How the coronavirus job cuts played out by sector and demographics

The job losses suffered in March as the U.S. economy shut down in the face of the novel coronavirus pandemic were widespread but still were disproportionately felt in a handful of employment sectors and by women, the young and the less educated.

In all, 701,000 jobs were reported lost last month, the Labor Department said on Friday, but even that massive number – the largest since the financial crisis 11 years ago – did not capture the true depth of the losses because the monthly survey was conducted too early in March.
Still, it shows that even in the earliest stages of the business closures that have since spread across the country, the cuts were most heavily felt in industries such as hotels, restaurants and education as the travel industry shut down, bars and eateries closed their doors, and day care centers shuttered, all in the aim of limiting the spread of the disease.
And, perhaps ironically in the middle of a health crisis, the health care sector was among the most afflicted as providers of nearly any service apart from acute care for sufferers of COVID-19, the lung ailment caused by the novel coronavirus, suspended operations and stopped seeing patients.
The following charts offer a picture of how March’s job losses – certain to be revised higher and followed by even larger cuts in April – played out across various industries and demographic groups.

The leisure and hospitality sector shed 459,000 jobs – 65% of all the positions lost in March. The loss, the largest monthly decline in the sector ever, effectively wiped out two years of employment gains in the industry.
The largest share of that came at restaurants and bars, which slashed 417,000 jobs.
Around 76,000 health and education jobs were eliminated led by 29,000 cuts at dentists and physicians offices and another 19,000 at day care centers.
The federal government sector stood out as a rare example of net job gains last month, thanks to the addition of 17,000 temporary workers for the 2020 census.

The unemployment rate shot up to 4.4% from a half-century low of 3.5%, the largest one-month increase in the jobless rate since 1975.
By race or ethnicity, the largest increases were seen among Asians and Latinos, with increases of 1.6 percentage points each, nearly twice the overall increase of 0.9 percentage point. Both whites and African Americans saw their rates rise at the same pace as the national rate, although the unemployment rate now for blacks – at 6.7% – is 65% higher than for whites at 4%.
The youngest workers were also the most likely to lose work in the early stages of the shutdown.
The unemployment rate for teenagers rose by 3.3 percentage points to 14.3% and for those between 20 and 24 years old by 2.3 points – the most since 1953 – to 8.7%.
By contrast, unemployment for those in the 25-to-34-year-old age bracket rose by just 0.4 percentage point to 4.1%. The jobless rate for workers aged 45 to 54 rose 0.7 percentage point to 3.2%, the lowest rate for any age group.

Workers with lower levels of education also found themselves thrown out of work at a higher rate in March.
The rate for workers without a high school diploma jumped by 1.1 percentage points to 6.8%, the highest in nearly three years.
For people with a college degree, meanwhile, the jobless rate rose by 0.6 percentage point to 2.5%. Still, it was the largest monthly increase in the rate for that demographic since the Labor Department began tracking it in the early 1990s.

And finally, there was a notable gender gap in the unemployment rate increase last month. The jobless rate for men rose by 0.7 percentage point, while the rate for women rose 0.9 percentage point, perhaps explained by their greater representation in the hardest-hit employment sectors such as hospitality and health care.
The overall rate for both sexes over the age of 20 now stands at 4%.
https://www.reuters.com/article/us-health-coronavirus-usa-jobs/how-the-coronavirus-job-cuts-played-out-by-sector-and-demographics-idUSKBN21M0EL

LI doctor tries new hydroxychloroquine twist for elderly COVID-19 patients

A New York doctor hopes to help his elderly COVID-19 patients with a treatment plan inspired by the success tentatively being reported with hydroxychloroquine — and which he says shows promising results.
Dr. Mohammud Alam, an infectious disease specialist affiliated with Plainview Hospital, said 81 percent of infected covid patients he treated at three Long Island nursing homes recovered from the contagion.
“In this crisis, I realized I had to do something,” Alam said. ”I realized if this was my dad, what would I do? And I would do anything I could to help.”
Alam said he decided he could not apply the touted combination of the antimalarial hydroxychloroquine and antibiotic azithromycin because the side effects could be potentially fatal for his high-risk patients, many of whom had underlying heart issues.
“I knew I could not jeopardize these patients,” Alam said.
“We know from the FDA that azithromycin can cause fatal arrhythmia and abnormal heart failure that can lead to death,” Alam said.
His patients were under long-term acute care and had comorbidities such as hypertension, coronary artery disease, chronic obstructive pulmonary disease or congestive heart failure.
The FDA has warnings that azithromycin “can cause abnormal changes in the electrical activity of the heart that may lead to a potentially fatal irregular heart rhythm.”
So instead, Alam replaced azithromycin with another decades-old antibiotic that doesn’t pose any known risks to the heart.
“Doxycycline is an anti-inflammatory with properties similar to azithromycin but without the safety concerns and without cardiac toxicity,” he said.
“So I decided why not choose that?” added Alam, a board-certified internist, who shared the results of an observational report consisting of 47 patients he treated.
”With the [limited]resources we have at the nursing home, we took a deep breath and realized we need to do something,” Alam said.
Alam is not the only one to begin using doxycycline in the fight against COVID-19.
Henry Ford Health System has started using combinations of the three drugs because of apparently fewer side effects, published reports state.
Alam began treating his patients, 45 of whom had tested positive for the coronavirus after they developed a high fever, shortness of breath and cough.
He received permission from their families before starting them on the medications, which have not yet undergone randomized controlled trials.
“The majority had clinical improvement,” said Alam. “We had very good outcomes.”
Alam said that 38 of 47 patients treated returned to their baseline and their symptoms resolved. Seven of the patients were transferred to a hospital and two died.
There was no control group in the study so Alam acknowledged more studies are needed to evaluate his protocol’s effectiveness.
Alam noted that an 87-year-old woman with hypertension and coronary issues beat the virus. “Her daughter was so thankful that I didn’t need to transfer her to a hospital.”
“At the end of the day we feel like we sent fewer patients to the hospitals, we saved ICU beds and we saved some of the ventilators at the hospital,“ Alam said.
One health expert said using the decades-old doxycycline, which has been studied since the 1960s, is a plausible alternative to azithromycin.
“Since we’re talking about the elderly being the most vulnerable, or people with underlying conditions, there is a theoretical benefit of doxycycline over azithromycin because doxycycline is not associated with cardiovascular disease,” said Dr. Sten H. Vermund, the dean of the Yale School of Public Health.
Vermund also cautioned a clinical trial is necessary and also noted that two patients did pass away.
“I am optimistic about this combination, but a well-designed clinical study is urgently needed to identify the appropriate patient population, optimize dosing regimen and assess the side effect profile of this combination therapy,” added Dr. Ryan Saadi, a Yale-trained infectious disease epidemiologist who is currently developing a ventilator technology at Quantaira Health.
Vermund also added that other treatment alternatives that could be just as good and less toxic should also be considered.
https://nypost.com/2020/04/04/long-island-doctor-tries-new-hydroxychloroquine-for-covid-19-patients/

GM seeks tariff relief for ventilator parts

General Motors (NYSE:GM) has asked the Trump administration to drop import tariffs on Chinese parts it needs to make ventilators, WSJ reports, citing a letter to the U.S. Trade Representative.

The company believes the levies will make it more expensive to build the machines, according to the report.

The existing tariffs on ventilator parts “could potentially impede the ability of GM and other U.S. manufacturers to source parts for critical care ventilators quickly, reliably, and at as reasonable a cost as possible,” GM says in the letter.

The U.S. government began collecting extra tariffs on most of ventilator parts in September 2018; they are being tariffed at a 25% rate.

https://seekingalpha.com/news/3558404-gm-seeks-tariff-relief-for-ventilator-parts-wsj

Amazon advances pandemic response

Amazon (NASDAQ:AMZN) has been talking to the CEOs of Abbott Laboratories (NYSE:ABT) and Thermo Fisher Scientific (NYSE:TMO) as it investigates how to screen its warehouse staff for COIVD-19, according to internal notes seen by Reuters.

Abbott Laboratories and Thermo Fisher Scientific Inc have indicated an interest in working with Amazon, but the U.S. government is taking up all of their testing capacity at the present time.

Amazon is introducing face masks and temperature checks for workers at all its U.S. and European warehouses next week.

https://seekingalpha.com/news/3558428-amazon-advances-pandemic-response

COVID-19 Infection and Renin Angiotensin System Blockers

The coronavirus disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has already surpassed the combined mortality inflicted by the severe acute respiratory syndrome (SARS) epidemic of 2002 and 2003 and the Middle East respiratory syndrome (MERS) epidemic of 2013. The pandemic is spreading at an exponential rate, with millions of people across the globe at risk of contracting SARS-CoV-2. Initial reports suggest that hypertension, diabetes, and cardiovascular diseases were the most frequent comorbidities in affected patients, and case fatality rates tended to be high in these individuals. In the largest Chinese study to date,¹ which included 44 672 confirmed cases, preexisting comorbidities that had high mortality rates included cardiovascular disease (10.5%), diabetes (7.3%), and hypertension (6.0%). Patients with such comorbidities are commonly treated with renin angiotensin system blockers, such as angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs). However, the use of ACEIs/ARBs in patients with COVID-19 or at risk of COVID-19 infection is currently a subject of intense debate. Below, we outline the mechanisms by which ACEIs/ARBs may be of benefit in those with COVID-19, what the current recommendations are for their use in infected patients, and suggested areas for further research.

SARS-CoV-2 uses the angiotensin-converting enzyme (ACE) 2 receptor for entry into target cells. ACE2 is predominantly expressed by epithelial cells of the lung, intestine, kidney, heart, and blood vessels. Both ACE and ACE2 belong to the ACE family of dipeptidyl carboxydipeptidases and exert distinct physiological functions. ACE cleaves angiotensin I to angiotensin II, which in turn binds and activates angiotensin II receptor type 1. This activation leads to vasoconstrictive, proinflammatory, and pro-oxidative effects. In contrast, ACE2 also degrades angiotensin II to angiotensin 1-7 and angiotensin I to angiotensin 1-9. When angiotensin 1-9 binds to the Mas receptor, it leads to anti-inflammatory, antioxidative, and vasodilatory effects. It is important to note that 2 forms of ACE2 exists: a structural transmembrane protein with extracellular domain that serves as a receptor for spike protein of SARS-CoV-2 and a soluble form that represents the circulating ACE2. Understanding the relationship between SARS-CoV-2 and membranous and soluble ACE2 may help us better understand the adaptive or maladaptive processes operative in COVID-19 infection.

Animal (mice) studies have shown that expression of ACE2 is substantially increased in patients treated with ACEIs/ARBs.^2,3 Similar to these observations, higher urinary ACE2 levels were seen in patients with hypertension treated with the ARB olmesartan. In another study,⁴ circulating ACE2 levels were increased in patients with diabetes treated with ACEIs. Based on these observations, some experts have speculated that use of ACEIs/ARBs leading to increased expression of ACE2 could potentially facilitate infection with COVID-19.

A recent study by Liu et al⁵ showed that serum angiotensin II levels in patients with COVID-19 pneumonia was significantly higher compared with healthy individuals and were linearly associated with viral load and lung injury. Based on this, it can be postulated that SARS-CoV-2 binding to ACE2 may attenuate residual ACE2 activity, skewing the ACE/ACE2 balance to a state of heightened angiotensin II activity leading to pulmonary vasoconstriction and inflammatory and oxidative organ damage, which increases the risk for acute lung injury (ALI). Conceivably, renin angiotensin system modulation, either by ACEIs/ARBs or recombinant ACE2, leading to increased expression of ACE2 may help mitigate some of these deleterious effects of angiotensin II. It is also postulated that increased levels of soluble form of ACE2 may act as a competitive interceptor of SARS-CoV-2 and slow virus entry into the cells and protect from lung injury.⁶ Presently, to our knowledge, there are no clinical data on the utility of initiating ACEI/ARB therapy in treating patients with COVID-19. There is some evidence that ACEIs/ARBs may be beneficial in patients with ALI or acute respiratory distress syndrome (ARDS). In a meta-analysis of 37 studies,⁷ ACEIs and ARBs were associated with reduced risk of pneumonia and pneumonia-related mortality compared with control treatment. In a small double-blind, placebo-controlled randomized clinical trial of 61 patients,⁸ those randomized to receive enalaprilat (up to 10 mg intravenously over 24 hours following a regimen based on blood pressure) had numerically higher ventilator-free days (12.3 vs 8.7 days; P = .18) and days alive outside the intensive care unit (8.9 vs 4.9 days; P = .09) compared with those randomized to placebo. The trial did not complete its intended sample size owing to slow enrollment. In a retrospective cohort study from Korea with 132 patients with ARDS,⁹ patients taking ACEIs/ARBs showed better survival compared with controls, albeit several confounding factors could have influenced the results. In a subgroup of patients with severe COVID-19, hyperinflammation and cytokine storm syndrome led to acute respiratory failure from ARDS. What drives such intense hyperinflammation is not yet known; however, through upregulation of ACE2, ACEIs/ARBs can exert anti-inflammatory and antioxidative effects, which may be beneficial in preventing ALI and ARDS.¹⁰ Based on the pathophysiology of SARS-CoV-2 infection and pleiotropic effects of ACEIs/ARBs, these agents may have a potential role in the management of select patients with severe COVID-19.

Several professional societies have put forward their guidance regarding the use of ACEIs/ARBs in patients with COVID-19. In summary, all guidelines recommend continuing ACEIs/ARBs in patients with COVID-19 unless clinically indicated (Table). Furthermore, they do not suggest initiation of ACEIs/ARBs in those without another clinical indication (eg, hypertension, heart failure, diabetes), given the lack of strong evidence showing benefit of these medications in COVID-19. We agree with these recommendations, given the current state of evidence. However, the biological plausibility of salutary effects of ACEIs/ARBs in those with COVID-19 is intriguing. A multicenter, double-blind, placebo-controlled phase 2 randomized clinical trial of starting losartan in patients with COVID-19 in outpatient settings (ClinicalTrials.gov identifier: NCT04311177) and in in-patient settings (ClinicalTrials.gov identifier: NCT04312009) is currently being planned. Accordingly, further epidemiological studies and prospective trials are urgently needed to investigate if use of ACEIs/ARBs can reduce the incidence or mortality associated with COVID-19–associated ALI or ARDS, both in patients with and without additional clinical indications for ACEIs/ARBs.

Table.  Recommendations on the Use of Angiotensin-Converting Enzyme Inhibitors (ACEIs) and Angiotensin Receptor Blockers (ARBs) in Patients With Coronavirus Disease 2019 (COVID-19)

Article Information

Corresponding Author: Franz H. Messerli, MD, Department of Cardiology, Bern University Hospital, University of Bern, Freiburgstrasse 18, 3010 Bern, Switzerland (messerli.f@gmail.com).

Published Online: April 3, 2020. doi:10.1001/jamacardio.2020.1282

Conflict of Interest Disclosures: Dr Maddox has received grants from the National Center for Advancing Translational Sciences, consulting fees from Creative Educational Concepts and Atheneum Partners, and honoraria and personal fees from the University of Utah, NewYork-Presbyterian, Westchester Medical Center, Sentara Heart Hospital, Henry Ford Health System, and University of California, San Diego; is the Executive Director of the Healthcare Innovation Lab at BJC HealthCare/Washington University School of Medicine in St Louis; advises Myia Labs through his institution, which receives equity compensation; and is the director of JF Maddox Foundation. Dr Messerli has received personal fees from Menarini, Medtronic, and Pfizer. No other disclosures were reported.

https://jamanetwork.com/journals/jamacardiology/fullarticle/2764299

How important is speech in transmitting coronavirus?

Normal speech by individuals who are asymptomatic but infected with coronavirus may produce enough aerosolized particles to transmit the infection, according to aerosol scientists at the University of California, Davis. Although it’s not yet known how important this is to the spread of COVID-19, it underscores the need for strict social distancing measures — and for virologists, epidemiologists and engineers who study aerosols and droplets to work together on this and other respiratory diseases.
Aerosols are particles small enough to travel through the air. Ordinary speech creates significant quantities of aerosols from respiratory particles, said William Ristenpart, professor of chemical engineering at UC Davis. Ristenpart is co-author on an editorial about the problem to be published in the journal Aerosol Science and Technology.
These respiratory particles are about one micron, or one micrometer, in diameter. That’s too small to see with the naked eye, but large enough to carry viruses such as influenza or SARS-CoV-2.
Some individuals superemitters
Last year, Ristenpart, graduate student Sima Asadi and colleagues published a paper showing that the louder one speaks, the more particles are emitted and that some individuals are “superemitters” who give off up to 10 times as many particles as others. The reasons for this are not yet clear. In a follow-up study published in January in PLOS One, they investigated which speech sounds are associated with the most particles.
Calculating just how easily a virus like SARS-CoV-2 spreads through droplets requires expertise from different fields. From virology, researchers need to know how many viruses are in lung fluids, how easily they form into droplets and how many viruses are needed to start an infection. Aerosol scientists can study how far droplets travel once expelled, how they are affected by air motion in a room and how fast they settle out due to gravity.
“The aerosol science community needs to step up and tackle the current challenge presented by COVID-19, and also help better prepare us for inevitable future pandemics,” Ristenpart and colleagues conclude.

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Other authors on the editorial are Asadi; Professor Anthony Wexler, UC Davis Department of Mechanical and Aerospace Engineering; and Nicole Bouvier, Icahn School of Medicine at Mount Sinai.
https://www.eurekalert.org/pub_releases/2020-04/uoc–hii040220.php

Possible coronavirus drug identified by Australian scientists

• Australian Scientists have shown that an anti-parasitic drug already available around the world can kill the virus within 48 hours.
• Scientists from Monash University in Melbourne showed that a single dose of the drug, Ivermectin, could stop the SARS-CoV-2 virus growing in cell culture – effectively eradicating all genetic material of the virus within 48 hours.
• The next steps are to determine the correct human dosage – ensuring the doses shown to effectively treat the virus in the test tube are safe levels for humans.
• The use of Ivermectin to combat COVID-19 depends on pre-clinical testing and clinical trials, with funding urgently required to progress the work.
• Ivermectin is an FDA-approved anti-parasitic drug that has also been shown to be effective in vitro against a broad range of viruses including HIV, Dengue, Influenza and Zika virus.
• The findings of the study were published today in Antiviral Research.

A collaborative study led by Monash University’s Biomedicine Discovery Institute (BDI) in Melbourne, Australia, with the Peter Doherty Institute of Infection and Immunity (Doherty Institute), has shown that an anti-parasitic drug already available around the world kills the virus within 48 hours.
The Monash Biomedicine Discovery Institute’s Dr Kylie Wagstaff, who led the study, said the scientists showed that the drug, Ivermectin, stopped the SARS-CoV-2 virus growing in cell culture within 48 hours.
“We found that even a single dose could essentially remove all viral RNA by 48 hours and that even at 24 hours there was a really significant reduction in it,” Dr Wagstaff said.
Ivermectin is an FDA-approved anti-parasitic drug that has also been shown to be effective in vitro against a broad range of viruses including HIV, Dengue, Influenza and Zika virus.
Dr Wagstaff cautioned that the tests conducted in the study were in vitro and that trials needed to be carried out in people.
“Ivermectin is very widely used and seen as a safe drug. We need to figure out now whether the dosage you can use it at in humans will be effective – that’s the next step,” Dr Wagstaff said.
“In times when we’re having a global pandemic and there isn’t an approved treatment, if we had a compound that was already available around the world then that might help people sooner. Realistically it’s going to be a while before a vaccine is broadly available.
Although the mechanism by which Ivermectin works on the virus is not known, it is likely, based on its action in other viruses, that it works to stop the virus ‘dampening down’ the host cells’ ability to clear it, Dr Wagstaff said.
Royal Melbourne Hospital’s Dr Leon Caly, a Senior Medical Scientist at the Victorian Infectious Diseases Reference Laboratory (VIDRL) at the Doherty Institute where the experiments with live coronavirus were conducted, is the study’s first author.
“As the virologist who was part of the team who were first to isolate and share SARS-COV2 outside of China in January 2020, I am excited about the prospect of Ivermectin being used as a potential drug against COVID-19,” Dr Caly said.
Dr Wagstaff made a previous breakthrough finding on Ivermectin in 2012 when she identified the drug and its antiviral activity with Monash Biomedicine Discovery Institute’s Professor David Jans, also an author on this paper. Professor Jans and his team have been researching Ivermectin for more than 10 years with different viruses.
Dr Wagstaff and Professor Jans started investigating whether it worked on the SARS-CoV-2 virus as soon as the pandemic was known to have started.
The use of Ivermectin to combat COVID-19 would depend on the results of further pre-clinical testing and ultimately clinical trials, with funding urgently required to keep progressing the work, Dr Wagstaff said.

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Read the full paper in Antiviral Research titled: The FDA-approved Drug Ivermectin inhibits the replication of SARS-CoV-2 in vitro: https://www.sciencedirect.com/science/article/pii/S0166354220302011
https://www.eurekalert.org/pub_releases/2020-04/mu-pcd040320.php