Recent Developments & Information
June 8, 2020
“Some schools may have no problem welcoming students back in the fall, but the decision to reopen depends on the rate of infection in specific areas. But, it won’t be necessary to keep schools closed next year.”Dr. Fauci
“The frequency of superspreading is beyond anything we could have imagined. If we could stop the superspreading from happening, we’d benefit the most people.”Ben Cowling, researcher
“Not everyone who has had the virus will produce detectable antibodies, and many may have used a different immune response in order to attack the virus.”Professor Karol Sikora, advisor to the World Health Organization
Index Of Featured Stories & Links
Note: All of the stories listed below are included in this Update, but we have included links to the stories upfront so that you can quickly jump to a story if you want.
- Statistics Point To Reality of Threat
- Immunological Dark Matter: Up to 80% Not Susceptible to C19
- Is the Virus Weakening?
- Coronavirus appears to be declining in potency
- New Scientific Findings
- Coronavirus Has Become Less Lethal (And Other Good News)
- Only 10% of coronavirus patients develop antibodies (!)
- Most infected people do not spread coronavirus to others (!)
- Scientists find link between C19 severity and genetics
- New Genetic Identification of C19 Susceptibility Will Aid Treatment
- Studies yield clearer picture of rare COVID-linked syndrome in kids
- Potential Treatments
- Breakthrough close on cloned antibodies that counteract C19
- FDA Approved Drug May Help Calm Cytokine Storm in C19
- PAC-MAN: Scientists Aim Gene-Targeting Breakthrough Against C19
- Projections & Our (Possible) Future
- When C19 Converges With the Next Flu Season – How Do We Prepare?
- New Model Predicts Peaks of the C19 Pandemic Around the World
- Practical Tips & Other Useful Information
- Scientists Test Best Fabric Choices for Homemade COVID Mask
- The Road Back?
- How Businesses Can Keep Employees Safe From Coronavirus
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A. Our World As Seen Through Headlines
(In No Particular Order)
- World Health Organization reverses position on face masks as coronavirus cases climb
- New Report Documents Most COVID-19 Deaths Occurred in Nursing Homes – Up to 81% in Some States
- High Blood Pressure Raises COVID Mortality Risk By 2x
- New York City reopens under Phase One on Monday
- NY Gov. Cuomo accelerates reopening plans as NY coronavirus deaths drop to record low
- It’s Covid Code Red in Latin America With No Signs of Peaking
- California Says Live Sports, Film Production Can Resume June 12
- Post-Lockdown Mideast Shows Signs of Virus Trouble Returning
- Amid reopenings and street protests, coronavirus transmission remains high in much of the U.S.
- Hurricane preparedness meets coronavirus caution as Cristobal bears down
- Dr. Fauci: China ‘did a disservice’ by withholding coronavirus info
- New York will allow groups of 150 to gather this month for graduations, Gov. Cuomo says
- NYC to open 15 coronavirus testing sites for protesters, Gov. Cuomo says
- NYPD eyes ‘pandemic drone’ nixed in Connecticut after backlash
- US Senator Rick Scott accuses China of trying to sabotage coronavirus vaccine
- Dr. Fauci: No Doubt Protests Can Spread Virus
- NY Gov. Cuomo says concerned protests could spark COVID resurgence
- Unemployment rate drops to 13.3% in May, signaling return of US jobs
- Trump touts surprise job gains, calls on states to end coronavirus lockdowns
- Some parts of the U.S. are facing financial ruin but have few coronavirus cases
- Coronavirus face masks should be worn in public, WHO says in updated guidance
- Officials who pushed strict lockdowns now argue protesters are an exception
- Mexico records more coronavirus deaths in a day than in United States
- Brazil’s daily deaths exceed 540, second highest in world
- Brazil has second highest number of total cases, and third highest number of total deaths
- Brazilian government stops publishing critical virus data on deaths and confirmed cases
- Chile’s daily deaths surge to 649, highest in world
- India Has Biggest 1-Day Jump in Cases, Again
- Hospitals in Delhi reserving more space for COVID-19 patients
- Saudi Arabia sees cases top 100,000
- Vaccines group raises $8.8 billion for immunization plans for poor countries
- MI Gov. Whitmer Joins Protests, Ignoring Her Social Distancing Guidelines, Surrounded by People Without Masks
- Dr. Fauci gives reassurance on school reopenings
- Restaurant bookings have fully recovered in Germany in a sign that activity rebounds quickly as lockdowns ease
- No lockdown for protests — so why keep businesses closed?
- U.S. Agencies Work With WHO Despite Trump Threat to Cut Ties
- U.S. Still Underprepared for Pandemic Threats, CDC Head Says
- German Economy Set to Shrink 7% Even With Recovery Underway
- Coronavirus casts cloud over D-Day commemoration in Normandy
- After Saying “Stay Home, Save Lives” And Shutting Parliament, Trudeau Attends Packed Protest Without Social-Distancing
- Health Professionals Support Floyd Protests – but Disapprove of Lockdown Protests
- The Expat Life Is Struggling to Survive Covid-19
- Singapore Considers Wearable Tech Devices For All to Trace Virus
- Fauci, Virus Task Force Vanish With Trump All-In on Reopen
- Roller-skating surges in popularity during the coronavirus pandemic
- Peru is running out of oxygen for coronavirus patients
- Support for four-day workweek soars amid coronavirus crisis
- Duh Blasio: Mayor can’t explain spike in NYC COVID-19 hospitalizations
- Huawei adds temperature-taking sensor to newest smartphone
- Cities will make a comeback after the coronavirus. They almost always do.
- China Denies Cover-Up, Rejects ‘Politicization’ of Coronavirus
- The CDC’s troubling blindspot
- Iran’s coronavirus cases surge again as strategic province becomes new epicenter
- AstraZeneca lays out plan for producing 2 billion doses of Covid-19 vaccine, if it works
- Race, Ethnicity Data To Be Required With Coronavirus Tests In U.S.
- Pandemic re-emphasizes need for universal flu vaccine
- Gavi launches innovative financing mechanism for access to COVID-19 vaccines
- Support for four-day workweek soars amid coronavirus crisis
- Apple reportedly offers coronavirus tests to returning employees
- De Blasio: Construction sites will be first step in coronavirus reopening
- Mexico is slowly reopening, but some worry that it’s still too fast
- The pandemic is making a no-deal Brexit more likely
- The U.S. is still confirming more than 20,000 new cases a day, with counts rising in the South and West
- The federal government undercounted the number of virus deaths in U.S. nursing homes
- Trump tells governor of Maine: ‘You better get the state open.’
- NYC Mayor de Blasio rips cops for not wearing masks to protests
- Michigan Supreme Court Unanimously Sides with 77-Year-Old Barber over Gov. Gretchen Whitmer
- Way too many Americans have gargled with bleach, sprayed their bodies with disinfectants to prevent COVID-19
- Las Vegas Casinos Reopen After 78-Day Coronavirus Lockdown
- Gamblers ignore COVID-19 safety measures as Las Vegas casinos reopen
- Las Vegas reopens with a new ethos: ‘Think dirty thoughts but keep your hands clean.’
B. Key Numbers & Trends
Note: Unless otherwise noted, all cases/deaths are confirmed cases/deaths that have been reported. All numbers reported in this Update as of the end of the most recent reporting period (reporting periods end each day at 11:59 pm Greenwich Time, or 7:59 pm NYC Time), and all changes reflect changes since the day preceding the end of the most recent reporting period. Please note that the reporting of cases/deaths for a state/country may be delayed (which often occurs over weekends and holidays), and the number of cases/deaths for a state/country can be revised, which can result in some unusual short-term changes in numbers.
1. Cases & Tests
- Total Cases = 7,082,212 (+1.6%)
- New Cases = 113,852 (-14,187)
- Growth Rate of New Cases (7 day average) = 1.8% (-0.1%)
- New Cases (7 day average) = 120,522 (+696)
- Although the number of new cases worldwide has been trending higher, the growth rate in new cases has declined significantly over the past 6 weeks.
- The current 7 day average growth rate for new cases (1.8%) is significantly less than the 7 day average growth rate for new cases for the week ending 4/26/20 (3.3%), which is a 45% reduction in the average daily growth rate over the past 6 weeks.
- Total Cases = 2,007,449 (+1.0%)
- New Cases = 18,905 (-3,931)
- Growth Rate of New Cases (7 day average) = 1.2% (+0%)
- New Cases (7 day average) = 22,203 (-260)
- Total Number of Tests = 21,291,677
- Percentage of positive tests (7 day average) = 4.6% (-0.3%)
- The 7 day average growth rate of new cases is stable, which is positive. But, more significantly, the current 7 day average growth rate of 1.2% is substantially less than the 7 day average growth rate for new cases for the week ending 4/26 (3.8%), which is a 68.5% reduction in the average daily growth rate over the past 6 weeks.
- The 7 day average number of new cases has decreased slightly, which is a positive trend, particularly in light of large number of tests
- The 7 day average percentage of positive tests continues to decline, which is also a positive trend and perhaps the best indicator that the virus is not spreading on a large scale (although there may be hotspots where the virus is spreading significantly)
- Total Deaths = 405,081 (+0.8%)
- New Deaths = 3,381 (-871)
- Growth Rate of Deaths (7 day average) = 1.6% (-0.1%)
- New Deaths (7 day average) = 4,483 (+27)
- Total Deaths = 112,469 (+0.3%)
- New Deaths = 373 (-333)
- Growth Rate of Deaths (7 day average) = 0.8% (-0.1%)
- New Deaths (7 day average) = 896 (-38)
- 373 deaths is the lowest number of daily deaths since March 26
- Growth rate of new deaths has been decreasing, which is a positive trend. The growth rate decreased from 1.17% to 0.33% over the last 4 days, a decrease of almost 72%.
C. Statistics Point To Reality of The Threat
[Note: While there is much we do not yet know about the coronavirus and C19, statistics is a powerful tool that can prove (or disprove) assumptions that have been made about the transmission and spread of the coronavirus. We have known for some time that the initial projections regarding the spread of the virus were off the mark by a substantial margin. But why? Some scientists are suggesting that the slowdown of the spread is not the result of lockdowns and something else is at play. If proven to be true, the implications for our society and economy cannot be overstated.]
1. Immunological Dark Matter: Up to 80% Not Susceptible to C19
- Just one month ago, the idea that most people aren’t susceptible to C19 — perhaps the overwhelming majority — was considered dangerous denialism. It was startling when Nobel-prize-winning scientist Michael Levitt argued at the start of May argued at the start of May that the growth curves of the disease were never truly exponential, suggesting that some sort of “prior immunity” must be kicking in very early. [Note: The story on Michael Levitt’s views can be found here.]
- Today, though, the presence of some level of prior resistance and immunity to C19 is fast becoming accepted scientific fact.
- Results have just been published of a study suggesting that 40%-60% of people who have not been exposed to coronavirus have resistance at the T-cell level from other similar coronaviruses like the common cold. [Note: This study can be found here.]
- Now, from the unlikely source of a prominent member of the “Independent SAGE committee”, the group set up by Sir David King to challenge government scientific advice and accused by some of being populated with Left-wing activists, comes a claim that the true portion of people who are not even susceptible to C19 may be as high as 80%.
- Professor Karl Friston, like Michael Levitt, is a statistician not a virologist; his expertise is in understanding complex and dynamic biological processes by representing them in mathematical models. Within the neuroscience field he was ranked by Science magazine as the most influential in the world, having invented the now standard “statistical parametric mapping” technique for understanding brain imaging — and for the past months he has been applying his particular method of Bayesian analysis, which he calls “dynamic causal modelling”, to the available C19 data.
- Friston referred to some kind of “immunological dark matter” as the only plausible explanation for the huge disparity in results between countries in an interview with the Guardian last weekend. The eye-catching phrase attracted a lot of attention on social media, with some commentators keen to dismiss it as rubbish, but he meant it in a quite precise way: like dark matter, the undetectable substance that makes up approximately 85% of the universe, it is provably there by its effects. We just don’t know anything about it. [Note: Friston’s interview with the Guardian can be found here.]
- His models suggest that the stark difference between outcomes in the UK and Germany, for example, is not primarily an effect of different government actions (such as better testing and earlier lockdowns) but is better explained by intrinsic differences between the populations that make the “susceptible population” in Germany — the group that is vulnerable to C19 — much smaller than in the UK.
- As he told me in our interview, even within the UK, the numbers point to the same thing: that the “effective susceptible population” was never 100%, and was at most 50% and probably more like only 20% of the population. He emphasizes that the analysis is not yet complete, but “I suspect, once this has been done, it will look like the effective non-susceptible portion of the population will be about 80%. I think that’s what’s going to happen.”
- Theories abound as to which factors best explain the huge disparities between countries in the portion of the population that seems resistant or immune — everything from levels of vitamin D to ethnic-genetic and social and geographical differences may come into play — but Professor Friston makes clear that it does not primarily seem to be a function of government coronavirus policy. “Solving that — understanding that source of variation in terms of this non-susceptibility — is going to be the key to understanding the enormous variation between countries,” he said.
- Professor Friston is ultra-cautious in his choice of words, and understandably so: the impact of this realization, if proven correct, is hard to overstate.
- Immediately it would change how we should think about lifting lockdown: a tube carriage in London might in theory have to be restricted to 15% capacity to maintain social distancing of 2 meters, but if, as Professor Friston believes, the susceptible population in London was only ever 26% and 80% or more of that group is now probably immune via antibody testing, you can put a lot more people in a tube carriage without increasing the level of risk. Ditto restaurants, pubs, theatres and most recently, MPs in parliament. It would question the whole idea of social distancing being a feature of any “new normal”.
- It would take the heat out of the political argument around the pandemic, and give the lie to the idea that it was ever primarily government actions (however incompetent or incompetently executed) that explain differing death rates. As Professor Friston puts it, once you put into the model sensible behaviors that people do anyway such as staying in bed when they are sick, the effect of legal lockdown “literally goes away”.
- His explanation for the remarkably similar mortality outcomes in Sweden (no lockdown) and the UK (lockdown) is that “they weren’t actually any different. Because at the end of the day the actual processes that get into the epidemiological dynamics — the actual behaviours, the distancing, was evolutionarily specified by the way we behave when we have an infection.”
- Most significantly, it would mean that the principal underlying assumption behind the global shutdowns, typified by the famous Imperial College forecasts — namely, that left unchecked this disease would rapidly pass through the entire population of every country and kill around 1% of those infected, leading to untold millions of deaths worldwide without draconian action — was wrong, by a large factor.
- The largest coordinated government action in history, forcibly closing down most of the world’s societies with consequences that may last for generations, would have been based on faulty science.
- When I put this to Professor Friston, he was the model of collegiate discretion. He said that the presumptions of Neil Ferguson’s models were all correct, “under the qualification that the population they were talking about is much smaller than you might imagine”. In other words, Ferguson was right that around 80% of susceptible people would rapidly become infected, and was right that of those between 0.5% and 1% would die — he just missed the fact that the relevant “susceptible population” was only ever a small portion of people in the UK, and an even smaller portion in countries like Germany and elsewhere. Which rather changes everything.
- With such elegant formulations are scientific reputations saved. Practically, it makes not much difference whether, as per Sunetra Gupta, the 40,000 officially-counted coronavirus deaths in the UK are 0.1% of 40 million people infected, or, as per Karl Friston’s theory implies, they are more like 0.5% of 8 million people infected with the remaining 32 million shielded from infection by mysterious “immunological dark material”. If you are exposed to the virus and it is destroyed in your body by mucosal antibodies or T-cells or clever genes so that you never become fully infected and don’t even notice it, should that count as an infection? The effect is the same: 40,000 deaths, not 400,000.
- This wouldn’t mean that most of the population is technically immune to C19 — scenarios with a very high viral load, such as doctors treating C19 patients in hospitals may still overpower these defenses — but it would mean under normal circumstances, most people would never have contracted the disease.
- The atmosphere in the UK continues to change irrespective of Government policy, and if people ever were afraid they are becoming less so, having intuited that, for now at least, the coronavirus threat seems to be in retreat. Gradually, the scientists are providing explanations for why that might be.
[Note: As an example of the importance of this theory, if proven to be correct, the fatality rate for C19 would drop from 0.026% to 0.008%. In other words, the fatality rate for C19 would drop from 2.6x the fatality rate of the flu to 0.8x (or 20% less than) the fatality rate of the flu. However, the population susceptible to dying from C19 may be quite different than the population susceptible to dying from the flu.]
D. Is the Virus Weakening
1. Coronavirus appears to be declining in potency
- Doctors at the University of Pittsburgh Medical Center say the coronavirus appears to be becoming less potent.
- Dr. Donald Yealy, chair of emergency medicine at UPMC, explained at a press conference on Thursday that people seem to be contracting the virus less easily and cases appear to be less severe then when the pandemic first took hold in the US early this year.
- ‘The virus may be changing,’ Yealy said. ‘Some patterns suggest the potency is diminished.’
- He noted that UPMC has successfully treated more than 500 coronavirus patients since March, and in recent weeks fewer patients are requiring ventilators to help them breathe.
- Less than 4% of all tests and only 0.2 percent of tests in asymptomatic patients are coming back positive, he said, indicating that the virus is less prevalent in the communities UPMC serves.
- The doctors’ findings that the virus could be declining in potency came days after researchers in Italy announced that patients there were showing much smaller amounts of the virus in their system, compared to samples taken during the peak of the crisis in March and April.
- Professor Alberto Zangrillo, head of intensive care at Italy’s San Raffaele Hospital in Lombardy, went so far as to say that the virus ‘clinically no longer exists’ during a Sunday interview on state television.
- But World Health Organization experts and a range of other scientists quickly rejected Zangrillo’s claims on Monday, saying there is no evidence to support the assertion that the coronavirus has been losing potency.
- ‘In terms of transmissibility, that has not changed, in terms of severity, that has not changed,’ WHO epidemiologist Maria Van Kerkhove told reporters.
- It is not unusual for viruses to mutate and adapt as they spread.
- Martin Hibberd, a professor of emerging infectious disease at the London School of Hygiene & Tropical Medicine, said major studies looking at genetic changes in the coronavirus did not support the idea that it was becoming less potent, or weakening in any way.
- ‘With data from more than 35,000 whole virus genomes, there is currently no evidence that there is any significant difference relating to severity,’ he said in an emailed comment.
- Zangrillo, well known in Italy as the personal doctor of former Prime Minister Silvio Berlusconi, said his comments were backed up by a study conducted by a fellow scientist, Massimo Clementi, which Zangrillo said would be published next week.
- Zangrillo told Reuters: ‘We have never said that the virus has changed, we said that the interaction between the virus and the host has definitely changed.’
- He said this could be due either to different characteristics of the virus, which he said they had not yet identified, or different characteristics in those infected.
- The study by Clementi, who is director of the microbiology and virology laboratory of San Raffaele, compared virus samples from C19 patients at the Milan-based hospital in March with samples from patients with the disease in May.
- ‘The result was unambiguous: an extremely significant difference between the viral load of patients admitted in March compared to’ those admitted last month, Zangrillo said.
- Oscar MacLean of the University of Glasgow’s Centre for Virus Research said suggestions that the virus was weakening were ‘not supported by anything in the scientific literature and also seem fairly implausible on genetic grounds’.
- Experts and representatives of Johns Hopkins University, Wake Forest Baptist Medical Center, George Washington University and Northwell Health also said they were not aware of evidence suggesting that the virus had changed.
- ‘The suggestion by the Italian doctor is potentially dangerous as it gives false reassurance based on no evidence,’ said Leana Wen, an emergency physician and public health professor at George Washington University.
- ‘There is no scientific evidence for there having been a change in the coronavirus. It’s a highly transmittable and highly contagious disease. We need to be as on guard as ever.’
[Note: One might think that the WHO, which just flip-flopped on the importance of wearing a mask and originally said that there was no evidence of person-to-person transmission of the coronavirus, might show a bit more humility in making pronouncements about a disease that they admittedly do not understand.]
E. New Scientific Findings & Other Research
1. Coronavirus Has Become Less Lethal (And Other Good News)
- A new study finds that the coronavirus has become less lethal over the past few months. While there’s no evidence that mutations are making the virus less deadly, treatments have improved enormously as scientists have learned more.
- Doctors have observed that the coronavirus case-fatality rate seems to have decreased considerably since the early days of the pandemic. But a pre-publication study from Italian universities and local public-health authorities comparing the case-fatality rates in two provinces (Ferrara and Pescara) during March and April is the first to show this might be true.
[Note: Read the study here.]
- After adjusting for age and comorbidities, the study found the overall death rate declined by some 40% from March to April with huge reductions in:
- Greater than age 80 (from 36.3% to 16.1%)
- Patients with hypertension (23% to 12.1%)
- Patients with diabetes (30.3% to 8.4%)
- Patients with cardiovascular disease (31.5% to 12.1%)
- Patients with COPD (29.7% to 11.4%)
- Patients with Renal disease (32.3% to 11.5%)
- The study’s findings need to be confirmed by more studies of fatality rates over time in other places. But the researchers note that the decline in death rates is unlikely to be due to less crowded hospitals since infection rates were low in the two provinces and never exceeded the intensive care unit capacity. Hospital utilization could confound results in other hot spots.
- They say their study confirms anecdotes from expert physicians that “the early administration of more tailored medications, is considerably improving the clinical course of C19.” Doctors are using a cocktail of targeted therapies including repurposed HIV antivirals, anticoagulants and monoclonal antibodies like tocilizumab that lower inflammatory cytokine attacks on organs.
- A European Journal of Internal Medicine study last month found that two of 62 patients receiving tocilizumab died compared to 11 of 23 in a group with similar characteristics. Randomized clinical trials are needed to draw solid conclusions about the efficacy of drug treatments, but they usually take months. So doctors have been experimenting and learning on the fly.
- We now know, for instance, that deaths among severely ill patients often result from an overreactive immune response known as “cytokine storms” as well as systemic blood clots. The FDA this week approved a new blood test by Roche that measures levels of the inflammatory-causing protein interleukin-6 and can help predict patients at risk for cytokine storms. Using drugs to break up blood clots and calm down the immune system earlier can prevent severe cases from turning deadly.
- Doctors have also observed that some patients with fatally low oxygen levels aren’t gasping for air or losing consciousness and their symptoms resemble altitude sickness [Hypoxia]—dizziness, nausea and headaches—more than pneumonia or acute respiratory distress. As a result they are using less intensive ventilation such as nasal cannulas and sleep-apnea machines.
- Mechanical ventilators can cause long-term brain and respiratory damage as well as secondary infections. A study in the Journal of the American Medical Association has found that a shockingly high 80% of those between ages 18 and 65 who were placed on ventilators in New York City died while just 2.4% were discharged alive during the study period. More targeted therapeutics can reduce the need for ventilators.
- The FDA last month approved Gilead’s antiviral remdesivir for emergency use after a phase-one trial found that the drug reduced recovery times in hospitalized patients on average to 11 days compared to 15 days for those in a control group. Remdesivir stops the virus from replicating, so it may be even more beneficial if administered earlier in the illness.
- The treatment learning curve has been as steep as the infection curve. But even if there’s a second C19 wave, it is likely to be less deadly than the first.
Source: Coronavirus Good News
2. Only 10% of coronavirus patients develop antibodies
- Only 10% of people who are infected with the coronavirus develop antibodies, a professor claims.
- Professor Karol Sikora, an advisor to the World Health Organization, said the majority would have a negative result on an antibody test, even though they have had the coronavirus.
- Governments have pinned their hopes on antibody testing to understand how much of the population has been infected to guide the easing of lockdown.
- These people – given the nicknames ‘immuno privileged’ or the ‘Covid elite’ – would be able to return to work or socially mingle with an ‘immunity passport’.
- But not everyone who has had the virus will produce detectable antibodies, and may have used a different immune response in order to attack the virus. For example, T cells are one of the first lines of defense and act before antibodies are even needed.
- Some parts of the immune response remain a complete mystery to scientists and are unable to measure.
- It means it may never be possible to measure the scale of the pandemic or pick out those who have definitely had the coronavirus and have some sort of protection.
- Surveillance testing suggests that 8.5% of people in England have already had the coronavirus, based on measuring antibodies. But scientists say the true figure is likely to be far higher.
- Antibodies are proteins that develop in response to a foreign pathogen over a few days. They are also created when a vaccine that imitates the virus is injected.
- The immune system remembers the antigen so that if a person is exposed to it again, it can produce antibodies quicker.
- These antibodies are present in the blood and the ‘have you had it’ tests are used to identify people who have previously had C19.
- ‘But there is a snag, and that’s that less than 10% of infected people have antibodies. That doesn’t mean only 10% have been infected. Probably far from it. ‘There are other immune defenses at play but we can’t measure that.’
- The immune system is a huge web of proteins that have different functions to protect the body against infection – and antibodies are just part of the picture.
- Professor Sikora, the chief medical officer at Rutherford Health, said the immune system is very sophisticated and there is a huge amount to uncover about how it works – especially in response to a coronavirus.
- He said: ‘There is what we call “immunological dark matter“. We don’t understand it, but it’s definitely protecting us. It may be one of the protections against the virus.’
- Antibodies, which latch on to the coronavirus and mark it for other immune cells to destroy, are part of the adaptive immune system.
- The adaptive immune response is much slower to respond to threats and infections than the ‘innate immune response’, which is primed and ready to fight at all times.
- The innate immune system is the immediate response to the virus, or the ‘first line of defense’. It includes some T cells, which both kill the virus directly and stimulate other immune cells to join in.
- Professor Sikora said there is ‘a hint’ that older people produce antibodies more often than those under 30 years old, and those who are more severely ill.
- ‘But other than that, there is nothing to identify them. There is nothing about racial characteristics either. It’s quite a mystery.’
- He added: ‘What you need is a test to identify those you don’t need to worry about. The problem is developing a test that is really specific, and we don’t know what to measure.’
- His comments follow research which shows most people who recover from the coronavirus generate a weak antibody response.
- Researchers from Rockefeller University in New York City looked at blood plasma samples from 149 recovered patients. They did not use an antibody test.
- They found every patient’s immune system seemed to be capable of generating the types of antibodies that neutralize and inactivate the virus, just not particularly enough of them.
- In fact, the neutralizing effect was undetectable in 33% of donors. The investigators say this may be because their immune systems cleared the infection before antibodies could be produced.
- They found that the effect was very high among 1% of patients, the so-called ‘elite’.
- Gus Dalgleish, a professor of oncology at University College London, told MailOnline he believes the majority of people fight the virus with T cells, based on research so far.
- He said: ‘If you have a good T cell response, it will protect you against the flu, the cold, or the coronavirus. This immune response declines dramatically over the age of 50 – which fits the people who get ill more quickly with the coronavirus.
- ‘Antibodies are a clear sign of many other infections. With this coronavirus, it doesn’t appear to be quite as clear.’
- It hasn’t stopped governments globally moving full steam ahead to buy millions of antibody tests in order to measure the size of the pandemic.
- The Department of Health and Social care have secured ten million antibody tests being conducted on NHS and social workers in the UK now. Health chiefs have lost at least £20million pounds trying to find one that reaches their standards.
- Health Secretary Matt Hancock said the deal with pharmaceutical companies Roche and Aboott was ‘an important milestone’ because it meant people on the frontline could finally find out if they had been infected.
- In the long term, the public may also be able to get their hands on a ‘have you had it’ test – either one that is sent to the laboratory or conducted from the comfort of your own home.
- Professor Sikora, former Director of WHO Cancer Programme, said: ‘When they [the Government] ordered the antibody tests they thought it would be of great importance. I don’t think it will be particularly helpful.
- ‘The hope was the antibody test would identify you as having recovered so you could get back to work. We were hoping it would be at least 50%, but it hasn’t worked out like that.
- ‘We started testing people in cancer centers six weeks ago and I was disappointed at the results. Less than 6% of people had antibodies. It’s not significant.
- ‘I have had the coronavirus, but I haven’t got antibodies.’
- An estimated 8.5 to 10% of England’s population (4.76 million to 5.6million) have had the coronavirus, according to the government-run surveillance scheme which uses blood samples taken from almost 8,000 people.
- Regional variations show that the rate of infection has been considerably higher in London, with 15.6% of the city’s population already affected. And it has been lowest in the South West, where only 2.6% of people are thought to have had the virus.
- Professor Dalgleish said he believes there are far more people who have had the virus but are being unaccounted for in estimations.
- Not only do the majority of people not appear to produce antibodies, but it’s not clear for how long they can be detected in somebody’s blood after infection.
- Professor Dalgleish said: ‘There is a picture emerging that people can have antibodies against it but they wane quite quickly.
- ‘I’ve seen evidence of people who have definitely had the virus but they can’t find antibodies in them months later.’
- ‘It makes finding the number of people who have been exposed to the virus very difficult to nail.’
- It also has implications for the vaccine, Professor Dalgleish warns.
- Speaking of vaccines in clinical trials, including that developed by Oxford University, he said: ‘It has been designed in a classical way, but is it going to work if the antibodies fade quickly?’
- Scientists are concerned that the focus on antibodies will off-rail the development of a vaccine.
- Vaccines help develop immunity by imitating an infection, causing the immune system to produce antibodies that remember how to fight the foreign pathogen.
- The early signs a vaccine works is conferred by the presence of antibodies – which scientists are warning is not a given and may not be as important as T cells.
- Professor Dalgleish said: ‘I propose a vaccine that uses T cells. We have a T cell boosting vaccine in cancer patients and none of them, even those over 70, get viral infections.’
3. Most infected people do not spread coronavirus to others
- Most coronavirus infections are caused by “superspreaders” – people who spread the infection to a large number of people, according to a new study carried out by a group of epidemiologists in Hong Kong.
- “Approximately 20% of coronavirus infections are responsible for 80% of all transmission events in Hong Kong,” the researchers noted.
- They also found that all incidents of spreading occurred indoors and that 70% of those infected did not spread the virus to others.
- “Superspreading events are happening more than we expected, more than what could be explained by chance. The frequency of superspreading is beyond what we could have imagined,” Ben Cowling, one of the study’s co-authors, told Business Insider. “”Now we know which measures might give you the most bang for your buck – if we could stop the superspreading from happening, we’d benefit the most people.”
- The researchers examined several clusters of infections in Hong Kong. While there were several causes for the spread of the coronavirus, most people were infected at social events where one person spread the infection.
- “Overall the majority (51.9%; 539/1,038) of coronavirus infections in Hong Kong have been associated with at least one of 135 known clusters,” the researchers noted. “The remaining 38.9% (210/539) of cluster cases solely involved imported cases where no onward local transmission could be identified.”
- Some 1,037 cases – occurring from when the first case was confirmed in Hong Kong on January 23 until April 28 – were examined.
- The research was published on the website Research Square, a pre-print publication, where research has yet to be peer reviewed and the results cannot therefore be considered conclusive.
- Read the study here.
4. Scientists find link between C19 severity and genetics
- Genetic variations may be what causes different people to suffer from different symptoms of the coronavirus, according to a new study by European scientists, The New York Times reported.
- The study, which has not been peer-reviewed yet, is the first to find a strong statistical link between genetic variations and C19, the illness caused by the coronavirus.
- Variations at two spots in the human genome are associated with an increased risk of respiratory failure in C19 patients, according to the study. Patients with Type A blood were linked to a 50% increase in the likelihood in needing to get oxygen or go on a ventilator, reported the Times.
- Oddly enough, variations in ACE2, the protein to which the virus attaches itself on the surface of human cells, did not seem to make a difference in the severity of the virus.
- “There are new kids on the block now,” said Andre Franke, a molecular geneticist at the University of Kiel in Germany and a co-author of the new study, according to the Times.
- While age and preexisting conditions have already been found to increase the risk of severe cases of C19, geneticists are hoping that DNA tests could help identify at-risk patients as well.
- The study was conducted by taking blood samples from 1,610 patients who needed an oxygen supply or were put on a ventilator and 2,205 blood donors with no evidence of C19. DNA was extracted from the samples and scanned with genotyping.
- The scientists found two spots in the genome, known as loci, shared by an unusually high number of severely ill patients compared with those who were not ill, including one locus which determines our blood type.
- Chinese scientists also found that patients with blood type A were more likely to develop a severe case of C19, according to the Times.
- While the Chinese study does support the new study, questions remain on why blood type affects the severity of the illness. “That is haunting me, quite honestly,” said Franke.
- The locus where the blood-type gene is located also contains DNA that acts an on-off switch for a gene producing a protein that triggers strong immune responses.
- The novel coronavirus triggers an overreaction of the immune system in some people, leading to inflammation and lung damage. It could be that genetic variations influence that response.
- The second locus found in the study, on Chromosome 3, has an even stronger statistical link to C19, but the spot houses six genes so it’s still unclear which one influences the severity of the illness, according to the Times.
- One of the six genes encodes a protein known to interact with ACE2, but another nearby gene encodes a potent immune-signaling molecule. It could be that this gene triggers an overreaction as well.
- A thousand researchers in 46 countries, including the European scientists involved in the new study, are collecting DNA samples from people with C19 and sharing the data on the website of the C19 Host Genetics Initiative.
- Andrea Ganna, a genetic epidemiologist at the University of Helsinki, said that the collected data of the initiative were beginning to point to a single spot on Chromosome 3 as a potentially important factor, according to the Times.
- Jonathan Sebat, a geneticist at the University of California, San Diego, told the Times that it’s uncommon for genetic variants to emerge out of studies of so few people.
- “We were all hoping optimistically this was one of those situations,” said Sebat, who is running a study in California to see if the two loci are as important as they seem.
- Sebat stressed that the study focused on patients with respiratory issues.
- Scientists conducting further studies may be able to zero in on exactly which gene in each locus affects the disease and may likely find many other genes with subtler influences on the course of the illness.
- The variation in severity between patients has been attributed to other factors, including different strains of the virus, as well.
- Over 30 different strains of the coronavirus were found in a study carried out in April by Professor Li Lanjuan and colleagues from Zhejiang University in Hangzhou, China and published in a non-peer reviewed paper released on website medRxiv.org.
- Li ‘s team infected cells with C19 strains carrying different mutations, of which the most aggressive strains were found to generate as much as 270 times as much viral load as the weakest strains. The aggressive strains also killed the human cells the fastest.
- The results indicated “that the true diversity of the viral strains is still largely underappreciated,” Li wrote.
- “Drug and vaccine development, while urgent, need to take the impact of these accumulating mutations into account to avoid potential pitfalls,” the scientists said.
5. New Genetic Identification of C19 Susceptibility Will Aid Treatment
- The clinical presentation of C19 varies from patient to patient, and understanding individual genetic susceptibility to the disease is therefore vital to prognosis, prevention, and the development of new treatments.
- For the first time, Italian scientists have been able to identify the genetic and molecular basis of this susceptibility to infection as well as to the possibility of contracting a more severe form of the disease.
- Professor Alessandra Renieri, Director of the Medical Genetics Unit at the University Hospital of Siena, Italy, said that her team’s GEN-COVID project to collect genomic samples from C19 patients across the whole of Italy in order to try to identify the genetic bases of the high level of clinical variability they showed. Using whole exome sequencing (WES) to study the first data from 130 Covid patients from Siena and other Tuscan institutions, they were able to uncover a number of common susceptibility genes that were linked to a favorable or unfavorable outcome of infection.
- “We believe that variations in these genes may determine disease progression,” says Prof Renieri. “To our knowledge, this is the first report on the results of WES in C19.”
- Searching for common genes in affected patients against a control group did not give statistically significant results with the exception of a few genes. So the researchers decided to treat each patient as an independent case, following the example of autism spectrum disorder.
- “In this way we were able to identify for each patient an average of three pathogenic (disease-causing) mutations involved in susceptibility to C19 infection,” says Prof Renieri. “This result was not unexpected, since we already knew from studies of twins that C19 has a strong genetic basis.”
- Although presentation of C19 is different in each individual, this does not rule out the possibility of the same treatment being effective in many cases. “The model we are proposing includes common genes and our results point to some of them.
- For example, ACE2 remains one of the major targets. All our Covid patients have an intact ACE2 protein, and the biological pathway involving this gene remains a major focus for drug development,” says Prof Renieri.
- ACE2 is an enzyme attached to the outer surface of several organs, including the lungs, that lowers blood pressure. It serves as an entry point for some coronaviruses, including C19.
- These results will have significant implications for health and healthcare policy. Understanding the genetic profile of patients may allow the repurposing of existing medicines for specific therapeutic approaches against C19 as well as speeding the development of new antiviral drugs. Being able to identify patients susceptible to severe pneumonia and their responsiveness to specific drugs will allow rapid public health treatment interventions. And future research will be aided, too, by the development of a Covid Biobank accessible to academic and industry partners.
- The researchers will now analyze a further 2,000 samples from other Italian regions, specifically from 35 Italian Hospitals belonging to the GEN-COVID project.
- “Our data, although preliminary, are promising, and now we plan to validate them in a wider population,” says Prof Renieri. “Going beyond our specific results, the outcome of our study underlines the need for a new method to fully assess the basis of one of the more complex genetic traits, with an environmental causation (the virus), but a high rate of heritability. We need to develop new mathematical models using artificial intelligence in order to be able to understand the complexity of this trait, which is derived from a combination of common and rare genetic factors.
- “We have developed this approach in collaboration with the Siena Artificial Intelligence Lab, and now intend to compare it with classical genome-wide association studies in the context of the C19 Host Genetics Initiative, which brings together the human genetics community to generate, share, and analyze data to learn the genetic determinants of C19 susceptibility, severity, and outcomes. As a research community, we need to do everything we can to help public health interventions move forward at this time.”
- Chair of the ESHG conference, Professor Joris Veltman, Dean of the Biosciences Institute at Newcastle University, Newcastle upon Tyne, UK, said: “We are very excited to have this work on the genetics of C19 susceptibility presented as one of our late-breaking abstract talks at the ESHG. Our Italian colleagues present the first insight into the role of genetic susceptibility influencing the severity of the response to a C19 infection. It needs to be expanded to encompass much larger populations, but it is impressive to see the speed at which research on this virus has proceeded in just a few months’ time.”
6. Studies yield clearer picture of rare COVID-linked syndrome in kids
- In a rapid communication published yesterday in Eurosurveillance, French researchers report 108 confirmed, probable, or possible cases of a rare multisystem inflammatory syndrome reported around the world in children with C19.
- And a separate small prospective observational study published this week in BMJ suggests that the syndrome, called pediatric multisystem inflammatory syndrome temporally associated with C19 (PIMS), is most common in those of African ancestry.
- In the first study, the largest known published series of PIMS cases, researchers mined nationwide French surveillance data to retrospectively identify all cases from Mar 1 to May 17.
- They identified 79 confirmed, 16 probable, and 13 possible coronavirus cases. Another 48 possible C19 cases were ruled out on the basis of case definition. Current or past C19 infection was confirmed by reverse-transcription polymerase chain reaction (RT-PCR) for 28 cases, by serology for 42 cases, and by both for 9 cases.
- The number of PIMS cases increased sharply after Apr 13, peaking 4 or 5 weeks after the peak of C19 cases, which the authors said suggests that PIMS is a post-infection syndrome.
- The PIMS cases and the 48 that had been ruled out had a very different pattern, particularly in age distribution, signs and symptoms, and disease severity. Median age of PIMS patients was 8 years, while it was 3 years in non-PIMS patients.
- In PIMS cases, the most common clinical features were Kawasaki-like disease (KLD) (61%) and inflammation of the heart muscle (70%), while 81% of the 48 non–C19 cases had KLD, probably representing classical Kawasaki disease, but only 5 (10%) had heart inflammation.
- Intensive care was needed in 67% of PIMS cases, 73% of them requiring vasopressors to regulate their blood pressure and 43% needing mechanical ventilation. One patient died. Of the 48 other patients, only 8% required intensive care.
- The geographic distribution of PIMS cases correlates with that of non-PIMS cases, which the authors said fits with the nearly simultaneous detection of PIMS in Italy, the United Kingdom, and New York City.
- “Conversely, the absence of identified PIMS cases in some countries may reflect (i) a smaller C19 epidemic, (ii) limited awareness of clinicians, (iii) a lack of a specific surveillance system for KLD or other systemic inflammatory symptoms in children, (iv) additional risk factors in our population such as genetic factors or (v) a combination of the above,” they wrote.
- C19 cases in children younger than 15 years reported to The European Surveillance System make up only 2.1% of all cases, the researchers said. Assuming that no more than 5% of French children in that age-group had the coronavirus, fewer than 2 of 10,000 children would be expected to have PIMS. A research protocol is being implemented to more accurately assess the incidence of PIMS during the pandemic.
- The authors said that while France is unlikely to see high numbers of PIMS in the short term, physicians in countries with a current high incidence of C19 should monitor for it.
- In the second study, of 21 children and adolescents with features of Kawasaki disease admitted to Necker Hospital for Sick Children in Paris from Apr 27 to May 11, 12 (57%) had at least one parent from sub-Saharan Africa or the Caribbean. Last follow-up was on Mar 15.
- Twelve children (57%) had Kawasaki disease shock syndrome, 16 (76%) had inflammation of the heart muscle, and 19 (90%) had evidence of recent C19 infection. All 21 patients had early gastrointestinal symptoms and elevated inflammatory markers in their blood. One patient had coronary artery dilation.
- Median time from onset of C19 symptoms to the beginning of signs and symptoms of Kawasaki disease was 45 days. Nineteen of 21 patients (90%) had antibodies against the coronavirus on serologic testing, and two had negative serologic and RT-PCR results for C19. Median patient age was 8 years.
- Eleven (52%) of the patients met the criteria for Kawasaki disease, while 10 were classified as having incomplete Kawasaki disease. Of the criteria, rash (76%), changes to the lips and mouth (76%), and conjunctivitis in both eyes (81%) were the most common.
- While 17 of 21 patients (81%) required intensive care, and 11 (52%) needed mechanical ventilation, all children were released from the hospital by May 15 after a stay of, on average, 8 days.
- That the syndrome appears most common in children of African descent may be related to social or living conditions or a genetic vulnerability, the authors said. Of note, none of the 21 patients reported living in unhealthy environments or having a relevant personal or family medical history.
- “These clinical findings should prompt high vigilance among primary care and emergency doctors, and preparedness during the coronavirus disease 2019 pandemic in countries with a high proportion of children of African ancestry and high levels of community transmission,” the authors conclude.
- In a commentary in the same journal, Mary Beth Son, MD, of Boston Children’s Hospital called for more research on “the incidence and spectrum of mild to severe PIMS through systematic surveillance; best treatment strategies; the incidence and clinical course of coronary artery dilation, aneurysms, and other cardiac complications and their association with risk factors such as severity of presenting illness; and non-cardiac long term health sequelae.”
F. Potential Treatments
1. Breakthrough close on cloned antibodies that counteract C19
- Scientists working on coronavirus treatments may be close to a breakthrough on an antibody treatment that could save the lives of people who become infected, it has been reported.
- An injection of cloned antibodies that counteract C19 could prove significant for those in the early stages of infection, according to the British-Swedish pharmaceutical company AstraZeneca.
- AstraZeneca’s chief executive Pascal Soriot told the newspaper that the treatment being developed is “a combination of two antibodies” in an injected dose “because by having both you reduce the chance of resistance developing to one antibody”.
- Antibody therapy is more expensive than vaccine production, with Soriot saying the former [antibody therapy] would be prioritized for the elderly and vulnerable “who may not be able to develop a good response to a vaccine”.
- One member of Cepi is the Serum Institute of India, which the Sunday Telegraph reports is considering other “parallel” partnerships with AstraZeneca that may lead to the antibody treatment being funded as a stand-alone treatment.
- Meanwhile UK-based vaccine manufacturer Seqirus announced it was working in partnership with parent company CSL, Cepi and the University of Queensland to help develop a candidate C19 vaccine in Australia. Its manufacturing base in Liverpool is producing an adjuvant, an agent that improves the immune response to a vaccine.
2. FDA Approved Drug May Help Calm Cytokine Storm in C19
- The drug acalabrutinib, FDA-approved for the treatment of several types of B cell cancers, improved the oxygenation levels and decreased molecular markers of inflammation in a majority of 19 patients hospitalized for the treatment of severe C19, according to a new study by Mark Roschewski and colleagues.
- The drug was administered to 11 patients on supplemental oxygen and 8 patients on mechanical ventilation over a 10-to-14-day course of treatment. At the end of treatment, 8 of 11 patients on supplemental oxygen were breathing room air, and 4 of 8 patients on ventilation were extubated, with 2 of the 8 breathing room air. Measurements of two proteins related to inflammation decreased in the majority of patients, with no signs of toxicity from the drug.
- The study is not a clinical trial, but rather an off-label observational study to see if acalabrutinib could help dampen the massive immune response — sometimes called a “cytokine storm” — that is associated with the most severe cases of C19.
- Acalabrutinib inhibits the Bruton tyrosine kinase (BTK) protein, which aids immune cells called macrophages in activating a variety of other proteins in the body’s innate immune response. Patients with severe C19 have a hyperinflammatory immune response that appears to be driven by macrophage activation, leading to acute respiratory distress syndrome (ARDS) and often death.
- Roschewski et al. also studied BTK activation and immune markers in whole blood from 4 C19 patients and 5 healthy individuals. BTK activation levels and the presence of the inflammatory protein IL-6 were higher in the C19 patients, further suggesting that BTK may play a critical role in the disease’s progression.
- An international prospective randomized controlled clinical trial is now underway to confirm the safety and efficacy of this BTK inhibitor as a therapeutic strategy against C19, the authors note.
3. PAC-MAN: Scientists Aim Gene-Targeting Breakthrough Against C19
- A team of scientists from Stanford University is working with researchers at the Molecular Foundry, a nanoscience user facility located at the Department of Energy’s Lawrence Berkeley National Laboratory (Berkeley Lab), to develop a gene-targeting, antiviral agent against C19.
- Last year, Stanley Qi, an assistant professor in the departments of bioengineering, and chemical and systems biology at Stanford University and his team had begun working on a technique called PAC-MAN – or Prophylactic Antiviral CRISPR in human cells – that uses the gene-editing tool CRISPR to fight influenza.
- But that all changed in January, when news of the C19 pandemic emerged. Qi and his team were suddenly confronted with a mysterious new virus for which no one had a clear solution. “So we thought, ‘Why don’t we try using our PAC-MAN technology to fight it?’” said Qi.
- Since late March, Qi and his team have been collaborating with a group led by Michael Connolly, a principal scientific engineering associate in the Biological Nanostructures Facility at Berkeley Lab’s Molecular Foundry, to develop a system that delivers PAC-MAN into the cells of a patient.
- Like all CRISPR systems, PAC-MAN is composed of an enzyme – in this case, the virus-killing enzyme Cas13 – and a strand of guide RNA, which commands Cas13 to destroy specific nucleotide sequences in the coronavirus’s genome. By scrambling the virus’s genetic code, PAC-MAN could neutralize the coronavirus and stop it from replicating inside cells.
It’s all in the delivery
- Qi said that the key challenge to translating PAC-MAN from a molecular tool into an anti-C19 therapy is finding an effective way to deliver it into lung cells. When the coronavirus invades the lungs, the air sacs in an infected person can become inflamed and fill with fluid, hijacking a patient’s ability to breathe.
- “But my lab doesn’t work on delivery methods,” he said. So on March 14, they published a preprint of their paper, and even tweeted, in the hopes of catching the eye of a potential collaborator with expertise in cellular delivery techniques.
- Soon after, they learned of Connolly’s work on synthetic molecules called lipitoids at the Molecular Foundry.
- Lipitoids are a type of synthetic peptide mimic known as a “peptoid” first discovered 20 years ago by Connolly’s mentor Ron Zuckermann. In the decades since, Connolly and Zuckermann have worked to develop peptoid delivery molecules such as lipitoids. And in collaboration with Molecular Foundry users, they have demonstrated lipitoids’ effectiveness in the delivery of DNA and RNA to a wide variety of cell lines.
- Today, researchers studying lipitoids for potential therapeutic applications have shown that these materials are nontoxic to the body and can deliver nucleotides by encapsulating them in tiny nanoparticles just one billionth of a meter wide – the size of a virus.
- Now Qi hopes to add his CRISPR-based C19 therapy to the Molecular Foundry’s growing body of lipitoid delivery systems.
- In late April, the Stanford researchers tested a type of lipitoid – Lipitoid 1 – that self-assembles with DNA and RNA into PAC-MAN carriers in a sample of human epithelial lung cells.
- According to Qi, the lipitoids performed very well. When packaged with coronavirus-targeting PAC-MAN, the system reduced the amount of synthetic coronavirus in solution by more than 90%. “Berkeley Lab’s Molecular Foundry has provided us with a molecular treasure that transformed our research,” he said.
- The team next plans to test the PAC-MAN/lipitoid system in an animal model against a live coronavirus. They will be joined by collaborators at New York University and Karolinska Institute in Stockholm, Sweden.
- If successful, they hope to continue working with Connolly and his team to further develop PAC-MAN/lipitoid therapies for the coronavirus and other coronaviruses, and to explore scaling up their experiments for preclinical tests.
- “An effective lipitoid delivery, coupled with CRISPR targeting, could enable a very powerful strategy for fighting viral disease not only against C19 but possibly against newly viral strains with pandemic potential,” said Connolly.
- “Everyone has been working around the clock trying to come up with new solutions,” added Qi, whose preprint paper was recently peer-reviewed and published in the journal Cell. “It’s very rewarding to combine expertise and test new ideas across institutions in these difficult times.”
G. Projections & Our (Possible) Future
1. When C19 Converges With the Next Flu Season – How Do We Prepare?
- As if the C19 pandemic isn’t scary enough, the flu season is not far away. How severe will the flu season be as it converges with the C19 outbreak? What can we do to prepare?
- Dr. Benjamin Singer, a Northwestern Medicine pulmonologist who treats C19 patients in the intensive care unit, outlines the best defense against influenza, which also may protect against coronavirus.
- In an editorial published May 29 in the journal Science Advances, Singer, an assistant professor of pulmonary and critical care and biochemistry and molecular genetics at Northwestern University Feinberg School of Medicine, examined the epidemiology and biology of the coronavirus and influenza to help inform preparation strategies for the upcoming flu season.
- He outlined the following four factors that could determine the severity of the upcoming flu season:
- Transmission: Social distancing policies designed to limit the spread of C19 are also effective against the flu. If C19 cases begin to spike in the fall of 2020, re-tightening social distancing measures could help mitigate early spread of the flu to flatten the curves for both viruses.
- Vaccination: As we await vaccine trials for C19, we should plan to increase rates of vaccination against the flu, particularly among older adults who are more susceptible to both the flu and C19.
- Co-infection: We need widespread availability of rapid diagnostics for C19 and other respiratory pathogens because co-infection with another respiratory pathogen, including the flu, occurred in more than 20% of C19-positive patients who presented with a respiratory viral syndrome early in the pandemic.
- Disparities: The C19 pandemic has highlighted unconscionable disparities among African Americans, Latinx and Native Americans so we must galvanize public health efforts aimed to limit viral spread, increase vaccination rates, deploy rapid diagnostics and expand other health care services for vulnerable populations, including communities of color, the poor and older adults.
- The CDC estimated that the 2019-2020 seasonal influenza epidemic resulted in tens of millions of cases and tens of thousands of deaths.
- “Even in non-pandemic years, the flu and other causes of pneumonia represent the eighth-leading cause of death in the United States, and respiratory viruses are the most commonly identified pathogens among hospitalized patients with community-acquired pneumonia,” Singer said.
Source: When COVID-19 meets flu season
2. New Model Predicts the Peaks of the C19 Pandemic Around the World
- Even though the worst seems to be over for countries like China and South Korea, public health experts warn that cases and fatalities will continue to surge in many parts of the world. Understanding how the disease evolves can help these countries prepare for an expected uptick in cases.
- In the journal Frontiers, researchers describe a single function that accurately describes all existing available data on active cases and deaths — and predicts forthcoming peaks. The tool uses q-statistics, a set of functions and probability distributions developed by Constantino Tsallis, a physicist and member of the Santa Fe Institute’s external faculty. Tsallis worked on the new model together with Ugur Tirnakli, a physicist at Ege University, in Turkey.
- “The formula works in all the countries in which we have tested,” says Tsallis.
- Neither physicist ever set out to model a global pandemic. But Tsallis says that when he saw the shape of published graphs representing China’s daily active cases, he recognized shapes he’d seen before — namely, in graphs he’d helped produce almost two decades ago to describe the behavior of the stock market.
- “The shape was exactly the same,” he says. For the financial data, the function described probabilities of stock exchanges; for C19, it described daily the number of active cases — and fatalities — as a function of time.
- Modeling financial data and tracking a global pandemic may seem unrelated, but Tsallis says they have one important thing in common. “They’re both complex systems,” he says, “and in complex systems, this happens all the time.”
- Disparate systems from a variety of fields — biology, network theory, computer science, mathematics — often reveal patterns that follow the same basic shapes and evolution.
- The financial graph appeared in a 2004 volume co-edited by Tsallis and the late Nobelist Murray Gell-Mann. Tsallis developed q-statistics, also known as “Tsallis statistics,” in the late 1980s as a generalization of Boltzmann-Gibbs statistics to complex systems.
- In the new paper, Tsallis and Tirnakli used data from China, where the active case rate is thought to have peaked, to set the main parameters for the formula. Then, they applied it to other countries including France, Brazil, and the United Kingdom, and found that it matched the evolution of the active cases and fatality rates over time.
- The model, says Tsallis, could be used to create useful tools like an app that updates in real-time with new available data, and can adjust its predictions accordingly. In addition, he thinks that it could be fine-tuned to fit future outbreaks as well.
- “The functional form seems to be universal,” he says, “Not just for this virus, but for the next one that might appear as well.”
[Note: The article, Predicting COVID-19 Peaks Around the World, can be found here.]
H. Practical Tips & Other Useful Information
1. Scientists Test Best Fabric Choices for Homemade COVID Mask
- University of Illinois at Urbana-Champaign, Editor’s note: Health authorities believe C19 spreads by the transmission of respiratory droplets, and the CDC recommends homemade cloth face coverings for use in public spaces. Starting today, Illinois joins many other states in requiring people to wear masks while out. However, initial uncertainty regarding the masks’ effectiveness in reducing exhaled droplets leaves some people unsure or skeptical of their usefulness during the current C19 pandemic. Mechanical science and engineering professor Taher Saif spoke with News Bureau physical sciences editor Lois Yoksoulian about a study that he and his graduate students, Onur Aydin and Bashar Emon, performed on the effectiveness of common household fabrics for use in homemade masks.
Physically speaking, are the respiratory droplets produced by talking and breathing the same as those that come from a cough or a sneeze?
- The droplets released during sneezing and coughing are larger than those released while speaking and breathing, and any of these droplets may carry many virus particles. The larger droplets tend to fall nearby due to gravity, but the smaller ones can go far, with the majority of them remaining within six feet of the infected individual. Unfortunately, because symptomatic, presymptomatic and asymptomatic carriers can shed the coronavirus, we cannot tell without testing which individuals are the sources of infection. Hence, a physical barrier, such as a mask, can prevent the spreading.
How does droplet type influence the fabric choice and the number of layers used to make a mask?
- The droplets released during coughing and sneezing come in various sizes and velocities. The fabric for any mask should be breathable and impermeable to high- and low-velocity droplets.
- It is important to realize that a highly impermeable fabric is likely to be less breathable. Low breathability will force airflow through the sides and will defeat the purpose of the mask. In that case, the mask simply gives a false sense of safety.
- The choice of fabric and the number of layers is a matter of compromise between breathability and droplet resistance. We need to maximize both.
- What fabric properties did you test?
- We tested the breathability and droplet blocking ability of common household fabrics. To quantify breathability, we simply measure the airflow velocity through the material. Measuring droplet blocking is a more complicated process that uses an inhaler to generate high-velocity droplets.
- We fill the nozzle of an inhaler with distilled water mixed with 100-nanometer fluorescent particles, which mimic the coronavirus in size. When puffed, the inhaler forces the water through the nozzle and generates high-momentum droplets that we collect on a plastic dish placed vertically in front of the inhaler. We then repeat the process with the fabric we are testing over the collection dish. We measure how much water landed on the dish in both cases by counting the nanoparticles using a microscope. We can then use the ratio of the volume collected with and without the fabric to give us a measure of droplet-blocking efficiency.
What types of fabric did you examine?
- We considered a set of 10 common household fabrics and compared their properties with those of a medical/dental-quality mask as a benchmark. The fabrics had different combinations of cotton, polyester and silk. We also measured the breathability and resistance for two- and three-layered T-shirt fabric. Our work produced two key findings.
- First, most common household fabrics, such as T-shirt material, have 40% or higher droplet blocking when used as a single layer. In two layers, to our surprise, T-shirt fabric had a 98% droplet blocking efficiency – exceeding that of the medical mask, while maintaining better breathability.
- Second, most common fabrics are hydrophilic, meaning they up soak water, whereas medical masks are hydrophobic, meaning they repel water. This tells us that common household fabrics use an alternative mechanism to hold droplets by retaining them. Incoming droplets are thus soaked and ‘held back’ by home fabrics, which might offer an as of yet untapped and understudied advantage of home-made cloth masks.
- Overall, our study suggests that most double-layered cloth face coverings may help reduce droplet transmission of respiratory infections.
[Note: The study, “Performance of fabrics for home-made masks against spread of respiratory infection through droplets: a quantitative mechanistic study”, can be found here.]
I. The Road Back?
1. How Businesses Can Keep Employees Safe From Coronavirus
Opinion by Scott Gottlieb and Lauren Silvis
- America is getting back to business against a backdrop of persistent C19 spread. The epidemic is under control, but not crushed. Essential to avoiding a second wave is widespread testing to detect and contain new infections.
- The good news is that many states have enough tests available to offer them to all citizens, regardless of symptoms. With new testing technologies coming online, it is becoming easier to deploy the right test in the right setting to the right patient. Part of the strategy should be testing at work sites where employees face higher risks.
- Employers have two approaches: trying to keep the virus from entering the workplace and, barring that, trying to contain spread. Fever checks or health questionnaires are only partially effective. Symptom monitoring is unlikely to detect more than about half of infections, and people may only develop symptoms days after being contagious.
- What kind of tests should employers use? There is obvious appeal to rapid tests. But current platforms can yield false negatives in about 20% of cases. This may be suitable for a doctor’s office, where a doctor can run another type of test to confirm a negative result. It may not be feasible for screening a mostly asymptomatic population at a job site, where running a second test on negative results isn’t practical given that most tests are likely to be negative, and there may not be symptoms to prompt further suspicion.
- A better option for some employers could be lab-based testing. Coming soon to the market are more kits that mail a test to a patient, who can collect a sample and send it back to the lab. The Food and Drug Administration took steps to make this type of testing more routine by issuing a standard template for how labs can get these tests authorized for use. This option is convenient for both patients and employers, and it will reduce strain on health-care workers, who need to preserve protective gear.
- People with symptoms of Covid should see a doctor, not show up at work for a test. Those tested at work are thus likely to be mostly asymptomatic but concerned about possible exposure. The risk of a false negative needs to be managed with especially accurate platforms.
- One technology, called next-generation sequencing, allows for pooled sampling. This tool is being deployed by several companies, including Tempus and Illumina. (Both authors of this article are employed by Tempus, and Dr. Gottlieb is on the board of Illumina.) Employees give saliva samples that are combined into pools of 10 or even 100 specimens and then screened at once. If you get a hit on a pool, then you go back and test each person in it. These can be very accurate and efficient. Sample pooling is how China claims it recently managed to screen 10 million citizens in Wuhan in 19 days.
- The next question is how often to test. A business could, say, offer tests to rotating groups of at risk employees based on who people come into regular contact with at work. Think of cohorts divided on different floors of an office building, or different parts of a shop floor. Sampling a representative group from each cohort on a regular basis can help detect outbreaks. Apps are now available to assist employers in implementing such protocols.
- As more testing tools become available, it is crucial to make sure screening is deployed where it is needed most. That means expanding testing opportunities in underserved communities, where there is both greater risk of spread and serious illness. States should help businesses like grocery stores, where risks are high but margins are low, establish testing regimes.
- Employers ought to anticipate other issues like protecting worker privacy, supporting self-isolation for infected individuals and reporting results to state health authorities. Employers also need systems to track close work contacts when they discover a positive case.
- But companies can be a big part of reducing America’s Covid risk and preventing another epidemic. Widespread testing may be the best bridge to a vaccine.
- Dr. Gottlieb is a resident fellow at the American Enterprise Institute, a partner at New Enterprise Associates and board member of health-care companies. He was commissioner of the Food and Drug Administration, 2017-19. Ms. Silvis is a senior vice president at Tempus Labs Inc. and was the deputy director of the FDA’s medical device center and the agency’s chief of staff from 2017-19.