Why It’s All Dr. Fauci’s Fault
Photos emerged last week of students, with very few wearing masks, in a crowded hallway in North Paulding High School, in Dallas, Georgia. Dallas, about 45 miles NW of Atlanta, is in Paulding County. Last week, Paulding County recorded 214 new cases of COVID-19 and an infection rate of 1,036 per 100k population. Nearby by Fulton county, home to Atlanta, had 1789 new cases and an infection ratio 1,922/100K. According to a CNN story, a sophomore student named Hannah posted the photos on social media, because, “I was concerned for the safety of everyone in that building and everyone in the county because precautions that the CDC and guidelines that the CDC has been telling us for months now, weren’t being followed,” she said.
On 16 July 2020, Georgia Governor Kemp sued the City of Atlanta for trying to enforce Atlanta’s mandate to wear masks in public.
Back in May, Trump has strongly urged states to reopen. Against CDC advice, Georgia was one of the first places in the US to allow nonessential businesses to reopen, with nail salons, massage therapists, bowling alleys, and gyms allowed to open on April 24. They were followed on April 27 by limited dine-in service for restaurants, movie theaters, and other entertainment venues. By May 4, some shopping malls had also reopened. By the end of June, Georgia’s hospitals were at maximum capacity. According to a Johns Hopkins Report, during the week Georgia set another all-time high for new cases. Governor Kemp said that he was of a mind to stay the course.
Since the pandemic struck, Georgia has suffered at least 4,177 deaths from COVID-19. During the week of 2-8 August, Georgia has seen at least 18,992 new infections and suffered at least 292 deaths from the virus.
On August 5, 2020, Dr. Fauci revealed to reporters that he has received death threats and that his daughters had been harassed.
Many people with the coronavirus don’t show symptoms. Researchers want to know why
Washington Post via @BostonGlobe – August 8
When researcher Monica Gandhi began digging deeper into outbreaks of the novel coronavirus, she was struck by the extraordinarily high number of infected people who had no symptoms.
A Boston homeless shelter had 147 infected residents, but 88% had no symptoms even though they shared their living space. A Tyson Foods poultry plant in Springdale, Ark., had 481 infections, and 95% were asymptomatic. Prisons in Arkansas, North Carolina, Ohio and Virginia counted 3,277 infected people, but 96% were asymptomatic.
During its seven-month global rampage, the coronavirus has claimed more than 700,000 lives. But Gandhi began to think the bigger mystery might be why it has left so many more practically unscathed.
What was it about these asymptomatic people, who lived or worked so closely to others who fell severely ill, she wondered, that protected them? Did the ‘’dose” of their viral exposure make a difference? Was it genetics? Or might some people already have partial resistance to the virus, contrary to our initial understanding?
Efforts to understand the diversity in the illness are finally beginning to yield results, raising hope that the knowledge will help accelerate development of vaccines and therapies – or possibly even create new pathways toward herd immunity in which enough of the population develops a mild version of the virus that they block further spread and the pandemic ends.
‘‘A high rate of asymptomatic infection is a good thing,’’ said Gandhi, an infectious-disease specialist at the University of California at San Francisco. ‘’It’s a good thing for the individual and a good thing for society.‘’
The coronavirus has left numerous clues – the uneven transmission in different parts of the world, the mostly mild impact on children. Perhaps most tantalizing is the unusually large proportion of infected people with mild symptoms or none at all. The Centers for Disease Control and Prevention last month estimated that rate at about 40%.
Those clues have sent scientists off in different directions: Some are looking into the role of the receptor cells, which the virus uses to infiltrate the body, to better understand the role that age and genetics might play. Others are delving into masks and whether they may filter just enough of the virus so those wearing them had mild cases or no symptoms at all.
The theory that has generated the most excitement in recent weeks is that some people walking among us might already have partial immunity.
When SARS-CoV-2, the technical name of the coronavirus that causes the disease covid-19, was first identified on Dec. 31, 2019, public health officials deemed it a ‘’novel” virus because it was the first time it had been seen in humans who presumably had no immunity from it whatsoever. There’s now some very early, tentative evidence suggesting that assumption might have been wrong.
One mind-blowing hypothesis – bolstered by a flurry of recent studies – is that a segment of the world’s population may have partial protection thanks to ‘’memory” T cells, the part of our immune system trained to recognize specific invaders. This could originate from cross-protection derived from standard childhood vaccinations. Or, as a paper published Tuesday in Science suggested, it could trace back to previous encounters with other coronaviruses, such as those that cause the common cold.
‘‘This might potentially explain why some people seem to fend off the virus and may be less susceptible to becoming severely ill,’’ National Institutes of Health Director Francis Collins remarked in a blog post this past week.
On a population level, such findings, if validated, could be far-reaching.
Hans-Gustaf Ljunggren, a researcher at Sweden’s Karolinska Institute, and others have suggested that public immunity to the coronavirus could be significantly higher than what has been suggested by studies. In communities in Barcelona, Boston, Wuhan and other major cities, the proportion of people estimated to have antibodies and therefore presumably be immune has mostly been in the single digits. But if others had partial protection from T cells, that would raise a community’s immunity level much higher.
This, Ljunggren said, would be ‘’very good news from a public health perspective.‘’
Some experts have gone so far as to speculate about whether some surprising recent trends in the epidemiology of the coronavirus – the drop in infection rates in Sweden where there have been no widespread lockdowns or mask requirements, or the high rates of infection in Mumbai’s poor areas but little serious disease – might be due to preexisting immunity.
Others say it’s far too early to draw such conclusions. Anthony Fauci, the United States’ top infectious-disease expert, said in an interview that while these ideas are being intensely studied, such theories are premature. He said at least some partial preexisting immunity in some individuals seems a possibility.
And he said the amount of virus someone is exposed to – called the inoculum – ‘’is almost certainly an important and likely factor’’ based on what we know about other viruses.
But Fauci cautioned that there are multiple likely reasons – including youth and general health – that determine whether a particular individual shrugs off the disease or dies of it. That reinforces the need, in his view, for continued vigilance in social distancing, masking and other precautions.
‘‘There are so many other unknown factors that maybe determine why someone gets an asymptomatic infection,’’ Fauci said. ‘’It’s a very difficult problem to pinpoint one thing.‘’
– – –
News headlines have touted the idea based on blood tests that 20% of some New York communities might be immune, 7.3% in Stockholm, 7.1% in Barcelona. Those numbers come from looking at antibodies in people’s blood that typically develop after they are exposed to a virus. But scientists believe another part of our immune system – T cells, a type of white blood cell that orchestrates the entire immune system – could be even more important in fighting against the coronavirus.
Recent studies have suggested that antibodies from the coronavirus seem to stick around for two to three months in some people. While work on T cells and the coronavirus is only getting started – testing T cells is much more laborious than antibody testing – previous research has shown that, in general, T cells tend to last years longer.
One of the first peer-reviewed studies on the coronavirus and T cells was published in mid-May in the journal Cell by Alessandro Sette, Shane Crotty and others at the La Jolla Institute for Immunology near San Diego.
The group was researching blood from people who were recovering from coronavirus infections and wanted to compare that to samples from uninfected controls who were donors to a blood bank from 2015 to 2018. The researchers were floored to find that in 40% to 60% of the old samples, the T cells seemed to recognize SARS-CoV-2.
‘‘The virus didn’t even exist back then, so to have this immune response was remarkable,’’ Sette said.
Research teams from five other locations reported similar findings. In a study from the Netherlands, T cells reacted to the virus in 20% of the samples. In Germany, 34%. In Singapore, 50%.
The different teams hypothesized this could be due to previous exposure to similar pathogens. Perhaps fortuitously, SARS-CoV-2 is part of a large family of viruses. Two of them – SARS and MERS – are deadly and led to relatively brief and contained outbreaks. Four other coronavirus variants, which cause the common cold, circulate widely each year but typically result in only mild symptoms. Sette calls them the ‘’less-evil cousins of SARS-CoV-2.‘’
This week, Sette and others from the team reported new research in Science providing evidence the T cell responses may derive in part from memory of ‘’common cold’’ coronaviruses.
‘‘The immune system is basically a memory machine,’’ he said. ‘’It remembers and fights back stronger.‘’
The researchers noted in their paper that the strongest reaction they saw was against the spike proteins that the virus uses to gain access to cells – suggesting that fewer viral copies get past these defenses.
‘‘The current model assumes you are either protected or you are not – that it’s a yes or no thing,’’ Sette added. ‘’But if some people have some level of preexisting immunity, that may suggest it’s not a switch but more continuous.‘’
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More than 2,300 miles away, at the Mayo Clinic in Cleveland, Andrew Badley was zeroing in the possible protective effects of vaccines.
Teaming up with data experts from Nference, a company that manages their clinical data, he and other scientists looked at records from 137,037 patients treated at the health system to look for relationships between vaccinations and coronavirus infection.
They knew that the vaccine for smallpox, for example, had been shown to protect against measles and whooping cough. Today, a number of existing vaccines are being studied to see whether any might offer cross-protection against SARS-CoV-2.
The results were intriguing: Seven types of vaccines given one, two or five years in the past were associated with having a lower rate of infection with the new coronavirus. Two vaccines in particular seemed to show stronger links: People who got a pneumonia vaccine in the recent past appeared to have a 28% reduction in coronavirus risk. Those who got polio vaccines had a 43% reduction in risk.
Venky Soundararajan, chief scientific officer of Nference, remembers when he first saw how large the reduction appeared to be, he immediately picked up his phone and called Badley: ‘’I said, ‘Is this even possible?‘’’
The team looked at dozens of other possible explanations for the difference. It adjusted for geographic incidence of the coronavirus, demographics, comorbidities, even whether people had had mammograms or colonoscopies, under the assumption that people who got preventive care might be more apt to social distance. But the risk reduction still remained large.
‘‘This surprised us completely,’’ Soundararajan recalled. ‘’Going in we didn’t expect anything or maybe one or two vaccines showing modest levels of protection.‘’
The study is only observational and cannot show a causal link by design, but Mayo researchers are looking at a way to quantify the activity of these vaccines on the coronavirus to serve as a benchmark to the new vaccines being created by companies such as Moderna. If existing vaccines appear as protective as new ones under development, he said, they could change the world’s whole vaccine strategy.
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Meanwhile, at NIH headquarters in Bethesda, Md., Alkis Togias has been laser-focused on one group of the mildly affected: children. He wondered whether it might have something to do with the receptor known as ACE2, through which the virus hitchhikes into the body.
In healthy people, the ACE2 receptors perform the important function of keeping blood pressure stable. The novel coronavirus latches itself to ACE2, where it replicates. Pharmaceutical companies are trying to figure out how to minimize the receptors or to trick the virus into attaching itself to a drug so it does not replicate and travel throughout the body.
Was it possible, Togias asked, that children naturally expressed the receptor in a way that makes them less vulnerable to infection?
He said recent papers have produced counterintuitive findings about one subgroup of children – those with a lot of allergies and asthma. The ACE2 receptors in those children were diminished, and when they were exposed to an allergen such as cat hair, the receptors were further reduced. Those findings, combined with data from hospitals showing that asthma did not seem to be a risk factor for the respiratory virus, as expected, have intrigued researchers.
‘‘We are thinking allergic reactions may protect you by down-regulating the receptor,’’ he said. ‘’It’s only a theory of course.‘’
Togias, who is in charge of airway biology for the National Institute of Allergy and Infectious Diseases, is looking at how those receptors seem to be expressed differently as people age, as part of a study of 2,000 U.S. families. By comparing those differences and immune responses within families, they hope to be able to better understand the receptors’ role.
Separately, a number of genetic studies show variations in genes associated with ACE2 with people from certain geographic areas, such as Italy and parts of Asia, having distinct mutations. No one knows what significance, if any, these differences have on infection, but it’s an active area of discussion in the scientific community.
– – –
Before the pandemic, Gandhi, the University of California researcher, specialized in HIV. But like other infectious-disease experts these days, she has spent many of her waking hours thinking about the coronavirus. And in scrutinizing the data on outbreaks one day, she noticed what might be a pattern: People were wearing masks in the settings with the highest percentage of asymptomatic cases.
The numbers on two cruise ships were especially striking. In the Diamond Princess, where masks weren’t used and the virus was likely to have roamed free, 47% of those tested were asymptomatic. But in the Antarctic-bound Argentine cruise ship, where an outbreak hit in mid-March and surgical masks were given to all passengers and N95 masks to the crew, 81% were asymptomatic.
Similarly high rates of asymptomatic infection were documented at a pediatric dialysis unit in Indiana, a seafood plant in Oregon and a hair salon in Missouri, all of which used masks. Gandhi was also intrigued by countries such as Singapore, Vietnam and the Czech Republic that had population-level masking.
‘‘They got cases,’’ she noted, ‘’but fewer deaths.‘’
The scientific literature on viral dose goes back to around 1938 when scientists began to find evidence that being exposed to one copy of a virus is more easily overcome than being exposed to a billion copies. Researchers refer to the infectious dose as ID50 – or the dose at which 50% of the population would become infected.
While scientists do not know what that level might be for the coronavirus (it would be unethical to expose humans in this way), previous work on other nonlethal viruses showed that people tend to get less sick with lower doses and more sick with higher doses. A study published in late May involving hamsters, masks and SARS-CoV-2 found that those given coverings had milder cases than those who did not get them.
In an article published this month in the Journal of General Internal Medicine, Gandhi noted that in some outbreaks early in the pandemic in which most people did not wear masks, 15% of the infected were asymptomatic. But later on, when people began wearing masks, the rate of asymptomatic people was 40% to 45%.
She said the evidence points to masks not just protecting others – as U.S. health officials emphasize – but protecting the wearer as well. Gandhi makes the controversial argument that while people mostly have talked about asymptomatic infections as terrifying due to how people can spread the virus unwittingly, it could end up being a good thing.
‘‘It is an intriguing hypothesis that asymptomatic infection triggering immunity may lead us to get more population-level immunity,’’ Gandhi said. ‘‘That itself will limit spread.‘’
Targets of T Cell Responses to SARS-CoV-2 Coronavirus in Humans with COVID-19 Disease and Unexposed Individuals
Cell – May 14
T cells found in COVID-19 patients ‘bode well’ for long-term immunity
Science – May 14
Excellent, Fred.
It is a fascinating disease. Terrible, yet interesting and exciting times.
Masks do not offer any significant protection. Here’s a review article from the Center for Infectious Disease Research and Policy at the U of Minnesota with 50+ journal references, including RCTs:
https://www.cidrap.umn.edu/news-perspective/2020/04/commentary-masks-all-covid-19-not-based-sound-data
Mike Osterholm, head of the Epidemiology Dept. at the U of M and lead state Epiemiologist explained why this is so in his first appearance on Joe Rogan’s podcast for those interested in another viewpoint.
There is no scientific basis for masks to be a mandatory component of “the new normal”. If you want to wear one, fine, go ahead, but as far as I’m concerned it’s one more emotional response to a situation that is drowning in them already.
The first report presents mounting evidence for the effectiveness of wearing face coverings in reducing the risk of transmission and presents new evidence suggesting that face coverings could also provide protection to the wearer. Authored by Paul Edelstein, Emeritus Professor of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, and Lalita Ramakrishan, Professor of Immunology and Infectious Diseases, University of Cambridge, it is an update on an earlier report from Data Evaluation and Learning for Viral Epidemics (DELVE), a multi-disciplinary group convened by the Royal Society. https://rs-delve.github.io/reports/2020/05/04/face-masks-for-the-general-public.html
The second report, by the Royal Society’s SET-C (Science in Emergencies Tasking – COVID-19) group and published jointly by the British Academy and the Royal Society, looks at the effectiveness of different face mask types and coverings and isolates behavioural factors that have limited adherence such as public understanding of the virus transmission, risk perception, trust, effectiveness of public messages and perceived barriers to wearing a mask. https://royalsociety.org/topics-policy/projects/set-c-science-in-emergencies-tasking-covid
Paul Edelstein, Emeritus Professor of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, said: “The evidence for the benefit of wearing face coverings in protecting others from infection is becoming clearer all the time. In fact, we have now identified convincing decades-old and apparently forgotten evidence, from the time when surgical masks were made of cloth and were reusable, showing that they help to prevent transmission of airborne infectious agents. There is now even some evidence that masks might directly benefit the wearer. The basics are simple to understand. There are people without symptoms going about their daily business who are unknowingly breathing out droplets that are carrying the virus. If they had their faces covered the majority of those droplets would be caught before they can infect other people. Wearing face coverings can help save lives and prevent disabling illnesses.” https://royalsociety.org/news/2020/07/president-of-the-royal-society-urges-everyone-to-wear-a-face-covering/
If you wish to blow yourself up, please do so without trying to take us with you.
There was some speculation that the virus originated in bats from Vietnam that were transported to Wuhan for sale. The low prevalence of coronavirus in that country (800 cases, 10 deaths with no lockdown) is possibly explained by the population having widespread immunity due to the prevalence of similar viruses in the past.
How the pandemic might play out in 2021 and beyond
Nature – August 5
This coronavirus is here for the long haul — here’s what scientists predict for the next months and years.
Illustration by Ana Kova
PDF version
June 2021. The world has been in pandemic mode for a year and a half. The virus continues to spread at a slow burn; intermittent lockdowns are the new normal. An approved vaccine offers six months of protection, but international deal-making has slowed its distribution. An estimated 250 million people have been infected worldwide, and 1.75 million are dead.
Scenarios such as this one imagine how the COVID-19 pandemic might play out1. Around the world, epidemiologists are constructing short- and long-term projections as a way to prepare for, and potentially mitigate, the spread and impact of SARS-CoV-2, the virus that causes COVID-19. Although their forecasts and timelines vary, modellers agree on two things: COVID-19 is here to stay, and the future depends on a lot of unknowns, including whether people develop lasting immunity to the virus, whether seasonality affects its spread, and — perhaps most importantly — the choices made by governments and individuals. “A lot of places are unlocking, and a lot of places aren’t. We don’t really yet know what’s going to happen,” says Rosalind Eggo, an infectious-disease modeller at the London School of Hygiene & Tropical Medicine (LSHTM).
“The future will very much depend on how much social mixing resumes, and what kind of prevention we do,” says Joseph Wu, a disease modeller at the University of Hong Kong. Recent models and evidence from successful lockdowns suggest that behavioural changes can reduce the spread of COVID-19 if most, but not necessarily all, people comply.
Last week, the number of confirmed COVID-19 infections passed 15 million globally, with around 650,000 deaths. Lockdowns are easing in many countries, leading some people to assume that the pandemic is ending, says Yonatan Grad, an epidemiologist at the Harvard T. H. Chan School of Public Health in Boston, Massachusetts. “But that’s not the case. We’re in for a long haul.”
If immunity to the virus lasts less than a year, for example, similar to other human coronaviruses in circulation, there could be annual surges in COVID-19 infections through to 2025 and beyond. Here, Nature explores what the science says about the months and years to come.
What happens in the near future?
The pandemic is not playing out in the same way from place to place. Countries such as China, New Zealand and Rwanda have reached a low level of cases — after lockdowns of varying lengths — and are easing restrictions while watching for flare-ups. Elsewhere, such as in the United States and Brazil, cases are rising fast after governments lifted lockdowns quickly or never activated them nationwide.
The latter group has modellers very worried. In South Africa, which now ranks fifth in the world for total COVID-19 cases, a consortium of modellers estimates that the country can expect a peak in August or September, with around one million active cases, and cumulatively as many as 13 million symptomatic cases by early November. In terms of hospital resources, “we’re already breaching capacity in some areas, so I think our best-case scenario is not a good one”, says Juliet Pulliam, director of the South African Centre for Epidemiological Modelling and Analysis at Stellenbosch University.
But there is hopeful news as lockdowns ease. Early evidence suggests that personal behavioural changes, such as hand-washing and wearing masks, are persisting beyond strict lockdown, helping to stem the tide of infections. In a June report, a team at the MRC Centre for Global Infectious Disease Analysis at Imperial College London found that among 53 countries beginning to open up, there hasn’t been as large a surge in infections as predicted on the basis of earlier data. “It’s undervalued how much people’s behaviour has changed in terms of masks, hand washing and social distancing. It’s nothing like it used to be,” says Samir Bhatt, an infectious-disease epidemiologist at Imperial College London and a co-author of the study.
Researchers in virus hotspots have been studying just how helpful these behaviours are. At Anhembi Morumbi University in São Paulo, Brazil, computational biologist Osmar Pinto Neto and colleagues ran more than 250,000 mathematical models of social-distancing strategies described as constant, intermittent or ‘stepping-down’ — with restrictions reduced in stages — alongside behavioural interventions such as mask-wearing and hand washing.
The team concluded that if 50–65% of people are cautious in public, then stepping down social-distancing measures every 80 days could help to prevent further infection peaks over the next two years. “We’re going to need to change the culture of how we interact with other people,” says Neto. Overall, it’s good news that even without testing or a vaccine, behaviours can make a significant difference in disease transmission, he adds.
Infectious-disease modeller Jorge Velasco-Hernández at the National Autonomous University of Mexico in Juriquilla and colleagues also examined the trade-off between lockdowns and personal protection. They found that if 70% of Mexico’s population committed to personal measures such as hand washing and mask-wearing following voluntary lockdowns that began in late March, then the country’s outbreak would decline after peaking in late May or early June. However, the government lifted lockdown measures on 1 June and, rather than falling, the high number of weekly COVID-19 deaths plateaued. Velasco-Hernández’s team thinks that two public holidays acted as superspreading events, causing high infection rates right before the government lifted restrictions.
In regions where COVID-19 seems to be on the decline, researchers say that the best approach is careful surveillance by testing and isolating new cases and tracing their contacts. This is the situation in Hong Kong, for instance. “We are experimenting, making observations and adjusting slowly,” says Wu. He expects that the strategy will prevent a huge resurgence of infections — unless increased air traffic brings a substantial number of imported cases.
But exactly how much contact tracing and isolation is required to contain an outbreak effectively? An analysis by the Centre for the Mathematical Modelling of Infectious Diseases COVID-19 Working Group at the LSHTM simulated fresh outbreaks of varying contagiousness, starting from 5, 20 or 40 introduced cases. The team concluded that contact tracing must be rapid and extensive — tracing 80% of contacts within a few days — to control an outbreak. The group is now assessing the effectiveness of digital contact tracing and how long it’s feasible to keep exposed individuals in quarantine, says co-author Eggo. “Finding the balance between what actually is a strategy that people will tolerate, and what strategy will contain an outbreak, is really important.”
Tracing 80% of contacts could be near-impossible to achieve in regions still grappling with thousands of new infections a week — and worse, even the highest case counts are likely to be an underestimate. A June preprint1 from a Massachusetts Institute of Technology (MIT) team in Cambridge analysing COVID-19 testing data from 84 countries suggests that global infections were 12 times higher and deaths 50% higher than officially reported (see ‘Predicting cases and deaths’). “There are many more cases out there than the data indicate. As a consequence, there’s higher risk of infection than people may believe there to be,” says John Sterman, co-author of the study and director of the MIT System Dynamics Group.
For now, mitigation efforts, such as social distancing, need to continue for as long as possible to avert a second major outbreak, says Bhatt. “That is, until the winter months, where things get a bit more dangerous again.”
What will happen when it gets cold?
It is clear now that summer does not uniformly stop the virus, but warm weather might make it easier to contain in temperate regions. In areas that will get colder in the second half of 2020, experts think there is likely to be an increase in transmission.
Many human respiratory viruses — influenza, other human coronaviruses and respiratory syncytial virus (RSV) — follow seasonal oscillations that lead to winter outbreaks, so it is likely that SARS-CoV-2 will follow suit. “I expect SARS-CoV-2 infection rate, and also potentially disease outcome, to be worse in the winter,” says Akiko Iwasaki, an immunobiologist at the Yale School of Medicine in New Haven, Connecticut. Evidence suggests that dry winter air improves the stability and transmission of respiratory viruses, and respiratory-tract immune defence might be impaired by inhaling dry air, she adds.
In addition, in colder weather people are more likely to stay indoors,
where virus transmission through droplets is a bigger risk, says Richard Neher, a computational biologist at the University of Basel in Switzerland. Simulations by Neher’s group show that seasonal variation is likely to affect the virus’s spread and might make containment in the Northern Hemisphere this winter more difficult.
In future, SARS-CoV-2 outbreaks could arrive in waves every winter.
The risk to adults who have already had COVID-19 could be reduced, as with flu, but it would depend on how rapidly immunity to this coronavirus wears off, says Neher. What’s more, the combination of COVID-19, flu and RSV in autumn and winter could be challenging, says Velasco-Hernández, who is setting up a model of how such viruses might interact.
It remains unknown whether infection with other human coronaviruses can offer any protection against SARS-CoV-2. In a cell-culture experiment involving SARS-CoV-2 and the closely related SARS-CoV, antibodies from one coronavirus could bind to the other coronavirus, but did not disable or neutralize it.
To end the pandemic, the virus must either be eliminated worldwide — which most scientists agree is near-impossible because of how widespread it has become — or people must build up sufficient immunity through infections or a vaccine. It is estimated that 55–80% of a population must be immune for this to happen, depending on the country.
Unfortunately, early surveys suggest there is a long way to go. Estimates from antibody testing — which reveals whether someone has been exposed to the virus and made antibodies against it — indicate that only a small proportion of people have been infected, and disease modelling backs this up. A study of 11 European countries calculated an infection rate of 3–4% up to 4 May, inferred from data on the ratio of infections to deaths, and how many deaths there had been. In the United States, where there have been more than 150,000 COVID-19 deaths, a survey of thousands of serum samples, coordinated by the US Centers for Disease Control and Prevention, found that antibody prevalence ranged from 1% to 6.9%, depending on the location.
What happens in 2021 and beyond?
The pandemic’s course next year will depend greatly on the arrival of a vaccine, and on how long the immune system stays protective after vaccination or recovery from infection. Many vaccines provide protection for decades — such as those against measles or polio — whereas others, including whooping cough and influenza, wear off over time. Likewise, some viral infections prompt lasting immunity, others a more transient response. “The total incidence of SARS-CoV-2 through 2025 will depend crucially on this duration of immunity,” wrote Grad, Harvard epidemiologist Marc Lipsitch and colleagues in a May paper exploring possible scenarios (see ‘What happens next?’).
Researchers know little so far about how long SARS-CoV-2 immunity lasts. One study of recovering patients found that neutralizing antibodies persisted for up to 40 days after the start of infection; several other studies suggest that antibody levels dwindle after weeks or months. If COVID-19 follows a similar pattern to SARS, antibodies could persist at a high level for 5 months, with a slow decline over 2–3 years. Still, antibody production is not the only form of immune protection; memory B and T cells also defend against future encounters with the virus, and little is known so far about their role in SARS-CoV-2 infection. For a clear answer on immunity, researchers will need to follow a large number of people over a long time, says Michael Osterholm, director of the Center for Infectious Disease Research and Policy (CIDRAP) at the University of Minnesota, Minneapolis. “We’re just going to have to wait.”
If infections continue to rise rapidly without a vaccine or lasting immunity, “we will see regular, extensive circulation of the virus”, says Grad. In that case, the virus would become endemic, says Pulliam. “That would be really painful.” And it is not unimaginable: malaria, a preventable and treatable disease, kills more than 400,000 people each year. “These worst-case scenarios are happening in many countries with preventable diseases, causing huge losses of life already,” says Bhatt.
If the virus induces short-term immunity — similar to two other human coronaviruses, OC43 and HKU1, for which immunity lasts about 40 weeks — then people can become reinfected and there could be annual outbreaks, the Harvard team suggests. A complementary CIDRAP report, based on trends from eight global influenza pandemics, points to significant COVID-19 activity for at least the next 18–24 months, either in a series of gradually diminishing peaks and valleys, or as a “slow burn” of continuing transmission without a clear wave pattern. Yet these scenarios remain only guesses, because this pandemic has so far not followed the pattern of pandemic flu, says Osterholm. “We’re in a coronavirus pandemic for which we have no precedents.”
Mounting evidence suggests coronavirus is airborne — but health advice has not caught up
Another possibility is that immunity to SARS-CoV-2 is permanent. In that case, even without a vaccine, it is possible that after a world-sweeping outbreak, the virus could burn itself out and disappear by 2021. However, if immunity is moderate, lasting about two years, then it might seem as if the virus has disappeared, but it could surge back as late as 2024, the Harvard team found.
That forecast, however, does not take the development of effective vaccines into account. It’s unlikely that there will never be a vaccine, given the sheer amount of effort and money pouring into the field and the fact that some candidates are already being tested in humans, says Velasco-Hernández. The World Health Organization lists 26 COVID-19 vaccines currently in human trials, with 12 of them in phase II trials and six in phase III. Even a vaccine providing incomplete protection would help by reducing the severity of the disease and preventing hospitalization, says Wu. Still, it will take months to make and distribute a successful vaccine.
The world will not be affected equally by COVID-19. Regions with older populations could see disproportionally more cases in later stages of the epidemic, says Eggo; a mathematical model from her team, published in June and based on data from six countries, suggests that the susceptibility to infection in children and people under 20 years old is approximately half that of older adults.
There is one thing that every country, city and community touched by the pandemic has in common. “There is so much we still don’t know about this virus,” says Pulliam. “Until we have better data, we’re just going to have a lot of uncertainty.”
A week ago my wife encountered maskless shoppers in a retailer that previously required masks for everyone. It was day 1 of Governor Evers’ mask mandate in Wisconsin. I speculated it was simply the retailer not being prepared on day 1 over how to handle the categories of people who were exempted from the mandate. My wife went back yesterday afternoon and saw one shopper without a mask. She asked and was told that if a shopper qualified for the exemption they could shop without a mask. Since I think that was the intent of the exemptions in the first place, it seems reasonable. That only one person was maskless (that she saw, but she probably saw 100+ other masked shoppers while in the store) it did not seem that it was being treated as an excuse to go maskless.
Rob,
Please check the original date of that UM perspective. It’s from April 1st, which means it was written sometime in March, long before we knew much about face masks. If you’ll reread it you’ll see that UM has walked back much of the original claim. In effect, what UM is now saying is that masks may not offer much protection if you wear a thin flimsy one that doesn’t fit well and isn’t washed regularly and if you don’t social distance and you hang around inside spaces with poor fresh air circulation. No kidding!!!
2slugbaits,
Well said and more polite than I. Thanks. Dan
2
The numbers are indeed fascinating. Think it was on an Amanpour Show that I heard a Scientist run the numbers on an N95, surgical, homemade, … I’ll look later, but the efficacy runs like 60-70 on the N95 and goes to 50 and below on the others. They were probability calculations, also. If I weren’t so lazy, I’d try doing them myself.
The revelations on asymptomatic in Fred’s yesterday post may really rock the boat.
Ken Melvin,
I’m assuming you had this CNN article in mind:
https://www.cnn.com/2020/08/08/us/duke-university-face-mask-test-trnd/index.html
One of the problems with this mask debate is that we’re getting opinions from people across various disciplines that may or may not have the relevant expertise. Epidemiologists understand epidemiology, but that doesn’t mean they understand the physics behind mask wearing. If I want to know how the virus behaves in a human, then I want to ask a doctor. If I want to understand how a virus spreads, then I want to ask an epidemiologist. If I want to understand the effectiveness of a mask, then I want to ask an experimental physicist or an engineer. Leonard Hofstadter or Howard Wolowitz are likely to have more expertise in the effectiveness of masks blocking particles than a doctor of medicine. There’s a reason why we have a division of labor & expertise.
9 cases of COVID-19 reported at North Paulding High
https://www.ajc.com/education/9-cases-of-covid-19-reported-at-north-paulding-high-school/OWH6MN7DZ5A2XDQMXX337AQEWI/
As US hits 5 million coronavirus cases, Europe is alarmed and astonished by American response to outbreak
AP via @BostonGlobe – August 9
ROME — With confirmed coronavirus cases in the US hitting 5 million Sunday, by far the highest of any country, the failure of the most powerful nation in the world to contain the scourge has been met with astonishment and alarm in Europe.
Perhaps nowhere outside the US is America’s bungled virus response viewed with more consternation than in Italy, which was ground zero of Europe’s epidemic. Italians were unprepared when the outbreak exploded in February, and the country still has one of the world’s highest official death tolls at over 35,000.
But after a strict nationwide, 10-week lockdown, vigilant tracing of new clusters and general acceptance of mask mandates and social distancing, Italy has become a model of virus containment.
“Don’t they care about their health?” a mask-clad Patrizia Antonini asked about people in the United States as she walked with friends along the banks of Lake Bracciano, north of Rome. “They need to take our precautions. … They need a real lockdown.‘’
Much of the incredulity in Europe stems from the fact that America had the benefit of time, European experience and medical know-how to treat the virus that the continent itself didn’t have when the first COVID-19 patients started filling intensive care units.
More than four months into a sustained outbreak, the US reached the 5 million mark, according to the running count kept by Johns Hopkins University. Health officials believe the actual number is perhaps 10 times higher, or closer to 50 million, given testing limitations and the fact that as many as 40% of all those who are infected have no symptoms. …
reading the title, i thought this post was about this:
Local TV stations across the country set to air discredited ‘Plandemic’ researcher’s conspiracy theory about Fauci — Local television stations owned by the Sinclair Broadcast Group are set to air a conspiracy theory over the weekend that suggests Dr. Anthony Fauci, the nation’s top expert on infectious diseases, was responsible for the creation of the coronavirus. The baseless conspiracy theory is set to air on stations across the country in a segment during the program "America This Week" hosted by Eric Bolling. The show, which is posted online before it is broadcast over the weekend, is distributed to Sinclair Broadcast Group’s network of local television stations, one of the largest in the country. A survey by Pew Research Group earlier this year showed that local news was a vital source of information on the coronavirus for many Americans, and more trusted than the media overall. In this week’s episode of the show, Bolling spoke with Judy Mikovits, the medical researcher featured in the discredited "Plandemic" video that went viral earlier this year and which was banned from platforms such as Facebook and YouTube. Throughout the segment, the on-screen graphic read, "DID DR. FAUCI CREATE COVID-19?" Bolling also spoke with Mikovits’ attorney, Larry Klayman, a right-wing lawyer who also has a history of pushing misinformation and representing conspiracy theorists. During the interview Mikovits told Bolling that Fauci had over the past decade "manufactured" and shipped coronaviruses to Wuhan, China, which became the original epicenter of the current outbreak. Bolling noted that this was a " hefty claim," but did not meaningfully challenge Mikovits and allowed her to continue making her case. Klayman also pushed conspiracy theories about the coronavirus. He said the "origins" of the virus were in the United States. Bolling didn’t meaningfully challenge Klayman either. .
North Paulding High School will close for cleaning
https://www.washingtonpost.com/education/2020/08/09/nine-people-test-positive-coronavirus-georgia-school-where-photos-packed-hallways-went-viral/?hpid=hp_hp-banner-main_school-photo-1145am%3Ahomepage%2Fstory-ans
Going from a race to the bottom to falling off the cliff, will America survive? How many more times can we get it wrong?
In the competition for economic advantage among sovereigns then there are only three things that matter: location; location; and location. So, the US was doing just fine when it was mostly in the restaurant business, but now the global pandemic has put that up against powerful headwinds. The one mistake that we did not make was stealing the territory that is now the present day US from primitive stone-age brown people. That put us on track for the gravy train until this day. What next? Who knows? The world is getting smaller every day in both literal and figurative ways.
Literal, you may ask? Well rising sea levels is some of that, but the physical world from our perspective should only consider the habitable part. So then, the habitable world is getting smaller every day.
The US does not need to get it wrong more times to fall off a cliff. We just need to wait for the bill to come due on all our past mistakes. Financialization can ruin the US economy for a while, but its bill come due is survivable thanks to our location. A lot of climate change deniers may secretly think that our location will allow us to survive the climate change bill when it comes due. Whether the US is largely safe from the worst effects of ACC or sitting at ground zero when the big one hits remains to be seen.