Coronavirus Update

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Coronavirus Update 7-3

Recent Developments & Information 

July 3, 2020

Reliable information is the best tool available to protect your family from the pandemic and its shockwaves

“I am not satisfied with what’s going on because we are going in the wrong direction if you look at the curves of the new cases, so we’ve really got to do something about that and we need to do it quickly.  If the U.S. does not get its act together, the country could see up to 100,000 new cases a day.”  

Dr. Fauci

Index

A. The Pandemic As Seen Through Headlines

B. Numbers & Trends

C. US Hotspots

1. Top 5 States in Deaths & Cases (7/2)

2. There are Many Reasons California’s C19 cases are soaring  

3. Are U.S. States Flattening the Curve?  

4. Do you live in a C19 hotspot? Map Created by Harvard will tell you  

D. Potential Treatments

1. Treatment with Hydroxychloroquine Cut Death Rate Significantly in C19 Patients, Henry Ford Health System Study Show   (!) 

2. An Old Vaccine May Help Against Coronavirus  [Recommended] 

E. New Scientific Findings & Research

1. Blood test at C19 diagnosis can predict disease severity  

2. C19 Causes ‘Hyperactivity’ in Blood-Clotting Cells  

F. Concerns & Unknowns

1. Fever checks are a flawed way to flag C19 cases, but smell tests might help  

2. Why are some people at greater risk of severe C19? 

3. Latinx people more vulnerable to C19 infection 

4. Most People With Coronavirus Won’t Spread It. Why Do a Few Infect Many? 

5. This coronavirus mutation has taken over the world. Scientists are trying to understand why.  

G. Herd Immunity

1. Herd Immunity Is Much Closer Than Antibody Tests Suggest  

2. The Tricky Math of Herd Immunity for C19  

H. Vaccines

1. Another experimental C19 vaccine shows promising early results 

2. FDA spells out guidelines for approving C19 vaccines  

I. Back to School!? 

1. Is it safe to send kids back to school?  

J. Projections & Our (Possible) Future

1. Increased restaurant spending Foreshadows Increase in new C19 cases 

K. Practical Tips & Other Useful Information

1. How to Clean an N95 mask? Use a microwave!  

L. Johns Hopkins Report: C19 At Six Months

A. The Pandemic As Seen Through Headlines

(In no particular order)

B. Numbers & Trends

Note: Unless otherwise noted, (i) all cases/deaths are confirmed cases/deaths that have been reported, (ii) all numbers reported in this update are as of the end of the most recent reporting period, and (iii) all changes reflect changes since the preceding day.  Green highlights indicate a decrease or no change and yellow highlights indicate an increase. 

Sources: https://www.worldometers.info/coronavirus/ and https://covidtracking.com/

1. Cases & Tests

Worldwide Cases:  
  • Total Cases = 10,974,421 (+1.9%)
  • New Cases = 208,864 (+11,442)
  • Growth Rate of New Cases (7 day average) = 4.9%
  • New Cases (7 day average) = 183,231 (+8,205)
Observations:
  • Record number of new cases on 7/1 
  • New cases have increased for 3 consecutive days (3 day average of cases has increased 13.1% since 6/29)
  • 7 day average growth rate in new cases is very high
  • 7 day average of new cases on 7/1 is at a record high
US Cases & Testing: 
  • Total Cases = 2,837,189 (+2.1%)
  • New Cases = 57,236 (+6,139)
  • Percentage of New Global Cases = 27.4% 
  • Growth Rate of New Cases (7 day average) = 5.4% 
  • New Cases (7 day average) = 47,243 (+2,429)
  • Total Number of Tests = 35,538,123 
  • Percentage of positive tests (7 day average) = 7.1% 
Observations:
  • Record number of new cases on 7/1 (second consecutive day record)
  • 7 day average of new cases, which has been rapidly rising since 6/9, set a new record high on 7/1 (7th consecutive daily record)
  • 7 day average growth rate in new cases is very high
  • 7 day average positive test percentage continues to increase

2. Deaths

Worldwide Deaths: 
  • Total Deaths = 523,242 (+0.7%) 
  • New Deaths = 5,184 (+337)
  • Growth Rate of New Deaths (7 day average) = -2.1% 
  • New Deaths (7 day average) = 4,485 (-95)
Observations:
  • 7 day average of new deaths as declined 2.1% over the last week (stable)
  • 3 day average of new deaths has increased by 31.3% since 6/29 (significant increase)
US Deaths: 
  • Total Deaths = 131,485 (+0.5%)
  • New Deaths = 687 (+11) 
  • Percentage of Global New Deaths = 13.2% 
  • Growth Rate of New Deaths (7 day average) = 0.9% 
  • New Deaths (7 day average) = 565 (+5)
Observations:
  • 7 day average of new deaths has generally been declining
  • 7 day average of new deaths continue to generally decline as 7 day average of new cases continue to rapidly rise

C. US Hotspots

1. Top 5 States in Deaths & Cases (7/2)

New Deaths
  1. California  98 
  2. Florida 64
  3. Massachusetts 51
  4. Texas 44
  5. Arizona 37
New Cases
  1. Florida  10,109
  2. California 9,312
  3. Texas 7,535
  4. Georgia 3,472
  5. Arizona 3,333
Most Deaths Per 1 Million Population 
  1. New Jersey 1,713
  2. New York 1,653
  3. Connecticut 1,213
  4. Massachusetts 1,180
  5. Rhode Island   893
Deaths Per 1 Million Population (Most Populated States)
  1. California   158
  2. Texas     89
  3. Florida   168
  4. New York  1,653
  5. Illinois   567

2. There are Many Reasons for California’s C19 cases soaring  

  • It’s troubling, though not surprising, to see C19 cases spiking across the American South and Southwest, where public officials delayed lockdowns, rushed to reopen businesses, or refused to require people to wear masks.
  • But what’s the matter with California? The nation’s most populous state was the first to enact statewide shelter-in-place rules, took decisive steps to build up the recommended testing and case tracing capacity, and has hammered the public health message on social distancing and masks.
  • Yet new cases are rising sharply in pockets throughout the sprawling state, even as they’re flat or falling across much of the East Coast. Positive tests over the last seven-day period have risen 45%, regularly topping 5,000 a day, Governor Gavin Newsom said during a press conference on Monday. Hospitalizations and intensive care unit admissions are both up around 40% over the past few weeks as well, threatening to overwhelm health-care systems.
  • In turn, Newsom has pressed Imperial County—the southernmost part of the state, where skyrocketing case loads have forced officials to move hundreds of patients to hospitals in neighboring areas—to fully reinstate stay-at-home orders. He’s also recommended or required that more than a dozen counties shut down their bars or keep them closed, including Los Angeles and Santa Clara, the home of Silicon Valley. Meanwhile, San Francisco’s mayor halted the city’s reopening plan on Friday.
  • So what’s driving the outbreaks in a state that supposedly did things right? Why weren’t its ambitious testing and contact tracing programs adequate to prevent the recent surge in cases?
  • “It’s not one thing, but four or five,” says George Rutherford, an epidemiologist at University of California, San Francisco, who is leading the university’s training program for the state’s contact tracing task force. “The state is so big—the population of California is larger than Canada—and there’s a lot of different things going on in different places.”
  • Health officials believe the state’s efforts to boost testing and rapidly track down infections is helping. California’s number of cases per capita—567 per 100,000—is well below the rates for states like Alabama, Arizona, or Florida. And Rutherford says about 85% of the people known to have interacted with positive patients are returning calls or answering questions from the state’s contact tracers, who are tasked with tracking down possible infections and encouraging people to quarantine or isolate themselves.
  • But clearly not enough people are strictly following these recommendations, and others, from public health officials—sometimes due to carelessness, and sometimes because of financial strains and other constraints.
  • Here are some of the main drivers at work:
Ethnic disparities
  • Throughout the state, Latinos make up by far the largest share of cases (56%) and deaths (42%), according to data from the California Department of Public Health. While Latinos make up 39% of the population, whites are a close second at 37% but represent only 17% of C19 cases.
  • These infections appear to be concentrated within low-income communities, where people are often essential workers who can’t do their jobs from home, can’t afford to call in sick and may live in crowded housing conditions, according to information from contact tracing programs as well as other research and reporting. Language, immigration status and financial issues can complicate efforts to successfully reach infected patients or their close contacts in these communities, and convince them to isolate themselves for extended periods.
  • Early results from a C19 screening project in San Francisco’s heavily Hispanic Mission neighborhood found that 95% of those who tested positive were “Hispanic or Latinx” (the difference is explained here). And 90% of infected patients said they couldn’t work from home.
People are becoming cavalier
  • Another major factor is that people are ignoring safety practices, according to a state breakdown of counties experiencing rising cases. As regions relax stay-at-home rules, families, friends, and strangers are increasingly gathering in homes, bars, restaurants, and other venues. Too often, they’re not wearing masks or staying far enough away from each other, said Mark Ghaly, secretary of California’s Health and Human Services Agency, during the Monday press conference.
  • Los Angeles County has become the nation’s largest epicenter of the disease, with nearly 98,000 confirmed cases, according to Johns Hopkins University’s coronavirus tracking map.
  • The Los Angeles County Department of Public Health announced on Sunday that it would heed Newsom’s directive to shut down bars, noting that the region’s sharp increase in cases and hospitalizations directly coincides with the reopening of businesses a few weeks earlier. Those include breweries, pubs, wineries, and other venues “where people remove their face covering to drink while they may be socializing with people not in their households,” the statement read.
  • “I implore that our residents and businesses follow the public health directives that will keep us healthy, safe, and on the pathway to recovery,” said Barbara Ferrer, the county’s director of public health. “Otherwise, we are quickly moving toward overwhelming our health-care system and seeing even more devastating illness and death.”
Explosions in prison cases
  • More than 2,500 state and federal prison inmates throughout California are infected with the coronavirus. More than 1,000 prisoners and staff members tested positive in San Quentin State Prison alone during the last few weeks, in an outbreak linked to the transfer of inmates from the California Institution for Men in Chino, where there are more than 500 active cases.
  • The spillover of patients into local hospitals has forced Marin County, where San Quentin is based, to pause its plans to reopen gyms, hotels, and other businesses.
An influx of cases from elsewhere
  • A variety of other factors are driving higher case counts, including increasingly widespread testing across the state (which totaled nearly 106,000 on Sunday), continuing outbreaks in nursing homes in several counties, and patients from outside California crowding into counties with better testing and treatment.
  • Part of what’s driving the soaring case loads in Imperial County is the influx of positive patients from Mexico. State officials say they’re primarily US citizens, hundreds of thousands of whom live in neighboring Baja, crossing back in search of superior health care.
  • The county has by far the state’s highest case numbers on a per capita basis, 3,414 per 100,000, as well as a positivity rate for tests that’s more than four times the state average.
  • The different drivers demand different interventions, health experts say. Officials need to make extra efforts to communicate with low-income Latino patients and provide money, food, housing, or other services to help them isolate while they’re infectious. (San Francisco has some programs like this in place, but clearly more are needed throughout the state.) Prison systems need to keep infected inmates isolated, and ensure that they’re no longer spreading the disease across facilities. And nursing homes should test patients and workers more often, and step in more rapidly at the earliest signs of an outbreak.
  • But pretty much all of this has been known from the start. Californians need to recognize that the dangers haven’t passed, even as regions relax certain rules. Everyone still has to maintain their distance from others, vigorously wash their hands, and wear masks. 

Source: Why California covid-19 cases are soaring, despite its aggressive efforts to combat the pandemic

3. Are U.S. States Flattening the Curve?  

  • The U.S. has counted more than 2.6 million C19 infections. The cumulative growth of cases published on Worldometers shows that the curve of total U.S. cases has been growing not exponentially, but quite gradually. While several states have for now made good progress on flattening the curve of infection, others have seen cases surge again.
  • While New York, New Jersey and Illinois – among the hardest-hit in the nation – stabilized their outbreaks, cases are again growing fast in California, Texas, Florida, Georgia and Arizona. Flattening curves could also be observed in other states in the Northeast and Midwest, including Massachusetts, Pennsylvania and Michigan (also among top 10 of states with the most cases in the U.S.), while more spikes in cases were registered in the South and the West, for example in North Carolina, Louisiana, New Mexico and Oregon.

Source: Chart: Are US States Flattening the Curve? 

4. Do you live in a C19 hotspot? Map Created by Harvard will tell you  

  • How likely are you to contract C19? That’s a complicated question with a lot of variables. Trying to get insight into your personal risk involves parsing state and county data on rates of infection, hospitalizations, and deaths.
  • But now there’s a tool that can help you cut through all the noise. Researchers at the Harvard Global Health Institute, in collaboration with a team of scientists, have launched a new interactive map and dashboard that allows you to quickly identify your risk level by state and county. It uses a four-color system, where green represents the lowest level of risk and red represents the highest. Check out the map here:  https://globalepidemics.org/key-metrics-for-covid-suppression/ 
  • According to Tom Tsai, a professor at the Harvard School of Public Health who helped create the dashboard, this tool was designed both for the general public and for policymakers. “The most effective public health policy occurs when the public and the policymakers are on the same page,” he says. In addition to the four color zones, it offers specific policy interventions for each zone. In the red, stay-at-home orders are necessary; in the green, testing and contact tracing are recommended.
  • The dashboard is the work of more than a dozen researchers from eight organizations, including Harvard’s Edmond J. Sacra Center for Ethics, CovidActNow, and the Rockefeller Foundation. Tsai says it was important to have a breadth of experiences represented, but also to have a clear, unified approach. “Science by definition is messy,” Tsai says. “There can be a diversity of opinion even among scientists. But what we could agree on is that we need a common language to help guide policymakers.”
  • While other organizations have developed maps and dashboards to help understand the spread of the virus, what’s notable about this one is that it uses a single metric, which is the number of daily new cases per 100,000 people. This standardizes the numbers and makes it easier to understand the specific risk level in your area. Tsai and his colleagues believe this is more helpful than hearing about the absolute number of new cases in a state or a county. “A thousand new cases in New York is very different from a thousand new cases in Idaho,” says Tsai. “We wanted to create a common metric across the population.”

Source: Do you live in a COVID-19 hotspot? Harvard created a simple map that will tell you 

D. Potential Treatments

1. Treatment with Hydroxychloroquine Cut Death Rate Significantly in C19 Patients, Henry Ford Health System Study Shows  

  • Treatment with hydroxychloroquine cut the death rate significantly in sick patients hospitalized with C19 – and without heart-related side-effects, according to a new study published by Henry Ford Health System.
  • In a large-scale retrospective analysis of 2,541 patients hospitalized between March 10 and May 2, 2020 across the system’s six hospitals, the study found 13% of those treated with hydroxychloroquine alone died compared to 26.4% not treated with hydroxychloroquine. 
  • None of the patients had documented serious heart abnormalities; however, patients were monitored for a heart condition routinely pointed to as a reason to avoid the drug as a treatment for C19.
  • The study was published today in the International Journal of Infectious Diseases, the peer-reviewed, open-access online publication of the International Society of Infectious Diseases (ISID.org).
  • Patients treated with hydroxychloroquine at Henry Ford met specific protocol criteria as outlined by the hospital system’s Division of Infectious Diseases. The vast majority received the drug soon after admission; 82% within 24 hours and 91% within 48 hours of admission. All patients in the study were 18 or over with a median age of 64 years; 51% were men and 56% African American.
  • “The findings have been highly analyzed and peer-reviewed,” said Dr. Marcus Zervos, division head of Infectious Disease for Henry Ford Health System, who co-authored the study with Henry Ford epidemiologist Dr. Samia Arshad. 
  • “We attribute our findings that differ from other studies to early treatment, and part of a combination of interventions that were done in supportive care of patients, including careful cardiac monitoring. Our dosing also differed from other studies not showing a benefit of the drug. And other studies are either not peer reviewed, have limited numbers of patients, different patient populations or other differences from our patients.”
  • Zervos said the potential for a surge in the fall or sooner, and infections continuing worldwide, show an urgency to identifying inexpensive and effective therapies and preventions.
  • “We’re glad to add to the scientific knowledge base on the role and how best to use therapies as we work around the world to provide insight,” he said. “Considered in the context of current studies on the use of hydroxychloroquine for C19, our results suggest that the drug may have an important role to play in reducing C19 mortality.”
  • The study also found those treated with azithromycin alone or a combination of hydroxychloroquine and azithromycin also fared slightly better than those not treated with the drugs, according to the Henry Ford data. The analysis found 22.4% of those treated only with azithromycin died, and 20.1% treated with a combination of azithromycin and hydroxychloroquine died, compared to 26.4% of patients dying who were not treated with either medication.
  • “Our analysis shows that using hydroxychloroquine helped saves lives,” said neurosurgeon Dr. Steven Kalkanis, CEO, Henry Ford Medical Group and Senior Vice President and Chief Academic Officer of Henry Ford Health System. “As doctors and scientists, we look to the data for insight. And the data here is clear that there was benefit to using the drug as a treatment for sick, hospitalized patients.”
  • Overall, hospital system patients in the study experienced an 18.1% in-hospital mortality rate. Regardless of treatment, mortality was highest in:
    • Patients older than 65,
    • Patients who identified as Caucasian,
    • Patients admitted with reduced oxygen levels, and
    • Patients who required ICU admission.
  • Patients who died commonly had serious underlying diseases, including chronic kidney and lung disease, with 88% dying from respiratory failure. 
  • According to CDC, hydroxychloroquine (also known as hydroxychloroquine sulfate) is a FDA-approved arthritis medicine that also can be used to prevent or treat malaria. It is available in the United States by prescription only. The drug is sold under the brand name Plaquenil and it is also sold as a generic medicine. It is commonly used by patients with arthritis, lupus or other rheumatic conditions.
  • Dr. Zervos also pointed out, as does the paper, that the study results should be interpreted with some caution, should not be applied to patients treated outside of hospital settings and require further confirmation in prospective, randomized controlled trials that rigorously evaluate the safety and efficacy of hydroxychloroquine therapy for C19.
  • “Currently, the drug should be used only in hospitalized patients with appropriate monitoring, and as part of study protocols, in accordance with all relevant federal regulations,” Dr. Zervos said.
  • Henry Ford Health System, as one of the region’s major academic medical centers with more than $100 million in annual research funding, is involved in numerous C19 trials with national and international partners.
  • Henry Ford Health System is currently also involved in a prophylactic hydroxychloroquine study: “Will Hydroxychloroquine Impede or Prevent COVID-19,” or WHIP COVID-19. 
  • The study is a 3,000-person, randomized, double-blinded look at whether hydroxychloroquine prevents healthcare and frontline workers from contracting the C19 virus. The WHIP C19 team is working on expanding study sites while there is a lull in the number of C19 cases in Southeast Michigan. This is in preparation for a potential increase of C19 cases as Fall flu season approaches, with additional sites available for convenient enrollment of healthcare workers and first responders. The WHIP C19 team is also taking this gift of time to reach out to other areas of the world that are seeing a blossoming of cases: Brazil and Argentina. There are currently 619 people enrolled in the study, out of a target of 3,000.

Source:  Treatment with Hydroxychloroquine Cut Death Rate Significantly in COVID-19 Patients

2. An Old Vaccine May Help Against Coronavirus 

Opinion by Robert C. Gallo and Daniel J. Arbess

  • Whether there will be a Covid-specific vaccine is still unclear. The sequence of the C19 viral genome, published in January by Chinese scientists, can identify proteins to be targeted by a vaccine. But verifying its safety and measuring the duration of its effectiveness, if any, will take at least another year. And what if the virus develops and mutates, as it is already doing? Vaccines against the common flu have been less than 50% reliable against new mutations in recent years. An innate-immunity vaccine can provide nonspecific protection against a range of viruses and become effective in hours, not weeks.
  • The innate immune system is the body’s first line of defense. Recent studies using one of innate immunity’s main components, interferon, have shown positive results in dampening the coronavirus and controlling the body’s inflammatory response.
  • We suggest the Sabin Oral Polio Vaccine, or OPV, as an ideal way to stimulate native emergency immune response to Covid while work on a targeted vaccine continues. OPV has a 70-year track record in protecting against polio, and almost 50 years ago Russian virologists discovered that it is also protective against other viruses. It reduced influenza by 3.8-fold—better than specific influenza vaccines. Other vaccines, including one for measles, can do the same.
  • We propose OPV because of its availability, simplicity (a tablet), very low cost and decades long safety record. No toxicity has been observed in populations already vaccinated against polio. Even in an unvaccinated population, side effects are rare. Billions of people have received OPV, including nearly everyone in the U.S. between 1962 and 2000.
  • Past studies suggest that this protection from innate immunity could last for several months, and repeat vaccination might be done to extend innate immunity considerably longer. This approach should provide ample time for economies to normalize while the investigation of Covid-specific vaccine candidates continues over the next year or two. Stimulating the innate immune system with OPV looks like a free and safe option for saving lives while we wait for an effective C19 vaccine.

Source: Opinion | An Old Vaccine May Help Against Coronavirus 

E. New Scientific Findings & Research  

1. Blood test at C19 diagnosis can predict disease severity  

  • Doctors can examine C19 patients’ blood to identify those at greatest risk of severe illness and to pinpoint those most likely to need a ventilator, new research from the University of Virginia School of Medicine suggests.
  • The discovery could lead to new treatments to prevent deadly “cytokine storms” seen in severe cases of C19. It also may help explain why diabetes contributes to worse outcomes in patients with the coronavirus.
  • The UVA scientists found that the levels of a particular cytokine in the blood upon diagnosis could be used to predict later outcomes. Cytokines—proteins produced by immune cells—are responsible for severe overreactions by the immune system, known as cytokine storms, associated with C19 and other serious illnesses.
  • The researchers say the discovery could become part of a scoring system to let doctors flag at-risk C19 patients for closer monitoring and personalized interventions. 
  • The finding also identifies cytokines doctors could target as a new treatment approach.
  • “The immune response that we discovered to predict severe shortness of breath in C19 is known in other pulmonary diseases to cause damage. So this could lead to a novel way to prevent respiratory failure in individuals infected with the new coronavirus, by inhibiting this immune cytokine,” said Dr. Bill Petri of UVA’s Division of Infectious Diseases and International Health. “We plan to test this in a model of C19 prior to considering a clinical trial.”
  • Cytokine storms, in which the immune system spirals out of control, are typically associated with an established group of cytokines. But the best predictor of C19 outcomes was an “underappreciated” cytokine more associated with allergies, the UVA researchers report. High levels of that cytokine, IL-13, were associated with worsened C19 outcomes regardless of patients’ gender, age or other health problems.
  • The researchers also identified two more cytokines associated with severe outcomes, though the duo had less ability to predict the need for a ventilator.
  • In addition, the researchers found that levels of two other cytokines were significantly higher in patients with elevated blood sugar. This “pro-inflammatory response,” they say, may help explain why diabetes is associated with worse C19 outcomes. In short, the body is primed to respond too strongly to the infection.
  • “This work was led by Allie Donlan, Mary Young and Mayuresh Abhyankar in my lab,” Petri said, “but it was also a huge team effort by the School of Medicine with the support of iTHRIV and the Global Infectious Diseases Institute.”
  • To draw their conclusions, the researchers identified 57 C19 patients treated at UVA who ultimately required a ventilator. They then tested blood samples taken from the patients within 48 hours of diagnosis or hospital admission. They compared the results with those from patients who did not wind up needing a ventilator.
  • The researchers say additional research is necessary to determine how the cytokines are contributing to C19 outcomes, but they hope the discovery will help doctors improve care for a disease that has now killed more than 125,000 Americans.

Source: Blood test at COVID-19 diagnosis can predict disease severity, study finds 

2. C19 Causes ‘Hyperactivity’ in Blood-Clotting Cells  

  • Changes in blood platelets triggered by C19 could contribute to the onset of heart attacks, strokes, and other serious complications in some patients who have the disease, according to University of Utah Health scientists. The researchers found that inflammatory proteins produced during infection significantly alter the function of platelets, making them “hyperactive” and more prone to form dangerous and potentially deadly blood clots.
  • They say better understanding the underlying causes of these changes could possibly lead to treatments that prevent them from happening in C19 patients. Their report appears in Blood, an American Society of Hematology journal.
  • “Our finding adds an important piece to the jigsaw puzzle that we call C19,” says Robert A. Campbell, Ph.D., senior author of the study and an assistant professor in the Department of Internal Medicine. “We found that inflammation and systemic changes, due to the infection, are influencing how platelets function, leading them to aggregate faster, which could explain why we are seeing increased numbers of blood clots in COVID patients.”
  • Emerging evidence suggests C19 is associated with an increased risk of blood clotting, which can lead to cardiovascular problems and organ failure in some patients, particularly among those with underlying medical problems such as diabetes, obesity, or high blood pressure.
  • To find out what might be going on, the researchers studied 41 C19 patients hospitalized at University of Utah Hospital in Salt Lake City. Seventeen of these patients were in the ICU, including nine who were on ventilators. They compared blood from these patients with samples taken from healthy individuals who were matched for age and sex.
  • Using differential gene analysis, the researchers found that SARS-CoV-2, the virus that causes C19, appears to trigger genetic changes in platelets. In laboratory studies, they studied platelet aggregation, an important component of blood clot formation, and observed C19 platelets aggregated more readily. They also noted that these changes significantly altered how platelets interacted with the immune system, likely contributing to inflammation of the respiratory tract that may, in turn, result in more severe lung injury.
  • Surprisingly, Campbell and his colleagues didn’t detect evidence of the virus in the vast majority of platelets, suggesting that it could be promoting the genetic changes within these cells indirectly.
  • One possible mechanism is inflammation, according to Bhanu Kanth Manne, Ph.D., one of the study’s lead authors and a research associate with the University of Utah Molecular Medicine Program (U2M2). In theory, inflammation caused by C19 could affect megakaryocytes, the cells that produce platelets. As a result, critical genetic alterations are passed down from megakaryocytes to the platelets, which, in turn, make them hyperactive.
  • In test tube studies, the researchers found that pre-treating platelets from SARS-CoV-2 infected patients with aspirin did prevent this hyperactivity. These findings suggest aspirin may improve outcomes; however, this will need further study in clinical trials. For now, Campbell warns against using aspirin to treat C19 unless recommended by your physician.
  • In the meantime, the researchers are beginning to look for other possible treatments.
  • “There are genetic processes that we can target that would prevent platelets from being changed,” Campbell says. “If we can figure out how C19 is interacting with megakaryocytes or platelets, then we might be able to block that interaction and reduce someone’s risk of developing a blood clot.”
  • Read the study here: Platelet Gene Expression and Function in C19

Source: COVID-19 Causes ‘Hyperactivity’ in Blood-Clotting Cells

F. Concerns & Unknowns

1. Fever checks are a flawed way to flag C19 cases, but smell tests might help  

  • Workplaces do it. Newly reopened public libraries do it. LAX does it. Some restaurants, bars, and retail stores started doing it when governors let them serve customers again: Use temperature checks — almost always with “non-contact infrared thermometers” — to identify people who might have, and therefore spread, the infectious disease.
  • Unfortunately, temperature checks could well join the long list of fumbled responses to the pandemic, from the testing debacle to federal officials’ about-face on masks.
  • Because many contagious people have no symptoms, using temperature checks to catch them is like trying to catch tennis balls in a soccer net: way too many can get through. On Tuesday, the head of the Transportation Security Administration told reporters, “I know in talking to our medical professionals and talking to the CDC … that temperature checks are not a guarantee that passengers who don’t have an elevated temperature also don’t have C19.” The reverse is also true: Feverish travelers might not have C19.
  • In this case, however, a growing body of science suggests a simple fix: make smell tests another part of routine screenings.
  • Of all the nose-to-toes symptoms of C19, the loss of the sense of smell — also known as anosmia — could work particularly well as an add-on to temperature checks, significantly increasing the proportion of infected people identified by screening in airports, workplaces, and other public places.
  • “My impression is that anosmia is an earlier symptom of C19 relative to fever, and some infected people can have anosmia and nothing else,” said physician Andrew Badley, who heads a virus lab at the Mayo Clinic. “So it’s potentially a more sensitive screen for asymptomatic patients.”
  • In a recent study, Badley and colleagues found that C19 patients were 27 times more likely than others to have lost their sense of smell. But they were only 2.6 times more likely to have fever or chills, suggesting that anosmia produces a clearer signal and may therefore be a better Covid-catching net than fever.
  • There is no definitive study on the predictive value of temperature checks for C19. But there are clues from when that strategy was used during the SARS epidemic of 2003. Deployed at airports, especially in Asia, the devices fell far short of the ideal, an analysis found. Although contactless thermometers are quite accurate if used correctly, many other conditions (including medications and inflammatory disease) can cause fever. As a result, the likelihood that someone with a fever had SARS ranged from 4% to 65%, depending on the underlying prevalence of the disease.
  • The likelihood that someone with a normal temperature reading was SARS-free was at least 86%. That suggests SARS fever checks didn’t miss many infected people. Unlike SARS, unfortunately, C19 can be contagious even before an infected person runs a fever, which makes missed cases more likely.

Source: Fever checks can’t catch all Covid-19 cases. Smell tests might help

2. Why are some people at greater risk of severe C19? 

A new study explores the interactions between airway cells and immune cells at the molecular level to identify why some people are at risk of severe C19 while others are not
  • There is plenty of evidence that the new coronavirus affects individuals differently. About 80% of those who have the coronavirus experience a clinically mild version of C19, meaning that they get better without needing to go to the hospital.
  • Risk factors for severe disease include being male, being older, and having underlying health conditions, among other factors.
  • What drives these risk factors is not entirely clear.
  • Some experts have suggested that an excessive immune reaction in response to the virus is at the heart of the damage to the lungs and other parts of the body that people with severe C19 experience.
  • Writing in Nature Biotechnology, scientists from the Center for Digital Health at the Berlin Institute of Health (BIH) and the Charité – Universitätsmedizin Berlin in Germany aimed to tease out the molecular actions that underpin such excessive immune reactions.
  • Prof. Roland Eils, chair and founding director of the Center for Digital Health, is one of the five senior study authors.
Analyzing individual cells
  • To pinpoint how different cells interact and communicate with each other, the multidisciplinary research team performed a single cell RNA sequencing analysis of upper and lower respiratory tract samples from 19 people in the hospital with C19 and five volunteers without the new coronavirus.
  • In total, the scientists analyzed 160,528 individual cells.
  • Of the 19 people with C19, eight had moderate disease, the authors write, while they classed 11 as critical. Two people died from the disease.
  • In the participants with C19, the team saw a three-fold increase in gene expression of the angiotensin converting enzyme 2 (ACE2) gene, which encodes the receptor that the new coronavirus uses to attach to cells during infection.
  • “It is interesting to note that in the case of C19, the signaling protein interferon, which is actually the immune system’s central defense strategy against viral infections, contributes to the epithelial cells producing more ACE2 and hence becoming more vulnerable to viral infection,” Prof. Irina Lehmann, head of the Molecular Epidemiology Research Group at the BIH and one of the study’s senior authors, explains.
  • “In C19, the immune system thus helps the virus to infect further cells, thereby amplifying the disease,” she continues.
  • Next, the team identified the specific subsets of epithelial and immune cells that were present in the samples and found proinflammatory cell types that may be driving cell death in the lungs.
  • Professor Roland Eils, a corresponding author said:
    • “Especially in severely ill patients, we observed that an overreactive immune system drives the destruction of the lung tissue.  This might explain why these patients are more severely affected by the infection than patients in whom the immune system reacts appropriately.” 
  • Professor Leif-Erik Sander, another of the study senior authors, also weighs in on the findings:
    • “These results suggest that our treatments in C19 patients should not only be directed against the virus itself but should also consider therapies that constrain the immune system, such as those now being used with dexamethasone, possibly even at the onset of the disease to prevent the immune system from overreacting.”
  • Specifically, the researchers suggest that targeting the proinflammatory “CCR1 and/or CCR5 pathways might suppress immune hyperactivation.”
  • The team acknowledges that their study has some shortcomings. Due to the relatively low number of people with C19 who required hospital care in Germany, the study was not large enough to look at the influences of age, sex, and underlying health conditions on the results.
  • The researchers were also not able to include people who had mild C19 and did not require hospital care.

Source: Why are some people at greater risk of severe COVID-19?

2. Latinx people more vulnerable to C19 infection 

An analysis of C19 testing in the Baltimore-Washington metropolitan area found that Latinx people were around 3 times as likely to test positive than any other ethnic or racial group.
  • The researchers who carried out the study believe that crowded living conditions and the economic necessity to continue working outside the home during the outbreak have contributed to higher rates of infection among Latinx communities.
Positive test results
  • The researchers analyzed results of tests for the coronavirus at five Johns Hopkins Health System hospitals and 30 outpatient clinics in the Baltimore-Washington metropolitan area.  All the tests were carried out between March 11 and May 25, 2020.
  • Of the 37,727 tests performed, 6,162 (16.3%) were positive for the new coronavirus. The occurrence of positive tests by ethnic and racial grouping was 42.6% for Latinx people, 17.6% for Black people, 17.2% for people identified as “other,” and 8.8% for white people.
  • Unusually for this infection, the majority of the Latinx patients who tested positive, 61.5%, were relatively young, aged 18–44 years.
  • By contrast, 28.6% of Black patients who tested positive and 28% of white patients who did so fell within this age range.
  • In another discrepancy, Latinx patients who tested positive and were hospitalized were much less likely to have been diagnosed with preexisting health conditions than people of other races and ethnicities.
  • Rates of hypertension, congestive heart failure, pulmonary disease, and chronic obstructive pulmonary disease were seemingly much lower among Latinx patients than Black or white patients.
Delayed peak
  • The study also found that the daily number of positive test results among Latinx people peaked several weeks later than the numbers among other ethnic and racial groups. The highest number among Latinx patients was on May 10, compared with April 19 for Black patients and April 16 for white patients.
  • Dr. Page says that a majority of Latinx patients with C19 are immigrants to the U.S. who work low-wage jobs, such as construction and cleaning, that are classed as “essential.”
  • “Many of these patients tell me they delayed coming to the hospital until absolutely necessary because they were worried about medical bills and were not sure if they could receive care because of their immigration status,” she says.
  • “Most of the patients I’ve met are not eligible for benefits, have no health insurance, and rent rooms in crowded houses. The need to work, lack of occupational protections, and crowded living conditions have led to high transmission in this community.”
  • A recently published study suggests that the new coronavirus spreads more easily in crowded homes.
Health disparities
  • The team suspects that disparities similar to those in the Baltimore-Washington area may exist elsewhere in the U.S., though their extent and causes may differ.
  • “Knowing what is driving these health disparities in each region is much-needed evidence to develop tailored policies and interventions to better serve all of our people,” says Diego A. Martinez, Ph.D., an assistant professor of emergency medicine at Johns Hopkins and the first author of the study.
  • The researchers hope that their findings will inform policy changes throughout the country and slow the spread of C19 among minority populations.
  • In their paper, the authors caution that their analysis was limited to patients using the Johns Hopkins Health System and may, therefore, not reflect infection rates regionally or nationally.
  • In addition, they acknowledge that their investigation was unable to determine the cause of higher positive test results among Latinx patients.

Source:  Latinx people more vulnerable to COVID-19, US study finds

3. Most People With Coronavirus Won’t Spread It. Why Do a Few Infect Many?  

  • Following a birthday party in Texas on May 30, one man reportedly infected 17 members of his family with the coronavirus.
  • Reading reports like these, you might think of the virus as a wildfire, instantly setting off epidemics wherever it goes. But other reports tell another story altogether.
  • In Italy, for example, scientists looked at stored samples of wastewater for the earliest trace of the virus. Last week they reported that the virus was in Turin and Milan as early as Dec. 18. But two months would pass before northern Italy’s hospitals began filling with victims of C19. So those December viruses seem to have petered out.
  • As strange as it may seem, these reports don’t contradict each other. Most infected people don’t pass on the coronavirus to someone else. But a small number pass it on to many others in so-called superspreading events.
  • “You can think about throwing a match at kindling,” said Ben Althouse, principal research scientist at the Institute for Disease Modeling in Bellevue, Wash. “You throw one match, it may not light the kindling. You throw another match, it may not light the kindling. But then one match hits in the right spot, and all of a sudden the fire goes up.”
  • Understanding why some matches start fires while many do not will be crucial to curbing the pandemic, scientists say. “Otherwise, you’re in the position where you’re always one step behind the virus,” said Adam Kucharski, an epidemiologist at the London School of Hygiene and Tropical Medicine.
  • When the virus first emerged in China, epidemiologists scrambled to understand how it spread from person to person. One of their first tasks was to estimate the average number of people each sick person infected, or what epidemiologists call the reproductive number.
  • The new coronavirus turned out to have a reproductive number somewhere between two and three. It’s impossible to pin down an exact figure, since people’s behavior can make it easier or harder for the virus to spread. By going into lockdown, for instance, Massachusetts drove its reproductive number down from 2.2 at the beginning of March to 1 by the end of the month; it’s now at .74.
  • This averaged figure can also be misleading because it masks the variability of spread from one person to the next. If nine out of 10 people don’t pass on a virus at all, while the 10th passes it to 20 people, the average would still be two.
  • In some diseases, such as influenza and smallpox, a large fraction of infected people pass on the pathogen to a few more. These diseases tend to grow steadily and slowly. “Flu can really plod along,” said Kristin Nelson, an assistant professor at Emory University.
  • But other diseases, like measles and SARS, are prone to sudden flares, with only a few infected people spreading the disease.
  • Epidemiologists capture the difference between the flare-ups and the plodding with something known as the dispersion parameter. It is a measure of how much variation there is from person to person in transmitting a pathogen.
  • But James Lloyd-Smith, a UCLA disease ecologist who developed the dispersion parameter 15 years ago, cautioned that just because scientists can measure it doesn’t mean they understand why some diseases have more superspreading than others. “We just understand the bits of it,” he said.
  • When C19 broke out, Dr. Kucharski and his colleagues tried to calculate that number by comparing cases in different countries.
  • If C19 was like the flu, you’d expect the outbreaks in different places to be mostly the same size. But Dr. Kucharski and his colleagues found a wide variation. The best way to explain this pattern, they found, was that 10 percent of infected people were responsible for 80 percent of new infections. Which meant that most people passed on the virus to few, if any, others.
  • Dr. Kucharski and his colleagues published their study in April as a preprint, a report that has not been reviewed by other scientists and published in a scientific journal. Other epidemiologists have calculated the dispersion parameter with other methods, ending up with similar estimates.
  • In Georgia, for example, Dr. Nelson and her colleagues analyzed over 9,500 C19 cases from March to May. They created a model for the spread of the virus through five counties and estimated how many people each person infected.
  • In a preprint published last week, the researchers found many superspreading events. Just 2 percent of people were responsible for 20 percent of transmissions.
  • Now researchers are trying to figure out why so few people spread the virus to so many. They’re trying to answer three questions: Who are the superspreaders? When does superspreading take place? And where?
  • As for the first question, doctors have observed that viruses can multiply to bigger numbers inside some people than others. It’s possible that some people become virus chimneys, blasting out clouds of pathogens with each breath.
  • Some people also have more opportunity to get sick, and to then make other people sick. A bus driver or a nursing home worker may sit at a hub in the social network, while most people are less likely to come into contact with others — especially in a lockdown.
  • Dr. Nelson suspects the biological differences between people are less significant. “I think the circumstances are a lot more important,” she said. Dr. Lloyd-Smith agreed. “I think it’s more centered on the events.”
  • A lot of transmission seems to happen in a narrow window of time starting a couple days after infection, even before symptoms emerge. If people aren’t around a lot of people during that window, they can’t pass it along.
  • And certain places seem to lend themselves to superspreading. A busy bar, for example, is full of people talking loudly. Any one of them could spew out viruses without ever coughing. And without good ventilation, the viruses can linger in the air for hours.
  • A study from Japan this month found clusters of coronavirus cases in health care facilities, nursing homes, day care centers, restaurants, bars, workplaces, and musical events such as live concerts and karaoke parties.
  • This pattern of superspreading could explain the puzzling lag in Italy between the arrival of the virus and the rise of the epidemic. And geneticists have found a similar lag in other countries: The first viruses to crop up in a given region don’t give rise to the epidemics that come weeks later.
  • Many countries and states have fought outbreaks with lockdowns, which have managed to draw down C19’s reproductive number. But as governments move toward reopening, they shouldn’t get complacent and forget the virus’s potential for superspreading.
  • “You can really go from thinking you’ve got things under control to having an out-of-control outbreak in a matter of a week,” Dr. Lloyd-Smith said.
  • Singapore’s health authorities earned praise early on for holding down the epidemic by carefully tracing cases of C19. But they didn’t appreciate that huge dormitories where migrant workers lived were prime spots for superspreading events. Now they are wrestling with a resurgence of the virus.
  • On the other hand, knowing that C19 is a superspreading pandemic could be a good thing. “It bodes well for control,” Dr. Nelson said.
  • Since most transmission happens only in a small number of similar situations, it may be possible to come up with smart strategies to stop them from happening. It may be possible to avoid crippling, across-the-board lockdowns by targeting the superspreading events.
  • “By curbing the activities in quite a small proportion of our life, we could actually reduce most of the risk,” said Dr. Kucharski.

Source: Most People With Coronavirus Won’t Spread It. Why Do a Few Infect Many? 

4. This coronavirus mutation has taken over the world. Scientists are trying to understand why.  

  • When the first coronavirus cases in Chicago appeared in January, they bore the same genetic signatures as a germ that emerged in China weeks before.
  • But as Egon Ozer, an infectious-disease specialist at the Northwestern University Feinberg School of Medicine, examined the genetic structure of virus samples from local patients, he noticed something different.
  • A change in the virus was appearing again and again. This mutation, associated with outbreaks in Europe and New York, eventually took over the city. By May, it was found in 95 percent of all the genomes Ozer sequenced.
  • At a glance, the mutation seemed trivial. About 1,300 amino acids serve as building blocks for a protein on the surface of the virus. In the mutant virus, the genetic instructions for just one of those amino acids — number 614 — switched in the new variant from a “D” (shorthand for aspartic acid) to a “G” (short for glycine).
  • But the location was significant, because the switch occurred in the part of the genome that codes for the all-important “spike protein” — the protruding structure that gives the coronavirus its crownlike profile and allows it to enter human cells the way a burglar picks a lock.
  • And its ubiquity is undeniable. Of the approximately 50,000 genomes of the new virus that researchers worldwide have uploaded to a shared database, about 70 percent carry the mutation, officially designated D614G but known more familiarly to scientists as “G.”
  • “G” hasn’t just dominated the outbreak in Chicago — it has taken over the world. Now scientists are racing to figure out what it means.
  • At least four laboratory experiments suggest that the mutation makes the virus more infectious, although none of that work has been peer-reviewed. Another unpublished study led by scientists at Los Alamos National Laboratory asserts that patients with the G variant actually have more virus in their bodies, making them more likely to spread it to others.
  • The mutation doesn’t appear to make people sicker, but a growing number of scientists worry that it has made the virus more contagious.
  • “The epidemiological study and our data together really explain why the [G variant’s] spread in Europe and the U.S. was really fast,” said Hyeryun Choe, a virologist at Scripps Research and lead author of an unpublished study on the G variant’s enhanced infectiousness in laboratory cell cultures. “This is not just accidental.”
  • But there may be other explanations for the G variant’s dominance: biases in where genetic data are being collected, quirks of timing that gave the mutated virus an early foothold in susceptible populations.
  • “The bottom line is, we haven’t seen anything definitive yet,” said Jeremy Luban, a virologist at the University of Massachusetts Medical School.
  • The scramble to unravel this mutation mystery embodies the challenges of science during the coronavirus pandemic. With millions of people infected and thousands dying every day around the world, researchers must strike a high-stakes balance between getting information out quickly and making sure that it’s right.
A better lock pick
  • SARS-CoV-2, the novel coronavirus that causes the disease C19, can be thought of as an extremely destructive burglar. Unable to live or reproduce on its own, it breaks into human cells and co-opts their biological machinery to make thousands of copies of itself. That leaves a trail of damaged tissue and triggers an immune system response that for some people can be disastrous.
  • This replication process is messy. Even though it has a “proofreading” mechanism for copying its genome, the coronavirus frequently makes mistakes, or mutations. The vast majority of mutations have no effect on the behavior of the virus.
  • But since the virus’s genome was first sequenced in January, scientists have been on the lookout for changes that are meaningful. And few genetic mutations could be more significant than ones that affect the spike protein — the virus’s most powerful tool.
  • This protein attaches to a receptor on respiratory cells called ACE2, which opens the cell and lets the virus slip inside. The more effective the spike protein, the more easily the virus can break into the bodies of its hosts. Even when the original variant of the virus emerged in Wuhan, China, it was obvious that the spike protein on SARS-CoV-2 was already quite effective.
  • But it could have been even better, said Choe, who has studied spike proteins and the way they bind to the ACE2 receptor since the severe acute respiratory syndrome outbreak in 2003.
  • The spike protein for SARS-CoV-2 has two parts that don’t always hold together well. In the version of the virus that arose in China, Choe said, the outer part — which the virus needs to attach to a human receptor — frequently broke off. Equipped with this faulty lock pick, the virus had a harder time invading host cells.
  • “I think this mutation happened to compensate,” Choe said.
  • Studying both versions of the gene using a proxy virus in a petri dish of human cells, Choe and her colleagues found that viruses with the G variant had more spike proteins, and the outer parts of those proteins were less likely to break off. This made the virus approximately 10 times more infectious in the lab experiment.
  • The mutation does not seem to lead to worse outcomes in patients. Nor did it alter the virus’s response to antibodies from patients who had the D variant, Choe said, suggesting that vaccines being developed based on the original version of the virus will be effective against the new strain.
  • Choe has uploaded a manuscript describing this study to the website bioRxiv, where scientists can post “preprint” research that has not yet been peer reviewed. She has also submitted the paper to an academic journal, which has not yet published it.
  • The distinctive infectiousness of the G strain is so strong that scientists have been drawn to the mutation even when they weren’t looking for it.
  • Neville Sanjana, a geneticist at the New York Genome Center and New York University, was trying to figure out which genes enable SARS-CoV-2 to infiltrate human cells. But in experiments based on a gene sequence taken from an early case of the virus in Wuhan, he struggled to get that form of the virus to infect cells. Then the team switched to a model virus based on the G variant.
  • “We were shocked,” Sanjana said. “Voilà! It was just this huge increase in viral transduction.” They repeated the experiment in many types of cells, and every time the variant was many times more infectious.
  • Their findings, published as a preprint on bioRxiv, generally matched what Choe and other laboratory scientists were seeing.
  • But the New York team offers a different explanation as to why the variant is so infectious. Whereas Choe’s study proposes that the mutation made the spike protein more stable, Sanjana said experiments in the past two weeks, not yet made public, suggest that the improvement is actually in the infection process. He hypothesized that the G variant is more efficient at beginning the process of invading the human cell and taking over its reproductive machinery.
  • Luban, who has also been experimenting with the D614G mutation, has been drawn to a third possibility: His experiments suggest that the mutation allows the spike protein to change shape as it attaches to the ACE2 receptor, improving its ability to fuse to the host cell.
  • Different approaches to making their model virus might explain these discrepancies, Luban said. “But it’s quite clear that something is going on.”

Source: The coronavirus is mutating – The Washington Post

G. Herd Immunity

1. Herd Immunity Is Much Closer Than Antibody Tests Suggest  

  • The prevalence of immunity to the coronavirus that causes C19 may be much higher than previous research suggests according to an intriguing new study by researchers associated with Karolinska Institute in Sweden. In addition, a new German study by researchers associated with the University Hospital Tübingen in Germany reports that people who have been previously infected with versions of the coronavirus that cause the common cold also have some immunity to the C19 virus. If these reports stand up to further scrutiny, it would be very good news because they suggest that the pandemic could be over sooner and ultimately be less lethal than feared.
  • In the Swedish study, researchers not only checked 200 participants for the presence of immunological proteins called antibodies produced in response to C19 infections, but also for T-cells which are another virus-fighting component of the immune system. Detecting and evaluating T-cells is a bit trickier than measuring antibodies. Read the Swedish study here: Robust T cell immunity in convalescent individuals with asymptomatic or mild COVID-19
  • The Karolinska researchers, according to the accompanying press release, “performed immunological analyses of samples from over 200 people, many of whom had mild or no symptoms of C19.” The study tested C19 patients, exposed asymptomatic family members, healthy blood donors who gave blood during 2020, and a 2019 donor control group.
  • “One interesting observation was that it wasn’t just individuals with verified C19 who showed T-cell immunity but also many of their exposed asymptomatic family members,” said Karolinska researcher Soo Aleman. “Moreover, roughly 30% of the blood donors who’d given blood in May 2020 had C19-specific T cells, a figure that’s much higher than previous antibody tests have shown.”
  • “Our results indicate that roughly twice as many people have developed T-cell immunity compared with those who we can detect antibodies in,” noted Karolinska Center for Infectious Medicine researcher Marcus Buggert.
  • Study co-author Hans-Gustaf Ljunggren told The Telegraph that if the study’s findings are replicated, they would apply to any country. London, for instance, might have about 30 percent immunity and New York above 40%. If so, some parts of the U.S. are much closer to herd immunity than population-wide antibody testing currently suggests.
  • Herd immunity is the resistance to the spread of a contagious disease that results if a sufficiently high proportion of a population is immune to the illness. Some people are still susceptible, but they are surrounded by immune individuals who serve as a barrier, preventing the microbes from reaching them. Epidemiologists typically estimate that the C19 threshold for herd immunity is around 60 to 70 percent.
  • Still the Swedish researchers caution, “It remains to be determined if a robust memory T cell response in the absence of detectable circulating antibodies can protect against [the virus].”
  • In a second study, German researchers analyzed blood samples of 365 people, of which 180 had had C19 and 185 had not. When they exposed the blood samples to the C19 coronavirus, they found, as expected, that blood from those who had had the illness produced a substantial immune response. More significantly, they also found that 81 percent of the subjects who had never had C19 also produced a T-cell immune reaction, reports The Science Times. If the German study’s results prove out, that would suggest that earlier common cold coronavirus infections may provide about eight in 10 people some degree of immune protection from the C19 virus. Read the German study here: SARS-CoV-2 T-cell epitopes define heterologous and COVID-19-induced T-cell recognition
  • The findings in both of these studies are potentially very good news with respect to public health and the course of the C19 pandemic. Here’s hoping that future replications will validate them.
  • A few caveats: both studies are based on small sample sizes and neither have yet been vetted by peer review.

Source: COVID-19 Herd Immunity Is Much Closer Than Antibody Tests Suggest, Say 2 New Studies

2. The Tricky Math of Herd Immunity for C19  

  • While much about the C19 pandemic remains uncertain, we know how it will likely end: when the spread of the virus starts to slow (and eventually ceases altogether) because enough people have developed immunity to it. At that point, whether it’s brought on by a vaccine or by people catching the disease, the population has developed “herd immunity.”
  • “Once the level of immunity passes a certain threshold, then the epidemic will start to die out because there aren’t enough new people to infect,” said Natalie Dean of the University of Florida.
  • While determining that threshold for C19 is critical, a lot of nuance is involved in calculating exactly how much of the population needs to be immune for herd immunity to take effect and protect the people who aren’t immune.
  • At first it seems simple enough. The only thing you need to know is how many people, on average, are infected by each infected person. This value is called R0 (pronounced “R naught”). Once you have that, you can plug it into a simple formula for calculating the herd immunity threshold: 1 − 1/R0.
  • Let’s say the R0 for C19 is 2.5, meaning each infected person infects, on average, two and a half other people (a common estimate). In that case, the herd immunity threshold for C19 is 0.6, or 60%. That means the virus will spread at an accelerating rate until, on average across different places, 60% of the population becomes immune.
  • At that point, the virus will still spread, but at a decelerating rate until it stops completely. Just as a car doesn’t come to a stop the moment you take your foot off the gas, the virus won’t vanish the moment herd immunity is reached.
  • “You could imagine that once 60% of the population is infected, the number of infections starts to drop. But it might be another 20% that gets infected while the disease is starting to die out,” said Joel Miller of La Trobe University in Australia.
  • That 60% is also the threshold past which new introductions of the virus — say, an infected passenger disembarking from a cruise ship into a healthy port with herd immunity — will quickly burn out.
  • “It doesn’t mean you won’t be able to start a fire at all, but that outbreak is going to die,” said Kate Langwig of Virginia Polytechnic Institute and State University.
  • However, things quickly get complicated. The herd immunity threshold depends on how many people each infected person actually infects — a number that can vary by location. The average infected person in an apartment building may infect many more people than the average infected person in a rural setting. So while an R0 of 2.5 for C19 may be a reasonable number for the whole world, it will almost certainly vary considerably on a more local level, averaging much higher in some places and lower in others. This means that the herd immunity threshold will also be higher than 60% in some places and lower in others.
  • “I think the range of R0 consistent with data for C19 is larger than most people give credit to,” said Marc Lipsitch of Harvard University, who has been advising health officials in Massachusetts and abroad. He cited data indicating it could be more than twice as high in some urban settings as the overall U.S. average.
  • And just as R0 turns out to be a variable, and not a static number, the way people acquire their immunity also varies, with important implications for calculating that herd immunity threshold.
  • Usually, researchers only think about herd immunity in the context of vaccine campaigns, many of which assume that everyone is equally likely to contract and spread a disease. But in a naturally spreading infection, that’s not necessarily the case. Differences in social behaviors lead some people to have more exposure to a disease than others. Biological differences also play a role in how likely people are to get infected.
  • “We are born different, and then these differences accumulate as we live different experiences,” said Gabriela Gomes of the University of Strathclyde in Scotland. “This affects how able people are to fight a virus.”
  • Epidemiologists refer to these variations as the “heterogeneity of susceptibility,” meaning the differences that cause some people to be more or less likely to get infected.
  • But this is too much nuance for vaccination campaigns. “Vaccines are generally not distributed in a population with respect to how many contacts people have or how susceptible they are, because we don’t know that,” said Virginia Pitzer of the Yale School of Public Health. Instead, health officials take a maximalist approach and, in essence, vaccinate everyone.
  • However, in an ongoing pandemic with no guarantee that a vaccine will be available anytime soon, the heterogeneity of susceptibility has real implications for the disease’s herd immunity threshold.
  • In some cases it will make the threshold higher. This could be true in places like nursing homes, where the average person might be more susceptible to C19 than the average person in the broader population.
  • But on a larger scale, heterogeneity typically lowers the herd immunity threshold. At first the virus infects people who are more susceptible and spreads quickly. But to keep spreading, the virus has to move on to people who are less susceptible. This makes it harder for the virus to spread, so the epidemic grows more slowly than you might have anticipated based on its initial rate of growth.
  • “The first person is going to be likely to infect the people who are most susceptible to begin with, leaving the people who are less susceptible toward the latter half of the epidemic, meaning the infection could be eliminated sooner than you’d expect,” Lipsitch said.
Estimating Heterogeneity
  • So how much lower is the herd immunity threshold when you’re talking about a virus spreading in the wild, like the current pandemic?
  • According to the standard models, about 60% of the U.S. population would need to be vaccinated against C19 or recover from it to slow and ultimately stop the spread of the disease. But many experts I talked to suspect that the herd immunity threshold for naturally acquired immunity is lower than that.
  • “My guess would be it’s potentially between 40 and 50%,” Pitzer said.
  • Lipsitch agrees: “If I had to make a guess, I’d probably put it at about 50%.”
  • These are mostly just educated estimates, because it’s so hard to quantify what makes one person more susceptible than another. Many of the characteristics you might think to assign someone — like how much social distancing they’re doing — can change from week to week.
  • “The whole heterogeneity problem only works if the sources of heterogeneity are long-term properties of a person. If it’s being in a bar, that’s not in itself sustained enough to be a source of heterogeneity,” Lipsitch said.
  • Heterogeneity may be hard to estimate, but it’s also an important factor in determining what the herd immunity threshold really is. Langwig believes that the epidemiological community hasn’t done enough to try and get it right.
  • “We’ve kind of been a little sloppy in thinking about herd immunity,” she said. “This variability really matters, and we need to be careful to be more accurate about what the herd immunity threshold is.”
  • Some recent papers have tried. In June the journal Science published a study that incorporated a modest degree of heterogeneity and estimated the herd immunity threshold for C19 at 43% across broad populations. But one of the study’s co-authors, Tom Britton of Stockholm University, thinks there are additional sources of heterogeneity their model doesn’t account for.
  • “If anything, I’d think the difference is bigger, so that in fact the herd immunity level is probably a bit smaller than 43%,” Britton said.
  • Another new study takes a different approach to estimating differences in susceptibility to C19 and puts the herd immunity threshold even lower. The paper’s 10 authors, who include Gomes and Langwig, estimate that the threshold for naturally acquired herd immunity to C19 could be as low as 20% of the population. If that’s the case, the hardest-hit places in the world may be nearing it.
  • “We’re getting to the conclusion that the most affected regions like Madrid may be close to reaching herd immunity,” said Gomes. An early version of the paper was posted in May, and the authors are currently working on an updated version, which they anticipate posting soon. This version will include herd immunity estimates for Spain, Portugal, Belgium and England.
  • Many experts, however, consider these new studies — not all of which have been peer-reviewed yet — to be unreliable.
  • In a Twitter thread in May, Dean emphasized that there’s too much uncertainty around basic aspects of the disease — from the different values of R0 in different settings to the effects of relaxing social distancing — to place much confidence in exact herd immunity thresholds. The threshold could be one number as long as a lot of people are wearing masks and avoiding large gatherings, and another much higher number if and when people let their guard down. 
  • Other epidemiologists are also skeptical of the low numbers. Jeffrey Shaman of Columbia University said that 20% herd immunity “is not consistent with other respiratory viruses. It’s not consistent with the flu. So why would it behave differently for one respiratory virus versus another? I don’t get that.”
  • Miller added, “I think the herd immunity threshold [for naturally acquired immunity] is less than 60%, but I don’t see clear evidence that any [place] is close to it.”
  • Ultimately, the only way to truly escape the C19 pandemic is to achieve large-scale herd immunity — everywhere, not just in a small number of places where infections have been highest. And that will likely only happen once a vaccine is in widespread use.
  • “I can’t think of any decision I’d make differently right now if I knew herd immunity was somewhere else in the range I think it is, which is 40-60%,” said Lipsitch.
  • Shaman, too, thinks that uncertainty about the naturally acquired herd immunity threshold, combined with the consequences for getting it wrong, leaves only one path forward: Do our best to prevent new cases until we can introduce a vaccine to bring about herd immunity safely.
  • “The question is: Could New York City support another outbreak?” he said. “I don’t know, but let’s not play with that fire.”

Source: The Tricky Math of Covid-19 Immunity

H. Vaccines

1. Another experimental C19 vaccine shows promising early results  

  • The news: An experimental C19 vaccine being developed by Pfizer and BioNTech provoked immune responses in 45 healthy volunteers, according to a preprint paper on medRXiv. The levels of antibodies were up to 2.8 times the level of those found in patients who have recovered. The study randomly assigned 45 people to get either one of three doses of the vaccine or a placebo. But there were side effects like fatigue, headache, and fever—especially at higher doses. The researchers decided to discontinue with the highest dose of 100-micrograms after the first round of treatments.
  • Some caveats required: It’s promising news but this is the first clinical data on this specific vaccine and it hasn’t been through the process of peer review yet. Higher antibody levels in patients who’d received the vaccine are a useful proxy for immunity to C19, but we don’t yet know for sure that they guarantee immunity. In order to find out, Pfizer will start conducting studies in larger groups of patients, starting this summer. It says its goal is to have 100 million doses of a vaccine available by the end of 2020.
  • A common approach: Pfizer is using the same experimental technique as Moderna, one of the other pharmaceutical companies developing a vaccine. Both vaccines are designed to provoke an immune response against the coronavirus through its messenger RNA, the genetic instructions for the virus to replicate inside the host. The method could provide a rapid way to develop a vaccine, but it’s yet to lead to a licensed one for sale. Currently, 178 vaccines are in various stages of development; 17 are now going through clinical trials.
  • Read the preprint paper here: Alefacept for psoriasis and psoriatic arthritis

Source: Another experimental covid-19 vaccine has shown promising early results

2. FDA spells out guidelines for approving C19 vaccines  

  • The FDA on Tuesday released final guidance laying out its standards for approving coronavirus vaccines, requiring that any vaccine candidate be at least 50 percent more effective than a placebo.
  • The agency also left open the possibility it would issue an emergency use authorization for a vaccine, but it said making that decision before the completion of large, randomized clinical trials could make it harder to determine a vaccine’s effectiveness.
  • FDA said it could issue an EUA if the agency feels there is enough data on safety and efficacy, but its preference is that vaccines undergo more vigorous scientific review. FDA recently revoked another set of EUAs that cleared hydroxychloroquine and chloroquine to treat C19, after the data for that decision was questioned and clinical trials showed the antimalarial drugs didn’t work.
  • There has been mounting concern from public health experts that FDA could make a hasty decision on an eventual vaccine, but Tuesday’s guidance may assuage some of those concerns. 
  • Before approval, manufacturers will also need to conduct animal studies to ensure that their candidates don’t provoke an immune response that actually worsens the infection, known as enhanced respiratory disease.
  • The agency said development can be sped up through creative clinical trial designs that allow for scientists to adapt dosing and options based on rolling data. Those designs, known as adaptive or seamless trials, are fleshed out in the guidance.
  • FDA said it will also be important to study vaccine candidates in patients with confirmed infections, since many people seeking out a vaccine may have already unknowingly contracted the virus without experiencing symptoms.
  • The agency said C19 vaccines must meet all the standard laws and regulatory requirements for any other vaccines to be approved, including manufacturing and control requirements.

Source: FDA spells out guidelines for approving Covid-19 vaccines 

I. Back to School!?

1. Is it safe to send kids back to school?  

  • C19 has been disruptive and bewildering for everyone, but especially for children. In the UK and in most US states, schools closed in March. Many of them will keep their doors shut until the fall. That’s six months without the normality of a school day, not to mention a significant break without any formal education for the many children who cannot access online classes.
  • It’s a global issue. Schools have had to close in 191 countries, affecting more than 1.5 billion students and 63 million teachers, according to the United Nations. But in many countries, schools are now cautiously reopening: in Germany, Denmark, Vietnam, New Zealand, and China, children are mostly back behind their desks. These countries all have two things in common: low levels of infection and a reasonably firm ability to trace outbreaks. 
  • What about the UK or the US, where the number of cases is relatively high and tracing systems are still in the early stages? How will we know when it’s safe for children to return? There can never be a cast-iron guarantee. But for parents to be able to gauge the level of risk, there are three questions that need answering. How susceptible are children to C19? How badly does it affect them? And do they spread it to others?
  • We know that children are less likely to catch C19 than adults. They’re about half as likely, to be precise, according to a recent study by the London School of Hygiene & Tropical Medicine (LSHTM) using data from China, Italy, Japan, Singapore, Canada, and South Korea, published in Nature Medicine. A survey of 149,760 people with C19 by the US Centers for Disease Control and Prevention found that children 17 and under, who make up 22% of the US population, account for fewer than 2% of confirmed infections across the United States. 
  • These findings were supported by a meta-analysis of 18 studies carried out by researchers at University College London, which found that under-18s were 56% less likely to catch coronavirus from an infected person than adults. On the flip side, children are likely to have more close contact with others than adults do, especially in a school, which could potentially mitigate the protective benefit they get from being less likely to catch the virus in the first place. Even so, the numbers look promising.
  • If children do become infected in spite of this, how badly does it affect them?
  • The LSHTM study suggests that when children catch C19, they usually get very mild effects. Only one in five of those aged 10-19 had any clinical symptoms, compared with 69% of adults over 70. Children are extremely unlikely to die from coronavirus: during the peak nine weeks of the pandemic in England and Wales, just five children 14 and under died, out of a population of almost 11 million in that age group, according to official data analyzed by David Spiegelhalter, a statistician at Cambridge University. A preprint in the journal Public Health found that across seven countries up to May 19, there were 44 C19 deaths out of over 137 million children 19 and under. That’s a rate of less than 1 in 3 million. There is an unpleasant new covid-linked inflammatory syndrome in children similar to Kawasaki disease, but it’s extremely rare. “I think there have been fewer than 500 cases reported worldwide,” says Tina Hartert, a medicine professor at the Vanderbilt Institute for Infection, Immunology, and Inflammation in Nashville, Tennessee. The message seems to be that parents should not worry unduly about what might happen to their kids should they catch the virus. 
  • The final crucial question: to what extent do children spread the coronavirus once infected? “If you look at the peer-reviewed literature, it’s very mixed. The simple answer is we don’t know,” says Jeffrey Shaman, an infectious diseases expert at Columbia University. A nine-year-old boy with coronavirus in the French Alps in February did not transmit the virus to anyone else despite exposure to more than 170 people, including close contact within schools. However, we shouldn’t read too much into a study of one. On the other hand, researchers from Berlin University tested 3,712 C19 patients, 127 of whom were under 20, and concluded that children can carry the same viral load as adults, which seems to correlate with infectiousness.
  • One of the biggest fears is that a child could pick up the coronavirus at school and then bring it home to Grandma. “The risk to the kids is low, and it’s not bad for me or my partner, but I do worry about them going back to school and then seeing my parents,” says Kirsten Minshall, a father of two boys aged 9 and 11 who lives in a seaside town in Kent in the UK.
  • It is possible for children to introduce C19 into their household—a study from China identified three occasions when a child under 10 was the “index case” in a home. But it seems to be rare.
  • The crux of the issue is data, or more precisely a lack of it. Because children are less likely to catch C19, and are likely to have milder symptoms if they do, they are less likely to be seen by doctors or tested. That means high-quality, reliable data on this question is hard to come by. 
  • A large National Institutes of Health–funded study in the US that launched last month should help. It’s going to test nasal swabs from nearly 2,000 families in 10 cities every two weeks. The aim is to work out what role children play in transmission, says Hartert, who is leading the study. Enrollment has just finished, and she expects the first results within weeks. 
  • Population-wide serological surveys—which test for the presence of antibodies against C19 in blood samples—will also help plug the data gap. Studies comparing areas where schools have reopened and those where they have not could be hugely helpful, too. If it ends up being the case that children are less susceptible to infection, that suggests closing schools won’t be a very important way to reduce transmission across society, says Rosalind Eggo, an infectious disease modeler at LSHTM, who was involved in the study. However, she warns that it’s tricky to disentangle the closure of schools from all the other actions that were taken at the start of the pandemic.
  • “It’s very difficult to work out what happened to transmission when schools closed, because that happened at the same time as a lot of other interventions, like a general lockdown, distancing, and increased hygiene,” she says.
  • But none of this addresses a major group, without which no school can function: teachers. 
  • “Some teachers will be elderly, and there’s no easy answer for them. They’re incredibly high risk,” says Hartert. Many of the schools that have reopened around the world have introduced distancing measures and schedules that minimize contact between school groups. 
  • “I’m less afraid of teaching than I am going to the supermarket,” says Marleen Slingenbergh, the head of biology at Alexandra Park School in London, where some schools have reopened for a small proportion of their students. She says that’s because the school has prioritized safety⁠—students have to sanitize their hands between lessons, teachers are required to stay at least two meters away from students at the front of the class, and there are strict “one at a time” bathroom policies, for example. 
  • That said, the majority of students haven’t returned yet. Slingenbergh fears it won’t be possible to maintain the safety measures when school returns in full in September. “With one week on, one week off, it’s possible. When we have 1,600 students, it will be tricky, especially during the changeover between lessons,” she says. 
  • Ultimately, the crucial thing for schools may be their ability to respond flexibly—closely monitoring for any potential outbreaks and quickly closing when necessary. 
  • There is, understandably, a lot of pressure from parents to keep their children safe, and many are still not comfortable with sending them back to school, says Slingenbergh. But most of them recognize it’s a delicate balance. “It’s all about weighing up the risks of covid, the kids getting proper schooling, and looking after their mental health,” Minshall says. 

Source: Is it safe to send kids back to school? 

J. Projections & Our (Possible) Future

1. Increased restaurant spending Foreshadows Increase in new C19 cases 

Key Points
  • JPMorgan analyzed data from 30 million Chase cardholders and Johns Hopkins University’s case tracker and found that higher restaurant spending in a state predicted a rise in new infections there three weeks later.
  • In-person restaurant spending was “particularly predictive.”
  • Conversely, higher spending at supermarkets predicted a slower spread of the virus.
  • Higher restaurant spending appears to be linked to a faster spread of the coronavirus, according to a JPMorgan study.
  • Analyst Jesse Edgerton analyzed data from 30 million Chase credit and debit cardholders and from Johns Hopkins University’s case tracker. He found that increased restaurant spending in a state predicted a rise in new infections there three weeks later.
  • He also said restaurant spending was the strongest predictor across all categories of card spending.
  • According to the research note, Louisiana, West Virginia and Arizona showed the smallest relative declines in restaurant spending by Chase cardholders compared with the year-earlier period, while the District of Columbia and Massachusetts saw the sharpest drops. 
  • Edgerton said in-person restaurant spending was “particularly predictive.”
  • The NPD Group found that transactions for the week ended June 14 were still improving at full-service chain restaurants in Arizona, California and Florida, even as those states reported spikes in new cases. The full-service segment was hardest hit by dining room closures and has taken the longest to recover.
  • The National Restaurant Association said in a statement that it shares the nation’s concern over rising C19 cases.
  • “It is irresponsible to pin the rise on a single industry,” the trade group said in a statement to CNBC. “Restaurants have historically operated with highly regulated safety protocols based on the FDA’s Food Code and now have taken new steps to meet social distancing guidelines required by state and federal officials. We all have responsibility for wearing masks, washing hands, and social distancing.”
  • Edgerton also gave the caveat that the states that are now seeing a surge in new infections share other factors outside of higher restaurant spending. 
  • Conversely, higher spending at supermarkets predicts a slower spread of the virus, which could indicate that states that buy more groceries are more mindful of social distancing measures. 
  • “For example, as of three weeks ago, supermarket spending was up 20% or more from last year’s levels in New York and New Jersey, while it was up less than 10% in Texas and Arizona,” Edgerton said.

Source: This chart shows the link between restaurant spending and new cases of coronavirus 

K. Practical Tips & Other Useful Information

1. How to Clean an N95 mask? Use a microwave!  

  • The researchers, from Beth Israel Deaconess Medical Center, Harvard University and Massachusetts General Hospital, have detailed a reproducible decontamination approach that all health care workers would be able to utilize. “We identified an effective method of N95 decontamination by microwave-generated steam utilizing universally accessible materials. Our method resulted in almost complete sterilization after only 3 min of treatment and did not appear to affect the integrity of N95 filtration or fit with repeated treatment,” the researchers write.
  • We selected a generic glass container sized at 17 × 17 × 7.5 cm (length [L] × width [W] × height [H]) that had an opening large enough to expose the entire N95 respirator to the vertical column of generated steam. We secured mesh from a produce bag over the top of the container with a rubber band and added 60 ml of distilled water to the basin (Fig. 3A and B). We repeated a sterilization time course against 1-cm2 N95 respirator coupons in 1-min increments. After 2 min of microwave steam treatment, we were unable to detect residual viable phage on the coupons (Fig. 3C). This represents a 1-min reduction in sterilization time compared to the ceramic mug decontamination assay, indicating that the glass container is a more efficient decontamination system.
  • We found that use of a generic glass container measuring 17 × 17 × 7.5 cm (L × W × H) resulted in the most efficient and practical N95 respirator decontamination system. Using this method, we observed almost complete sterilization of the N95 respirator after a single 3-min treatment. On average, we found a 6-log10 reduction in viable MS2 phage with a minimum of a 5-log10 reduction. During decontamination treatments, we positioned the N95 respirator with its convex surface pointed downward, onto the mesh-covered container, maximizing steam exposure. Placement was otherwise made without regard to specific orientation of the respirator, simulating real world application. Posttreatment water retention by the N95 respirator was not detected, eliminating a need for drying time before reuse. Importantly, this method was validated for use of 20 times on a single respirator without detrimental effect on respirator integrity or fit. In contrast, a recent preprint demonstrated that fit and seal integrity was compromised in UV- and heat-treated N95 respirators after 3 treatment cycles and in ethanol-treated respirators after 2 treatment cycles (16). Given these findings, decontamination by microwave-generated steam may provide an ideal solution for broad N95 respirator reuse, with minimal treatment duration, minimal posttreatment processing, and maximal reuse potential.
  • Read the study here: Microwave-Generated Steam Decontamination of N95 Respirators Utilizing Universally Accessible Materials

Source: Researchers Identify N95 Decontamination Method Using a Microwave 

L. Johns Hopkins Report: C19 At Six Months

July 2, 2020

1. C19 at Six Months

  • Six months ago, in late December 2019, reports emerged about 27 cases of unidentified pneumonia in Wuhan, China, potentially linked to a local market. At that time, very little was known about the disease, pathogen, or origin of the outbreak, and while we have learned much over the past 6 months, many mysteries remain.
  • The pandemic has grown to more than 10 million cases and 500,000 deaths across nearly every country around the world. As of July 1, the WHO reported 10.36 million cases and 508,055 deaths worldwide, covering more than 200 countries and territories. Among these countries and territories, 86 are reporting “Community Transmission”—the WHO’s highest tier—which indicates “larger outbreaks of local transmission,” “large numbers of cases not linkable to transmission chains,” and “multiple unrelated clusters in several areas of the country.”
  • The United States continues to lead the world in cumulative incidence, and it has recently alternated with Brazil as #1 for daily incidence. In total, 38 US states are reporting increasing COVID-19 incidence over the past 2 weeks, 24 are reporting increasing COVID-19 hospitalizations, and 20 are reporting test positivity greater than 5% and increasing. These concerning trends have prompted 13 states to pause their recovery plans and an additional 6 states to reverse course and re-implement or strengthen certain social distancing restrictions.
  • From the first reports of cases in China, our team at the Johns Hopkins Center for Health Security has been following and analyzing this situation closely. Thank you for reading our COVID-19 situation reports and learning alongside us as the pandemic spreads. We are grateful to our technical team, who pulls together these updates with diligence and rigor—Divya Hosangadi, Amanda Kobokovich, Elena Martin, Christina Potter, Marc Trotochaud, Rachel Vahey, and Matthew Watson; led by Matthew Shearer and Dr. Caitlin Rivers—as well as our communications team, Margaret Miller and Julia Cizek. Finally, thank you to our funders and donors who make these reports and the rest of our work possible. 
  • In order to provide some context for the past 6 months, we have compiled a timeline of selected events since the onset of the pandemic:
  • December 31: Wuhan Municipal Health Commission publishes the initial report of unidentified pneumonia, potentially linked to a local market
  • January 6: US CDC issues a Level 1 travel watch for Wuhan, China
  • January 11: First reported C19 death in China
  • January 13: First C19 case reported outside of China
  • January 21: First C19 case reported in the US
  • January 23: China implements “lockdown” in Wuhan
  • January 24: First imported C19 cases reported in Europe (France)
  • January 27: US CDC issues Level 3 travel warning for China, recommending against non-essential travel
  • January 27: First documented SARS-CoV-2 transmission in Europe (Germany)
  • January 29: First C19 cases reported in Eastern Mediterranean Region (United Arab Emirates)
  • January 30: WHO declares C19 a Public Health Emergency of International Concern
  • January 30: US CDC confirms first domestic transmission of SARS-CoV-2
  • January 31: US implements travel restrictions for Mainland China
  • February 5: The Diamond Princess cruise ship is quarantined in Yokohama, Japan, due to an ongoing C19 outbreak onboard that resulted in at least 712 confirmed cases, including 9 deaths
  • February 25: First C19 case reported in the African Region (Algeria)
  • February 27: South Korea surpasses China as #1 globally in terms of daily C19 incidence
  • February 29: US implements travel restrictions for Iran
  • March 4: Seattle and King County, Washington (US), advises high-risk individuals to avoid large gatherings
  • March 8: Italy implements “lockdown” for affected areas of the Lombardy region in Northern Italy
  • March 10: Italy expands “lockdown” measures to the entire country
  • March 11: US implements travel restrictions for all of Europe
  • March 11: WHO declares C19 a pandemic
  • March 13: US declares the C19 epidemic to be a national emergency
  • March 14: US implements travel restrictions for the UK and Ireland
  • March 15: National “lockdown” goes into effect in Spain
  • March 16: Six counties in the San Francisco Bay Area, California (US), issue the country’s first shelter-in-place orders
  • March 18: The WHO announces the SOLIDARITY Trial, a global collaboration to conduct clinical trials for prospective C19 medical countermeasures
  • March 19: California (US) issues the first statewide “stay at home” order
  • March 23: The University of Oxford (UK) begins enrolling patients for the RECOVERY Trial, a nationwide clinical trial effort in the UK for C19 MCMs
  • March 24: National “lockdown” ordered in India
  • March 24: The International Olympic Committee announces that the 2020 Olympic Games, scheduled to be hosted in Japan, are postponed
  • March 27: US CDC expands travel restrictions to cover all other countries
  • March 28: US CDC issues domestic travel advisory for New York, New Jersey, and Connecticut
  • March 28: Italy surpasses China as #1 globally in terms of cumulative C19 incidence
  • March 29: US surpasses Italy as #1 globally in terms of cumulative C19 incidence (and remains #1 today)
  • April 4: 1 million global cases
  • May 15: US government unveils Operation Warp Speed, a program to drive development and production of medical countermeasures against C19
  • May 17: WHO reports more than 100,000 new cases in a single day
  • May 23: 5 million global cases
  • May 24: US implements travel restrictions for Brazil
  • May 28: US surpasses 100,000 cumulative reported C19 deaths
  • May 29: New York (US) enters Phase 1 of recovery (NYC on June 8)
  • June 8: New Zealand declares SARS-CoV-2 eliminated
  • June 11: European Commission recommends that European countries remove internal border restrictions by June 15 to enable travel within the continent
  • June 29: 10 million global cases
  • June 30: 500,000 global deaths
  • June 30: European Council announces that European countries would lift travel restrictions for 15 countries beginning July 1
  • The global situation has evolved dramatically since the onset of the pandemic. The initial focus was on Wuhan, as China instituted a strict “lockdown” of the city and its 11 million inhabitants that lasted months. The “lockdown” involved highly restrictive social and physical distancing measures, including a prohibition on entering or leaving the lockdown area. The virus quickly spread to and within countries around the world, gaining a foothold in communities in Europe, the Eastern Mediterranean, and the US that ultimately resulted in major national epidemics. As transmission increased across Europe and in the US, China successfully contained its epidemic. In addition to the “lockdown” in Wuhan, Chinese officials implemented intense contact tracing and testing efforts and rapidly expanded local health system capacity, including through the construction of modular hospital facilities.
  • As China contained the disease, the global C19 burden shifted toward Europe and the US. As some countries began to gain control of their national epidemics, they looked ahead to relaxing social distancing measures and resuming social and economic activities. Some took slow, incremental approaches, while others progressed more rapidly. The pandemic continued to shift, sparking major epidemics in the Central and South American, Eastern Mediterranean, and South Asian regions, preying on areas that had not yet been severely affected. Portions of the US, particularly the New York City area, were severely affected early in the pandemic, but the country was able to begin bringing its epidemic under control from mid-April through the end of May, even as incidence shifted away from New York to other states and regions. As states began to ease social distancing measures, allowing “stay at home” and other statewide or regional orders to expire and promoting social and economic activity, areas that had not yet been severely affected began to report rapidly increasing incidence and other concerning C19 trends.
  • Six months into the pandemic, the situation does not necessarily appear promising, but there is hope for the future. 
  • Global incidence continues to increase exponentially, largely driven by major epidemics in multiple large countries, including Brazil, India, Mexico, and the US. And while most African countries have not reported elevated incidence, there is concern that limitations in testing and reporting may not be fully capturing the scale of the pandemic on the continent. Many experts believe that C19 risk is growing and that we could be at the very beginning of a more serious “wave” of transmission that could last for months or longer. 
  • Despite these concerning trends, there remains hope for the coming months. Numerous countries—including China, Italy, South Korea, Spain, and others that were severely affected early in the pandemic—have successfully brought their epidemics under control and achieved relatively low levels of transmission. New Zealand stands as an example to the rest of the world, having successfully eliminated C19 earlier in June. These countries are providing templates for successful national-level responses and sharing lessons that other countries can leverage to improve their containment efforts.
  • Numerous efforts around the world are ongoing to develop, identify, and produce effective medical countermeasures against C19. Several treatments have demonstrated some efficacy against C19, including remdesivir and dexamethasone, and efforts are ongoing to develop and evaluate other treatment options. Perhaps even more critically, multiple promising vaccine candidates are progressing through various stages of clinical trials, and governments and other organizations are already investing to establish and scale up production capacity, in anticipation of positive future results, in order to increase availability as soon as an efficacious product is identified. Efforts are also ongoing to ensure that treatments and vaccines are available globally to promote equitable distribution for all countries as soon as possible.
  • The C19 pandemic is far from over, but we are gaining experience and tools on a daily basis to improve our ability to combat it. Scientists, health practitioners, and other experts continue to learn more about the disease and the virus that causes it. We have a long way to go and a lot of hard work ahead of us, but we can and will bring this pandemic under control. Each of us plays an important role, whether contributing directly to response operations as a frontline healthcare worker or public health official, ensuring the continuation of community services and infrastructure as an essential worker, developing and implementing policies as a researcher or elected official, or taking appropriate protective measures as part of your daily life.
  • Wear your mask, maintain physical distance, wash your hands, and stay home when you are sick. We are all in this together, even if we are 6 feet apart.
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