurosciences. "We need to figure out where the fire is coming from."

Recently, there's been speculation that some of COVID-19's seemingly disparate symptoms may stem from trouble in the blood. Blood clots, for example, are showing up in cases of COVID-19 frequently enough for clinicians to take notice. "There's something unique about the coagulation system in these patients," says nephrologist Kathleen Liu, M.D. '99, Ph.D. '97, MAS '07, a UCSF professor of medicine. In caring for COVID-19 patients on dialysis machines, she's been surprised to see blood clots block dialysis tubes more than usual. Clotted tubes are common, she says, "but this is extreme."

That may be because, as growing evidence suggests, SARS-CoV-2 can infect cells in the walls of blood vessels that help regulate blood flow and coagulation, or clotting. If true, this behavior could explain some of the virus's weirder (and rarer) manifestations, such as heart attacks, strokes, and even "COVID toes."
Most symptomatic cases of COVID-19 are mild. Credit: UCSF

"Our vasculature is a contiguous system," says cardiologist Parikh. "Thus injury in one area, such as blood vessels in the lungs, can set off clotting cascades that affect multiple organs." Some of that trouble likely results from inflammation triggered by the immune system, she points out, although another culprit may be the body's RAAS, or renin-angiotensin-aldosterone system, a hormone system that controls blood pressure and fluid balance. Because RAAS involves ACE2 receptors, Parikh suspects it may become disrupted when the virus infects cells through these receptors, thus triggering coagulation and other downstream effects. Her lab is now studying this system in COVID-19 patients to better understand how SARS-CoV-2 infection affects it.

Inevitably, some ailments may turn out to be red herrings. During a pandemic, when people are flocking to hospitals with infections, clinicians will also see a rise in other health problems, simply by the rules of statistics, points out S. Andrew Josephson, M.D., the Francheschi-Mitchell Professor, chair of UCSF's neurology department, and a member of the Weill Institute for Neurosciences. "If the prevalence of infection is high, then almost any condition—a broken leg, if you will—you might conclude is associated with COVID-19."

"As clinicians, we want to get information to our medical community and to the public as quickly as possible," Josephson says, "but we have to be cautious about not making too big a deal of a little blip."

The long tail

As with any infection, how long a bout of COVID-19 lasts varies from person to person. If you're ill enough to need critical care, you can expect the disease to take at least a few weeks to run its course. In some cases, symptoms persist for months. For a typical milder case, though, you should feel better within a couple weeks.

At that point, the question foremost on your mind will be: Am I immune? There are now more than a dozen antibody tests on the market, but most are unreliable, according to UCSF research. And even the best tests can't tell you whether you have enough of the right kinds of antibodies to protect you against reinfection. "There is a lot of hope and belief that we'll have an antibody test that actually informs us of immunity, but we're not quite there yet," says Chaz Langelier, M.D., Ph.D., a UCSF assistant professor of medicine who is working to improve diagnostic tools for COVID-19.

What we have in the meantime are a lot of unknowns: If you do become immune to SARS-CoV-2, when and how does that occur? Will you gain immunity from a mild or asymptomatic case, as well as a severe one? How long will that immunity last?

"The answers will have huge implications for social distancing and masking and for getting the economy back up and running," says Michael Peluso, M.D., a clinical fellow who came to UCSF three years ago to help fight HIV. Now he's co-leading a new study called LIINC (Long-term Impact of Infection with Novel Coronavirus), which is enrolling people who have been infected with SARS-CoV-2 and will follow them for two years. Besides illuminating changes in immunity over time, LIINC is investigating chronic effects of infection on the immune system, lungs, heart, brain, blood, and other parts of the body.

"I hope people will recover and immunity will be protective and long-lasting, and that will be that," Peluso says.

It's what we all hope. We hope we will beat an infection swiftly—or, better yet, avoid the virus until there is a vaccine. We hope that if we do fall gravely ill, we will be cared for by the best providers and tended to by people we love. The reality, as we already know, is more complicated. And even if COVID-19 doesn't batter our bodies, the pandemic will surely leave scars—on our psyches, our livelihoods, our institutions, and our health—that we are only beginning to fathom. In truth, we don't know how our cards will fall, as individuals or as a people. Only time—and data—will tell.

Provided by University of California, San Francisco

Frontline healthcare workers more likely to test positive for SARS-CoV-2 despite PPEby King's College London

Credit: CC0 Public Domain

A new study published today in Lancet Public Health has found that front-line healthcare workers with adequate personal protective equipment (PPE) have a three-fold increased risk of a positive SARS-CoV-2 test, compared to the general population. Those with inadequate PPE had a further increase in risk. The study also found that healthcare workers from Black, Asian and minority ethnic (BAME) backgrounds were more likely to test positive.

Using the COVID Symptom Tracker App, researchers from King's College London and Harvard looked at data from 2,035,395 individuals and 99,795 front-line health-care workers in the UK and US. The prevalence of SARS-CoV-2 was 2747 cases per 100,000 front-line health-care workers compared with 242 cases per 100,000 people in the general community. A little over 20 percent of front-line health-care workers reported at least one symptom associated with SARS-CoV-2 infection compared with 14·4 percent of the general population; fatigue, loss of smell or taste, and hoarse voice were especially frequent.

BAME health-care workers were at an especially high risk of SARS-CoV-2 infection, with at least a fivefold increased risk of infection compared with the non-Hispanic white general community.

Professor Sebastien Ourselin, senior author from King's College London said: "The findings of our study have tremendous impact for healthcare workers and hospitals. The data is clear in revealing that there is still an elevated risk of SARS-CoV-2 infection despite availability of PPE.

"In particular we note that that the BAME community experience elevated risk of infection and in some cases lack access to adequate PPE, or frequently reuse equipment."

Researchers say their study not only shows the importance of adequate availability and use of PPE, but also the crucial need for additional strategies to protect healthcare workers, such as ensuring correct application and removal of PPE and avoiding reuse which was associated with increased risk. 

Differences were also noted in PPE adequacy according to race and ethnicity, with non- Hispanic white health-care workers more frequently reporting reuse of or inadequate access to PPE, even after adjusting for exposure to patients with COVID-19.

Joint first author Dr. Mark Graham from King's College London said: "The work is important in the context of the widely reported higher death rates amongst healthcare workers from BAME backgrounds. Hopefully a better understanding of the factors contributing to these disparities will inform efforts to better protect workers."

Dr. Claire Steves, lead clinical researcher from King's College London said: "I'm very pleased we have now introduced masks and social distancing where possible for all interactions in hospitals—to protect ourselves and the population we serve. We need to ensure this is reinforced and sustained throughout the health service—including in health care settings outside hospitals, for example in care homes.

"Additional protective strategies are equally as important, such as implementing social distancing among healthcare staff. Stricter protocols for socialising among healthcare staff also need to be considered."


Explore further COVID risk calculator aims to help keep BAME healthcare workers safer

Journal information: The Lancet Public Health

Provided by King's College London

High COVID-19 risk among health care workers, especially those from minority backgrounds
by Massachusetts General Hospital

Credit: CC0 Public Domain

New research indicates that at the peak of the COVID-19 pandemic in the U.S. and the U.K., frontline healthcare workers—particularly those from Black, Asian, and minority ethnic backgrounds—faced much higher risks of testing positive for COVID-19 than individuals in the general community. The study, which was conducted by a team led by researchers at Massachusetts General Hospital (MGH), is published in The Lancet Public Health.


Among 2,035,395 individuals in the community and 99,795 frontline healthcare workers who voluntarily used the COVID Symptom Study smartphone app developed by Zoe Global Ltd with scientific input from MGH and Kings College London, 5,545 new reports of a positive COVID-19 test were documented between March 24 and April 23, 2020.

Frontline healthcare workers had at least a threefold increased risk of COVID-19, after accounting for differences in testing frequency between frontline healthcare workers and the general community. Black, Asian, and minority ethnic healthcare workers appeared to be disproportionately affected, with a nearly twofold higher risk compared with white healthcare workers.

Also, frontline healthcare workers who reported inadequate availability of personal protective equipment (PPE) such as masks, gloves, and gowns, had an especially elevated risk; however, adequate availability of PPE did not seem to completely reduce risk among healthcare workers caring for patients with COVID-19.

"Although it is clear that healthcare workers on the front line of the fight against COVID-19 have an increased risk of infection, our country continues to face vexing shortages of PPE," said senior author Andrew T. Chan, MD, Ph.D., chief of the Clinical and Translational Epidemiology Unit at MGH and director of Cancer Epidemiology at the MGH Cancer Center. "Our results underscore the importance of providing adequate access to PPE and also suggest that systemic racism associated with inequalities to access to PPE likely contribute to the disproportionate risk of infection among minority frontline healthcare workers."

Dr. Chan hopes the study's findings bring greater awareness to the importance of ensuring an equitable supply chain of PPE and of developing additional strategies to protect all frontline healthcare workers. "This study demonstrates how the two major crises that the U.S. faces— the COVID-19 pandemic and systemic racism—are inextricably linked and need immediate attention," he added.


More information: Long H Nguyen et al, Risk of COVID-19 among front-line health-care workers and the general community: a prospective cohort study, The Lancet Public Health (2020). DOI: 10.1016/S2468-2667(20)30164-X

Journal information: The Lancet Public Health

Provided by Massachusetts General Hospital 

Google searches during pandemic hint at future increase in suicide

by Columbia University Irving Medical Center

Credit: CC0 Public Domain

U.S. Google searches for information about financial difficulties and disaster relief increased sharply in March and April compared to pre-pandemic times, while googling related to suicide decreased, researchers at Columbia University Irving Medical Center have found.

Because previous research has shown that financial distress is strongly linked to suicide mortality, the researchers fear that the increase may predict a future increase in deaths from suicide.

The findings were published online in PLOS One.

"The scale of the increase in Google searches related to financial distress and disaster relief during the early months of the pandemic was remarkable, so this finding is concerning," says Madelyn Gould, Ph.D., MPH, Irving Philips Professor of Epidemiology in Psychiatry at Columbia University Vagelos College of Physicians and Surgeons and senior author of the study.
Pandemics and suicide

Researchers in the United States and elsewhere have begun studying the effects of the COVID-19 pandemic on mental health, but the impact on suicidal behavior and deaths is difficult to assess due to lag time in the availability of mortality data.

Previous studies suggest that suicide rates often decrease in the immediate aftermath of national disasters, such as 9/11, but may increase several months later, as seen after the 1918 flu pandemic and the 2003 SARS outbreak in Hong Kong.

Studies in the U.S. and internationally have linked Google search behavior with suicidal behavior, so in the current study, the researchers evaluated online searches about suicide and suicide risk factors during the early part of the pandemic and potential long-term impact on suicide.

The researchers used an algorithm to analyze Google trends data from March 3, 2019, to April 18, 2020, and identify proportional changes over time in searches for 18 terms related to suicide and known suicide risk factors.

"We didn't have a clear hypothesis about whether there would be an increase in suicide-related queries during this period of time, but we anticipated a national sense of community during the pandemic that might mitigate suicidal behavior in the short term," says Emily Halford, MPH, data analyst and the study's first author.

Unemployment, panic attacks, and loneliness may predict future suicide

The researchers found dramatic relative increases (in the thousands of percentages, in some cases) in Googling search terms related to financial distress—e.g., "I lost my job," "unemployment," and "furlough"—and for the national Disaster Distress Helpline.

The proportion of queries related to depression was slightly higher than the pre-pandemic period, and moderately higher for panic attack.

"It seems as though individuals are grappling with the immediate stresses of job loss and isolation and are reaching out to crisis services for help, but the impact on suicidal behavior hasn't yet manifested," says Gould. "Generally, depression can take longer to develop, whereas panic attacks may be a more immediate reaction to job loss and having to deal with emotionally charged events amidst the social isolation of the pandemic."

Searches for terms related to loneliness were also meaningfully higher during the early pandemic period versus the prior year.

Gould adds that social distancing is one of the primary measures implemented to slow the spread of the coronavirus, "but this approach may have detrimental secondary effects, such as loneliness and exacerbation of preexisting mental illnesses, which are known suicide risk factors."

Meeting the anticipated need for crisis services

The researchers say that in light of an anticipated increase in suicidal crises, it will be important to ensure continued availability and accessibility of crisis services and other mental health services during the later stages of the pandemic.

"The current findings give us insight into how people have been dealing with the immediate emotional and financial effects of the pandemic," says Gould. "Encouragingly, individuals who Google terms related to suicide are directed to the National Suicide Prevention Lifeline. We are hoping that accessing this crisis service may ameliorate suicide risk among the individuals who have Googled suicide-related terms."

More Information

If you or someone you know is thinking about suicide, contact the National Suicide Prevention Lifeline 24/7 for free, confidential support by calling 1-800-273-8255 (1-800-273-TALK) and through online chats.

The paper is titled, "Google searches for suicide and suicide risk factors in the early stages of the COVID-19 pandemic," and was published online in PLOS One on July 24, 2020.


Explore further COVID-19 impact on suicide

More information: Emily A. Halford et al, Google searches for suicide and suicide risk factors in the early stages of the COVID-19 pandemic, 

PLOS ONE (2020). DOI: 10.1371/journal.pone.0236777

Journal information: PLoS ONE


Provided by Columbia University Irving Medical Center