From Creekside: The B.C. provincial government is trying to green light the construction of a massive LNG terminal on Lelu Island in the Skeena Estuary — Pacific Northwest LNG, backed by Malaysian energy giant Petronas — without the consent of the people who rejected a $1.15 billion dollar deal from Petronas to gain that consent. […]

It’s amazing what happens if you just get out there, writes Ernie Schramayr.

Big East commissioner Val Ackerman discussed the hurdles for sports to return to her league in 2020-21.

'It's inevitable many desperate patients will resort to 'DIY dentistry'

After months of wrangling following the Russia probe, prosecutors will not go ahead with the case against Michael Flynn based on the former national security adviser's false statements to the FBI.

Police say the recovery operation in Truro, N.S., will continue over the weekend after a three-year-old boy disappeared from his grandmother’s yard Wednesday afternoon.

Follow our live coronavirus updates here Coronavirus: the symptoms

Follow our live coronavirus updates here

Boris Johnson will not take part in Prime Minister's Questions today following the birth of his son.

The pair announced the exciting news this morning

He has now been absent from the front line of the Government response for a month, after his three-week recovery period at the Chequers official residence in Buckinghamshire.

Britain will not enjoy a "V-shaped bounce" out of the crisis caused by coronavirus but will take years to recover fully, two former chancellors today warned.

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Scotland Yard has said Professor Neil Ferguson's behaviour is "plainly disappointing" but officers do not intend to take any further action.

It seems like people who get infected with SARS-CoV-2 retain immunity, but we can’t be sure how long that immunity will last. We still lack the testing capabilities to be certain.eamesBot / Shutterstock

This story was updated post-publication to include information from a study published on the preprint server medRxiv on April 17, 2020.

With more than half a million cases of COVID-19 in the United States1 and the number of deaths increasing daily, it remains unclear when and how we might return to some semblance of pre-pandemic life. This leaves many grappling with an important question: Do you become immune after SARS-CoV-2 infection? And, if so, how long might that immunity last?

In 2019, the virus SARS-CoV-2 jumped to a human host for the first time, causing the disease COVID-19. When you become infected with a new virus, your body does not possess the antibodies necessary to mount a targeted immune response. Antibodies, proteins belonging to the immunoglobulin family, consist of four chains of amino acids that form a characteristic Y-shaped structure. Antibodies are manufactured by the immune system to bind to antigens (viral proteins) to neutralize viral infectivity.

When you inhale an aerosolized droplet containing SARS-CoV-2, the virus encounters the cells of the mucous membrane lining the respiratory tract. If effective contact is made, the virus binds to a particular receptor on these cells called ACE-2. After binding ACE-2, a host enzyme is co-opted to cleave the virus’ surface protein, called the spike protein, allowing the virus to enter the cell.

It appears that individuals with COVID-19 do create neutralizing antibodies—the basis of immunity.

Within the first few hours of infection, the body’s first line of defense—the innate immune response—is activated. The innate immune response is non-specific. When a “foreign” molecule is detected, innate immune cells signal to other cells to alter their response or prepare to combat infection.

In the following days, the adaptive immune response is activated, which is more specific. The adaptive immune response will peak one to two weeks post-infection and consists of antibodies and specialized immune cells. It is called the “adaptive” immune response because of its ability to tailor the response to a specific pathogen. Antibodies can neutralize viral infectivity by preventing virus from binding to receptors, blocking cell entry, or causing virus particles to aggregate.2 Once an infection has resolved, some of these antibodies remain in the body as immunological memory to be recruited for protection in the case of reinfection. To be immune to a virus is to possess this immunological memory.

Many vaccines work by activating the adaptive immune response. Inactivated virus, viral protein, or some other construct specific to a particular virus are introduced into the body as vaccines to initiate an immune response. Ideally, the body creates antibodies against the viral construct so that it can mount a succinct response when infected by the virus. However, in order to work effectively, a vaccine must provoke an immune response that is sufficiently robust. If the body only produces low concentrations of neutralizing antibodies, adequate immunological memory may not be sustained.

While there is still much that we have to learn about SARS-CoV-2, it appears that individuals with COVID-19 do create neutralizing antibodies—the basis of immunity. However, we don’t know for certain how long that immunity might offer protection. On the question of COVID-19 re-infection, Matt Frieman, a coronavirus researcher at the University of Maryland School of Medicine, commented in a recent interview with NPR: “We don’t know very much … I think there’s a very likely scenario where the virus comes through this year, and everyone gets some level of immunity to it, and if it comes back again, we will be protected from it—either completely or if you do get reinfected later, a year from now, then you have much less disease. That’s the hope, but there is no way to know that.”3

Immunity to a virus is measured by serological testing—patient blood is collected and analyzed for the presence of antibodies against a particular virus. Serological data is most informative when collected long-term, so the data we have been able to obtain on SARS-CoV-2 is limited. However, data on other coronaviruses that we’ve had the opportunity to study in more depth can inform our estimations on how this outbreak may evolve.

First, we can look to the coronaviruses that are known to cause the common cold. Following infection with one of these coronaviruses, disease is often mild; therefore, the concentration of antibodies detected in the blood is low. This is because mild disease often indicates a less robust immune response. Interestingly, it is not the virus itself that causes us to feel sick, but, rather, our body’s response to it. Typically, the sicker we feel, the stronger the immune response; therefore, after a cold, we are often only protected for a year or two against the same virus.4 While SARS-CoV-2 wouldn’t necessarily act like these common coronaviruses, the body’s response to these coronaviruses serves as a point of reference upon which to make predictions in the absence of virus-specific data.

We can also look to coronaviruses that are known to cause severe disease, such as SARS-CoV, which caused the 2002-2003 outbreak of SARS in China. One study discovered that antibodies against SARS-CoV remained in the blood of healthcare workers for 12 years after infection.5 While it is not certain that SARS-CoV-2 will provoke a response similar to that of SARS-CoV, this study provides us with information that can inform our estimates on immunity following COVID-19 and provide hope that immunity will provide long-term protection.

If immunity to SARS-CoV-2 diminishes as it does for common cold coronaviruses, it is likely that wintertime outbreaks will recur.

Scientists have also been working to analyze antibodies in samples from individuals infected with SARS-CoV-2. A research group in Finland recently published a study detailing the serological data collected from a COVID-19 patient over the course of their illness.6 Antibodies specific to SARS-CoV-2 were present within two weeks from the onset of symptoms. Similarly, another recent report analyzing patients with confirmed COVID-19 indicated that it took approximately 11-14 days for neutralizing antibodies to be detected in blood.7 Both of these studies, while preliminary, suggest that the basis for immunity is present in patients infected with SARS-CoV-2.

Another report looked at the possibility for recurrence of COVID-19 following re-infection with SARS-CoV-2.8 In this study, rhesus macaques were infected with SARS-CoV and allowed to recover after developing mild illness. Once blood samples were collected and confirmed to test positive for neutralizing antibodies, half of the infected macaques were re-challenged with the same dose of SARS-CoV-2. The re-infected macaques showed no significant viral replication or recurrence of COVID-19. While macaques “model” human immunity, not predict it, these data further support the possibility that antibodies manufactured in response to SARS-CoV-2 are protective against short-term re-infection.

We can also analyze a virus’ structure, and the information gained from sequencing the viral genome, when trying to predict its behavior. All viruses continually undergo mutation in the process of rapid replication. They lack the necessary machinery to repair changes incurred to the genetic sequence (we as humans also incur mutations to our genetic sequence daily, but we have more sophisticated genetic repair mechanisms in place). The occurrence of significant genetic changes to the viral genome that result in viable genetic changes to a virus is termed antigenic variation. We see a lot of antigenic variation in influenza viruses (thus the need to create new vaccines each year); but the coronaviruses seem to be relatively stable antigenically.4 This is because most coronaviruses have an enzyme that allows them to correct genetic errors sustained during replication. The more stable a virus remains over time, the more likely that antibodies manufactured in response to infection or vaccination will remain effective at neutralizing viral infectivity.

All this considered, it appears that immunity is retained following SARS-CoV-2 infection. So too, that immunity might persist long enough to warrant the implementation of vaccination. However, we still have much to learn about this virus, and whether there may be some cross-immunity between SARS-CoV-2 and other coronaviruses. The widespread variation in patient immune responses adds an additional layer of complexity. We still don’t have a good understanding of why people have different responses to viral infection—some of this variation is owed to genetic variation, but how and why some people have more robust immune responses and more severe disease is still unknown.4 In some cases, individuals show a high immune response because the concentration of virus is high. In other cases, individuals show a high immune response because they differ in some aspect of immune regulation or efficiency. However, as levels of immunity increase generally across a population, the population approaches what is called “herd immunity”—when the percentage of a population immune to a particular virus is sufficiently high that viral load drops below the threshold required to sustain the infection in that population.9

How the pandemic will evolve in the coming months is uncertain. Outcomes depend on a myriad of factors—the duration of immunity, the dynamics of transmission and how we mitigate those dynamics through social distancing, the development of therapeutics and or vaccines, and the ability of healthcare systems to handle COVID-19 caseloads. If immunity to SARS-CoV-2 diminishes as it does for common cold coronaviruses, it is likely that wintertime outbreaks will recur in coming years.10 Whether immunity to other coronaviruses might offer some cross protective immunity to SARS-CoV-2 will also play a role, albeit to a lesser extent. Widespread serological testing to assess the duration of immunity to SARS-CoV-2 is imperative, but many countries still lack this capability.

A recent study looking at serological data from 3,300 symptomatic and asymptomatic individuals in California estimates that there may be as many as 48,000-81,000 people who have been infected with SARS-Cov-2 in Santa Clara County, which is 50- to 85-fold more cases than we previously thought.11 This small-scale survey emphasizes the importance of serological testing in determining the true extent of infection.

The continuation of rigid social distance also hangs in a balance—one-time social distancing measures may drive the SARS-CoV-2 epidemic peak into the fall and winter months, especially if there is increased wintertime transmissibility.10 New therapeutics, vaccines, or measures such as contact tracing and quarantine—once caseloads have been reduced and testing capacity increased—might reduce the need for rigid social distancing. However, if such measures are not put in place, mathematical models predict that surveillance and recurrent social distancing may be required through 2022.10 Only time will tell.

Helen Stillwell is a research associate in immunobiology at Yale University.

References

1. The COVID Tracking Project https://covidtracking.com/data/us-daily (2020).

2. Virology Blog: About Viruses and Viral Disease. Virus neutralization by antibodies. virology.ws (2009).

3. GreenfieldBoyce, N. Do you get immunity after recovering from a case of coronavirus? NPR (2020).

4. Racaniello, V., Langel, S., Leifer, C., & Barker, B. Immune 29: Immunology of COVID-19. Immune Podcast. microbe.tv (2020).

5. Guo, X., et al. Long-Term persistence of IgG antibodies in SARS-CoV infected healthcare workers. bioRxiv (2020). Retrieved from doi: 10.1101/20202/02/12/20021386

6. Haveri, A., et al. Serological and molecular findings during SARS-CoV-2 infection: the first case study in Finland, January to February 2020. Euro Surveillance 25, (2020).

7. Zhao, J., et al. Antibody responses to SARS-CoV-2 in patients of novel coronavirus disease 2019. Clinical Infectious Diseases (2020). Retrieved from doi: 10.1093/cid/ciaa344

8. Bao, L., et al. Reinfection could not occur in SARS-CoV-2 infected rhesus macaques. bioRxiv (2020). Retrieved from doi: 10.1101/20202.03.13.990226

9. Virology Blog: About Viruses and Viral Disease. Herd immunity. virology.ws (2008).

10. Kissler, S.M. Tedijanto, C., Goldstein, E., Grad, Y.H., & Lipsitch, M. Projecting the transmission dynamics of SARS-CoV-2 through the post-pandemic period. Science eabb5793 (2020).

11. Bendavid, E., et al. COVID-19 antibody seroprevalence in Santa Clara County, California. medRxiv (2020). Retrieved from doi: 10.1101/2020.04.14.20062463

The marquee on my closed neighborhood movie theater reads, “See you on the other side.” I like reading it every day as I pass by on my walk. It causes me to envision life after the coronavirus pandemic. Which is awfully hard to envision now. But it’s out there. When you have a disease and are in a hospital, alone and afraid, intravenous tubes and sensor wires snaking from your body into digital monitors, all you want is to be normal again. You want nothing more than to have a beer in a dusky bar and read a book in amber light. At least that’s all I wanted last year when I was in a hospital, not from a coronavirus. When, this February, I had that beer in a bar with my book, I was profoundly happy. The worst can pass.

With faith, you can ask how life will be on the other side. Will you be changed personally? Will we be changed collectively? The knowledge we’re gaining now is making us different people. Pain demands relief, demands we don’t repeat what produced it. Will the pain of this pandemic point a new way forward? It hasn’t before, as every war attests. This time may be no different. But the pandemic has slipped a piece of knowledge into the body public that may not be easy to repress. It’s an insight scientists and poets have voiced for centuries. We’re not apart from nature, we are nature. The environment is not outside us, it is us. We either act in concert with the environment that gives us life, or the environment takes life away.

Guess which species is the bully? No animal has had the capacity to modify its niche the way we have.

Nothing could better emphasize our union with nature than the lethal coronavirus. It’s crafted by a molecule that’s been omnipresent on Earth for 4 billion years. Ribonucleic acid may not be the first bridge from geochemical to biochemical life, as some scientists have stated. But it’s a catalyst of biological life. It wrote the book on replication. RNA’s signature molecules, nucleotides, code other molecules, proteins, the building blocks of organisms. When RNA’s more chemically stable kin, DNA, arrived on the scene, it outcompeted its ancestor. Primitive organisms assembled into cells and DNA set up shop in their nucleus. It employed its nucleotides to code proteins to compose every tissue in every multicellular species, including us. A shameless opportunist, RNA made itself indispensable in the cellular factory, shuttling information from DNA into the cell’s power plant, where proteins are synthesized.

RNA and DNA had other jobs. They could be stripped down to their nucleotides, swirled inside a sticky protein shell. That gave them the ability to infiltrate any and all species, hijack their reproductive machinery, and propagate in ways that make rabbits look celibate. These freeloading parasites have a name: virus. But viruses are not just destroyers. They wear another evolutionary hat: developers. Viruses “may have originated the DNA replication system of all three cellular domains (archaea, bacteria, eukarya),” writes Luis P. Villareal, founding director of the Center for Virus Research at the University of California, Irvine.1 Their role in nature is so successful that DNA and RNA viruses make up the most abundant biological entities on our planet. More viruses on Earth than stars in the universe, scientists like to say.

Today more RNA than DNA viruses thrive in cells like ours, suggesting how ruthless they’ve remained. RNA viruses generally reproduce faster than DNA viruses, in part because they don’t haul around an extra gene to proofread their molecular merger with others’ DNA. So when the reckless RNA virus finds a new place to dwell, organisms become heartbreak hotels. Once inside a cell, the RNA virus slams the door on the chemical saviors dispatched by cells’ immunity sensors. It hijacks DNA’s replicative powers and fans out by the millions, upending cumulative cellular functions. Like the ability to breathe.

Humans. We love metaphors. They allow us to compare something as complex as viral infection to something as familiar as an Elvis Presley hit. But metaphors for natural processes are seldom accurate. The language is too porous, inviting our anthropomorphic minds to close the gaps. We imagine viruses have an agenda, are driven by an impetus to search and destroy. But nature doesn’t act with intention. It just acts. A virus lives in a cell like a planet revolves around a sun.

Biologists debate whether a virus should be classified as living because it’s a deadbeat on its own; it only comes to life in others. But that assumes an organism is alive apart from its environment. The biochemist and writer Nick Lane points out, “Viruses use their immediate environment to make copies of themselves. But then so do we: We eat other animals or plants, and we breathe in oxygen. Cut us off from our environment, say with a plastic bag over the head, and we die in a few minutes. One could say that we parasitize our environment—like viruses.”2

Our inseparable accord with the environment is why the coronavirus is now in us. Its genomic signature is almost a perfect match with a coronavirus that thrives in bats whose habitats range across the globe. Humans moved into the bats’ territory and the bats’ virus moved into humans. The exchange is just nature doing its thing. “And nature has been doing its thing for 3.75 billion years, when bacteria fought viruses just as we fight them now,” says Shahid Naeem, an upbeat professor of ecology at Columbia University, where he is director of the Earth Institute Center for Environmental Sustainability. If we want to assign blame, it lies with our collectively poor understanding of ecology.

Organisms evolve with uniquely adaptive traits. Bats play many ecological roles. They are pollinators, seed-spreaders, and pest-controllers. They don’t die from the same coronavirus that kills humans because the bat’s anatomy fights the virus to a draw, neutralizing its lethal moves. What’s the deal with the human immune system? We don’t fly. “Bats are flying mammals, which is very unusual,” says Christine K. Johnson, an epidemiologist at the One Health Institute at the University of California, Davis, who studies virus spillover from animals to humans. “They get very high temperatures when they fly, and have evolved immunological features, which humans haven’t, to accommodate those temperatures.”

A viral invasion can overstimulate the chemical responses from a mammal’s immune system to the point where the response itself causes excessive inflammation in tissues. A small protein called a cytokine, which orchestrates cellular responses to foreign invaders, can get over-excited by an aggressive RNA virus, and erupt into a “storm” that destroys normal cellular function—a process physicians have documented in many current coronavirus fatalities. Bats have genetic mechanisms to inhibit that overreaction. Similarly, bat flight requires an increased rate of metabolism. Their wing-flapping action leads to high levels of oxygen-free radicals—a natural byproduct of metabolism—that can damage DNA. As a result, states a 2019 study in the journal Viruses, “bats probably evolved mechanisms to suppress activation of immune response due to damaged DNA generated via flight, thereby leading to reduced inflammation.”3

Bats don’t have better immune systems than humans; just different. Our immune systems evolved for many things, just not flying. Humans do well around the cave fungus Pseudogymnoascus destructans, source of the “white-nose syndrome” that has devastated bats worldwide. Trouble begins when we barge into wildlife habitats with no respect for differences. (Trouble for us and other animals. White-nose syndrome spread in part on cavers’ shoes and clothing, who tracked it from one site to the next.) We mine for gold, develop housing tracts, and plow forests into feedlots. We make other animals’ habitats our own.

Our moralistic brain sees retribution. Karma. A viral outbreak is the wrath that nature heaps on us for bulldozing animals out of their homes. Not so. “We didn’t violate any evolutionary or ecological laws because nature doesn’t care what we do,” Naeem says. Making over the world for ourselves is just humans being the animals we are. “Every species, if they had the upper hand, would transform the world into what it wants,” Naeem says. “Birds build nests, bees build hives, beavers build dams. It’s called niche construction. If domestic cats ruled the world, they would make the world in their image. It would be full of litter trays, lots of birds, lots of mice, and lots of fish.”

But nature isn’t an idyllic land of animal villages constructed by evolution. Species’ niche-building ways have always brought them into contact with each other. “Nature is ruled by processes like competition, predation, and mutualism,” Naeem says. “Some of them are positive, some are negative, some are neutral. That goes for our interactions with the microbial world, including viruses, which range from super beneficial to super harmful.”

Nature has been doing its thing for 3.75 billion years, when bacteria fought viruses as we fight them now.

Ultimately, nature works out a truce. “If the flower tries to short the hummingbird on sugar, the hummingbird is not going to provide it with pollination,” Naeem says. “If the hummingbird sucks up all the nectar and doesn’t do pollination well, it’s going to get pinged as well. Through this kind of back and forth, species hammer out an optimal way of getting along in nature. Evolution winds up finding some middle ground.” Naeem pauses. “If you try to beat up everybody, though, it’s not going to work.”

Guess which species is the bully? “There’s never been any species on this planet in its entire history that has had the capacity to modify its niche the way we have,” Naeem says. Our niche—cities, farms, factories—has made the planet into a zoological Manhattan. Living in close proximity with other species, and their viruses, means we are going to rub shoulders with them. Dense living isn’t for everyone. But a global economy is. And with it comes an intercontinental transportation system. A virus doesn’t have a nationality. It can travel as easily from Arkansas to China as the other way around. A pandemic is an inevitable outcome of our modified niche.

Although nature doesn’t do retribution, our clashes with it have mutual consequences. The exact route of transmission of SARS-CoV-2 from bat to humans remains unmapped. Did the virus pass directly into a person, who may have handled a bat, or through an intermediate animal? What is clear is the first step, which is that a bat shed the virus in some way. University of California, Davis epidemiologist Johnson explains bats shed viruses in their urine, feces, and saliva. They might urinate on fruit or eat a piece of it, and then discard it on the ground, where an animal may eat it. The Nipah virus outbreak in 1999 was spurred by a bat that left behind a piece of fruit that came in contact with a domestic pig and humans. The Ebola outbreaks in the early 2000s in Central Africa likely began when an ape, who became bushmeat for humans, came in contact with a fruit bat’s leftover. “The same thing happened with the Hendra virus in Australia in 1994,” says Johnson. “Horses got infected because fruit bats lived in trees near the horse farm. Domesticated species are often an intermediary between bats and humans, and they amplify the outbreak before it gets to humans.”

Transforming bat niches into our own sends bats scattering—right into our backyards. In a study released this month, Johnson and colleagues show the spillover risk of viruses is the highest among animal species, notably bats, that have expanded their range, due to urbanization and crop production, into human-run landscapes.4 “The ways we’ve altered the landscape have brought a lot of great things to people,” Johnson says. “But that has put wildlife at higher pressures to adapt, and some of them have adapted by moving in with us.”

Pressures on bats have another consequence. Studies indicate physiological and environmental stress can increase viral replication in them and cause them to shed more than they normally do. One study showed bats with white-nose syndrome had “60 times more coronavirus in their intestines” as uninfected bats.5 Despite evidence for an increase in viral replication and shedding in stressed bats, “a direct link to spillover has yet to be established,” concludes a 2019 report in Viruses.3 But it’s safe to say that bats being perpetually driven from their caves into our barns is not ideal for either species.

As my questions ran out for Columbia University’s Naeem, I asked him to put this horrible pandemic in a final ecological light for me.

“We think of ourselves as being resilient and robust, but it takes something like this to realize we’re still a biological entity that’s not capable of totally controlling the world around us,” he says. “Our social system has become so disconnected from nature that we no longer understand we still are a part of it. Breathable air, potable water, productive fields, a stable environment—these all come about because we’re part of this elaborate system, the biosphere. Now we’re suffering environmental consequences like climate change and the loss of food security and viral outbreaks because we’ve forgotten how to integrate our endeavors with nature.”

A 2014 study by a host wildlife ecologists, economists, and evolutionary biologists lays out a plan to stem the tide of emergent infectious diseases, most of which spawned in wildlife. Cases of emergent infectious diseases have practically quadrupled since 1940.6 World leaders could get smart. They could pool money for spillover research, which would identify the hundreds of thousands of potentially lethal viruses in animals. They could coordinate pandemic preparation with international health regulations. They could support animal conservation with barriers that developers can’t cross. The scientists give us 27 years to cut the rise of infectious diseases by 50 percent. After that, the study doesn’t say what the world will look like. I imagine it will look like a hospital right now in New York City.

Patients lie on gurneys in corridors, swaddled in sheets, their faces shrouded by respirators. They’re surrounded by doctors and nurses, desperately trying to revive them. In pain, inconsolable, and alone. I know they want nothing more than to see their family and friends on the other side, to be wheeled out of the hospital and feel normal again. Will they? Will others in the future? It will take tremendous political will to avoid the next pandemic. And it must begin with a reckoning with our relationship with nature. That tiny necklace of RNA tearing through patients’ lungs right now is the world we live in. And have always lived in. We can’t be cut off from the environment. When I see the suffering in hospitals, I can only ask, Do we get it now?

Kevin Berger is the editor of Nautilus.

References

1. Villareal, L.P. The Widespread Evolutionary Significance of Viruses. In Domingo, E., Parrish, C.R., & Hooland, J. (Eds.) Origin and Evolution of Viruses Elsevier, Amsterdam, Netherlands (2008).

2. Lane, N. The Vital Question: Energy, Evolution, and the Origins of Complex Life W.W. Norton, New York, NY (2015).

3. Subudhi, S., Rapin, N., & Misra, V. Immune system modulation and viral persistence in Bats: Understanding viral spillover. Viruses 11, E192 (2019).

4. Johnson, C.K., et al. Global shifts in mammalian population trends reveal key predictors of virus spillover risk. Proceedings of The Royal Society B 287 (2020).

5. Davy, C.M., et al. White-nose syndrome is associated with increased replication of a naturally persisting coronaviruses in bats. Scientific Reports 8, 15508 (2018).

6. Pike, J., Bogich, T., Elwood, S., Finnoff, D.C., & Daszak, P. Economic optimization of a global strategy to address the pandemic threat. Proceedings of the National Academy of Sciences 111, 18519-18523 (2014).

Lead image: AP Photo / Mark Lennihan

The final outcome of COVID-19 is still unclear. It will ultimately be decided by our patience and the financial bottom line.Castleski / Shutterstock

On January 5, six days after China officially announced a spate of unusual pneumonia cases, a team of researchers at Shanghai’s Fudan University deposited the full genome sequence of the causal virus, SARS-CoV-2, into Genbank. A little more than three months later, 4,528 genomes of SARS-CoV-2 have been sequenced,1 and more than 883 COVID-related clinical trials2 for treatments and vaccines have been established. The speed with which these trials will deliver results is unknown—the delicate bаlance of efficacy and safety can only be pushed so far before the risks outweigh the benefits. For this reason, a long-term solution like vaccination may take years to come to market.3

The good news is that a lack of treatment doesn’t preclude an end to the ordeal. Viral outbreaks of Ebola and SARS, neither of which had readily available vaccines, petered out through the application of consistent public health strategies—testing, containment, and long-term behavioral adaptations. Today countries that have previously battled the 2002 SARS epidemic, like Taiwan, Hong Kong, and Singapore, have shown exemplary recovery rates from COVID. Tomorrow, countries with high fatality rates like Sweden, Belgium, and the United Kingdom will have the opportunity to demonstrate what they’ve learned when the next outbreak comes to their shores. And so will we.

The first Ebola case was identified in 1976,4 when a patient with hemorrhagic symptoms arrived at the Yambuku Mission Hospital, located in what is now the Democratic Republic of Congo (DRC). Patient samples were collected and sent to several European laboratories that specialized in rare viruses. Scientists, without sequencing technology, took about five weeks to identify the agent responsible for the illness as a new member of the highly pathogenic Filoviridae family.

The first Ebola outbreak sickened 686 individuals across the DRC and neighboring Sudan. 453 of the patients died, with a final case fatality rate (CFR)—the number of dead out of number of sickened—of 66 percent. Despite the lethality of the virus, sociocultural interventions, including lockdowns, contact-tracing, campaigns to change funeral rites, and restrictions on consumption of game meat all proved effective interventions in the long run.

That is, until 2014, when there was an exception to the pattern. Ebola appeared in Guinea, a small country in West Africa, whose population had never before been exposed to the virus. The closest epidemic had been in Gabon, 13 years before and 2,500 miles away. Over the course of two years, the infection spread from Guinea into Liberia and Sierra Leone, sickening more than 24,000 people and killing more than 10,000.

Countries that have previously battled the 2002 SARS epidemic, like Taiwan and Hong Kong, have shown exemplary recovery rates.

During the initial phase of the 2014 Ebola outbreak, rural communities were reluctant to cooperate with government directives for how to care for the sick and the dead. To help incentivize behavioral changes, sociocultural anthropologists like Mariane Ferme of the University of California, Berkeley, were brought in to advise the government. In a recent interview with Nautilus, Ferme indicated that strategies that allowed rural communities to remain involved with their loved ones increased cooperation. Villages located far from the capital, she said, were encouraged to “deputize someone to come to the hospital, to come to the burial, so they could come back to the community and tell the story of the body.” For communities that couldn’t afford to send someone to the capital, she saw public health officials adopt a savvy technological solution—tablets to record video messages that were carried between convalescent patients and their families.

However, there were also systemic failures that, in Ferme’s opinion, contributed to the severity of the 2014 West African epidemic. In Sierra Leone, she said, “the big mistake early on was to distribute [weakly causal] information about zoonotic transmission, even when it was obviously community transmission.” In other words, although there had been an instance of zoonotic transmission—the virus jumping from a bat to a human—that initiated the epidemic, the principle danger was other contagious individuals, not game meat. Eventually, under pressure from relief groups, the government changed its messaging to reflect scientific consensus.

But the retraction shook public faith in the government and bred resentment. The mismatch between messaging and reality mirrors the current pandemic. Since the COVID outbreak began, international and government health officials have issued mixed messages. Doubts initially surfaced about the certainty of the virus being capable of spreading from person to person, and the debate over the effectiveness of masks in preventing infection continues.

Despite the confused messaging, there has been general compliance with stay-at-home orders that has helped flatten the curve. Had the public been less trusting of government directives, the outcome could have been disastrous, as it was in Libera in 2014. After a two-week lockdown was announced, the Liberian army conducted house-to-house sweeps to check for the sick and collect the dead. “It was a draconian method that made people hide the sick and dead in their houses,” Ferme said. People feared their loved ones would be buried without the proper rites. A direct consequence was a staggering number of active cases, and an unknown extent of community transmission. But in the end, the benchmark for the end of Ebola and SARS was the same. The WHO declared victory when the rate of new cases slowed, then stopped. By the same measure, when an entire 14-day quarantine period passes with no new cases of COVID-19, it can be declared over.

It remains possible that even if we manage to end the epidemic, it will return again. Driven by novel zoonotic transmissions, Ebola has flared up every few years. Given the extent of COVID-19’s spread, and the potential for the kind of mutations that allow for re-infection, it may simply become endemic.

Two factors will play into the final outcome of COVID-19 are pathogenicity and virulence. Pathogenicity is the ability of an infectious agent to cause disease in the host, and is measured by R0—the number of new infections each patient can generate. Virulence, on the other hand, is the amount of harm the infectious agent can cause, and is best measured by CFR. While the pathogenicity of Ebola, SARS, and SARS-CoV-2 is on the same order—somewhere between 1 to 3 new infections for each patient, virulence differs greatly between the two SARS viruses and Ebola.

The case fatality rate for an Ebola infection is between 60 to 90 percent. The spread in CFR is due to differences in infection dynamics between strains. The underlying cause of the divergent virulence of Ebola and SARS is largely due to the tropism of the virus, meaning the cells that it attacks. The mechanism by which the Ebola virus gains entry into cells is not fully understood, but it has been shown the virus preferentially targets immune and epithelial cells.5 In other words, the virus first destroys the body’s ability to mount a defense, and then destroys the delicate tissues that line the vascular system. Patients bleed freely and most often succumb to low blood pressure that results from severe fluid loss. However, neither SARS nor SARS-CoV-2 attack the immune system directly. Instead, they enter lung epithelial cells through the ACE2 receptor, which ensures a lower CFR. What is interesting about these coronaviruses is that despite their similar modes of infection, they demonstrate a range of virulence: SARS had a final CFR of 10 percent, while SARS-CoV-2 has a pending CFR of 1.4 percent. Differences in virulence between the 2002 and 2019 SARS outbreaks could be attributed to varying levels of care between countries.

The chart above displays WHO data of the relationship between the total number of cases in a country and the CFR during the 2002-2003 SARS-CoV epidemic. South Africa, on the far right, had only a single case. The patient died, which resulted in a 100 percent CFR. China, on the other hand, had 5,327 cases and 349 deaths, giving a 7 percent CFR. The chart below zooms to the bottom left corner of the graph, so as to better resolve critically affected countries, those with a caseload of less than 1,000, but with a high CFR.

Here is Hong Kong, with 1,755 cases and a 17 percent CFR. There is also Taiwan, with 346 cases and an 11 percent CFR. Finally, nearly tied with Canada is Singapore with 238 cases and a 14 percent CFR.

With COVID-19, it’s apparent that outcome reflects experience. China has 82,747 cases of COVID, but has lowered their CFR to 4 percent. Hong Kong has 1,026 cases and a 0.4 percent CFR. Taiwan has 422 cases at 1.5 percent CFR, and Singapore with 8,014 cases, has a 0.13 percent CFR.

It was the novel coronavirus identification program established in China in the wake of the 2002 SARS epidemic that alerted authorities to SARS-CoV-2 back in November of 2019. The successful responses by Taiwan, Hong Kong, and Singapore can also be attributed to a residual familiarity with the dangers of an unknown virus, and the sorts of interventions that are necessary to prevent a crisis from spiraling out of control.

In West Africa, too, they seem to have learned the value of being prepared. When Ferme returned to Liberia on March 7, she encountered airport staff fully protected with gowns, head covers, face screens, masks, and gloves. By the time she left the country, 10 days later, she said, “Airline personnel were setting up social distancing lines, and [rural vendors] hawking face masks. Motorcycle taxis drivers, the people most at risk after healthcare workers—all had goggles and face masks.”

The sheer number of COVID-19 cases indicates the road to recovery will take some time. Each must be identified, quarantined, and all contacts traced and tested. Countries that failed to act swiftly, which allowed their case numbers to spiral out of control, will pay in lives and dollars. Northwestern University economists Martin Eichenbaum et al. modeled6 the cost of a yearlong shutdown to be $4.2 trillion, a cost that proactive countries will not face. A recent Harvard study7 published in Science suggests the virus will likely make seasonal appearances going forward, potentially requiring new waves of social distancing. In other words, initial hesitancy will have repercussions for years. In the future, smart containment principles,6 where restrictions are applied on the basis of health status, may temper the impact of these measures.

Countries that failed to act swiftly, which allowed their case numbers to spiral out of control, will pay in lives and dollars.

Inaction was initially framed as promoting herd immunity, where spread of the virus is interrupted once everyone has fallen sick with it. This is because getting the virus results in the same antibody production process as getting vaccinated—but doesn’t require the development of a vaccine. The Johns Hopkins Bloomberg School of Public Health estimates that 70 percent of the population will need to be infected with or vaccinated against the virus8 for herd immunity to work. Progress toward it has been slow, and can only be achieved through direct infection with the virus, meaning many will die. A Stanford University study in Santa Clara County9 suggests only 2.5 percent to 4.2 percent of the population have had the virus. Another COVID hotspot in Gangelt, Germany, suggests 15 percent10—higher, but still nowhere near the 70 percent necessary for herd immunity. Given the dangers inherent in waiting on herd immunity, our best hope is a vaccine.

A key concern for effective vaccine development is viral mutation. This is because vaccines train the immune system to recognize specific shapes on the surface of the virus—a composite structure called the antigen. Mutations threaten vaccine development because they can change the shape of the relevant antigen, effectively allowing the pathogen to evade immune surveillance. But, so far, SARS-CoV-2 has been mutating slowly, with only one mutation found in the section most accessible to the immune system, the spike protein. What this suggests is that the viral genome may be sufficiently stable for vaccine development.

What we know, though, is that Ebola was extinguished due to cooperation between public health officials and community leaders. SARS-CoV ended when all cases were identified and quarantined. The Spanish Flu in 1918 vanished after two long, deadly seasons.

The final outcome of COVID-19 is still unclear. It will ultimately be decided by our patience and the financial bottom line. With 26 million unemployed and protests erupting around the country, it seems there are many who would prefer to risk life and limb rather than face financial insolvency. Applying smart containment principles in the aftermath of the shutdown might be the best way to get the economy moving again, while maintaining the safety of those at greatest risk. Going forward, vigilance and preparedness will be the watchwords of the day, and the most efficient way to prevent social and economic ruin.

Anastasia Bendebury and Michael Shilo DeLay did their PhDs at Columbia University. Together they created Demystifying Science, a science literacy organization devoted to providing clear, mechanistic explanations for natural phenomena. Find them on Twitter @DemystifySci.

References

1. Genomic epidemiology of novel coronavirus - Global subsampling. Nextstrain www.nextstrain.org.

2. Covid-19 TrialsTracker. TrialsTracker www.trialstracker.net.

3. Struck, M. Vaccine R&D success rates and development times. Nature Biotechnology 14, 591-593 (1996).

4. Breman, J. & Johnson, K. Ebola then and now. The New England Journal of Medicine 371 1663-1666 (2014).

5. Baseler, L., Chertow, D.S., Johnson, K.M., Feldmann, H., & Morens, D.M. THe pathogenesis of Ebola virus disease. The Annual Review of Pathology 12, 387-418 (2017).

6. Eichenbaum, M., Rebell, S., & Trabandt, M. The macroeconomics of epidemics. The National Bureau of Economic Research Working Paper: 26882 (2020).

7. Kissler, S., Tedijanto, C., Goldstein, E., Grad, Y., & Lipsitch, M. Projecting the transmission dynamics of SARS-CoV-2 through the postpandemic period. Science eabb5793 (2020).

8. D’ Souza, G. & Dowdy, D. What is herd immunity and how can we achieve it with COVID-19? Johns Hopkins COVID-19 School of Public Health Insights www.jhsph.edu (2020).

9. Digitale, E. Test for antibodies against novel coronavirus developed at Stanford Medicine. Stanford Medicine News Center Med.Stanford.edu (2020).

10. Winkler, M. Blood tests show 14%of people are now immune to COVID-19 in one town in Germany. MIT Technology Review (2020).

On January 5, six days after China officially announced a spate of unusual pneumonia cases, a team of researchers at Shanghai’s Fudan University deposited the full genome sequence of the causal virus, SARS-CoV-2, into Genbank. A little more than three months later, 4,528 genomes of SARS-CoV-2 have been sequenced,1 and more than 883 COVID-related clinical trials2 for treatments and vaccines have been established. The speed with which these trials will deliver results is unknown—the delicate bаlance of efficacy and safety can only be pushed so far before the risks outweigh the benefits. For this reason, a long-term solution like vaccination may take years to come to market.3

The good news is that a lack of treatment doesn’t preclude an end to the ordeal. Viral outbreaks of Ebola and SARS, neither of which had readily available vaccines, petered out through the application of consistent public health strategies—testing, containment, and long-term behavioral adaptations. Today countries that have previously battled the 2002 SARS epidemic, like Taiwan, Hong Kong, and Singapore, have shown exemplary recovery rates from COVID. Tomorrow, countries with high fatality rates like Sweden, Belgium, and the United Kingdom will have the opportunity to demonstrate what they’ve learned when the next outbreak comes to their shores. And so will we.

The first Ebola case was identified in 1976,4 when a patient with hemorrhagic symptoms arrived at the Yambuku Mission Hospital, located in what is now the Democratic Republic of Congo (DRC). Patient samples were collected and sent to several European laboratories that specialized in rare viruses. Scientists, without sequencing technology, took about five weeks to identify the agent responsible for the illness as a new member of the highly pathogenic Filoviridae family.

The first Ebola outbreak sickened 686 individuals across the DRC and neighboring Sudan. 453 of the patients died, with a final case fatality rate (CFR)—the number of dead out of number of sickened—of 66 percent. Despite the lethality of the virus, sociocultural interventions, including lockdowns, contact-tracing, campaigns to change funeral rites, and restrictions on consumption of game meat all proved effective interventions in the long run.

That is, until 2014, when there was an exception to the pattern. Ebola appeared in Guinea, a small country in West Africa, whose population had never before been exposed to the virus. The closest epidemic had been in Gabon, 13 years before and 2,500 miles away. Over the course of two years, the infection spread from Guinea into Liberia and Sierra Leone, sickening more than 24,000 people and killing more than 10,000.

Countries that have previously battled the 2002 SARS epidemic, like Taiwan and Hong Kong, have shown exemplary recovery rates.

During the initial phase of the 2014 Ebola outbreak, rural communities were reluctant to cooperate with government directives for how to care for the sick and the dead. To help incentivize behavioral changes, sociocultural anthropologists like Mariane Ferme of the University of California, Berkeley, were brought in to advise the government. In a recent interview with Nautilus, Ferme indicated that strategies that allowed rural communities to remain involved with their loved ones increased cooperation. Villages located far from the capital, she said, were encouraged to “deputize someone to come to the hospital, to come to the burial, so they could come back to the community and tell the story of the body.” For communities that couldn’t afford to send someone to the capital, she saw public health officials adopt a savvy technological solution—tablets to record video messages that were carried between convalescent patients and their families.

However, there were also systemic failures that, in Ferme’s opinion, contributed to the severity of the 2014 West African epidemic. In Sierra Leone, she said, “the big mistake early on was to distribute [weakly causal] information about zoonotic transmission, even when it was obviously community transmission.” In other words, although there had been an instance of zoonotic transmission—the virus jumping from a bat to a human—that initiated the epidemic, the principle danger was other contagious individuals, not game meat. Eventually, under pressure from relief groups, the government changed its messaging to reflect scientific consensus.

But the retraction shook public faith in the government and bred resentment. The mismatch between messaging and reality mirrors the current pandemic. Since the COVID outbreak began, international and government health officials have issued mixed messages. Doubts initially surfaced about the certainty of the virus being capable of spreading from person to person, and the debate over the effectiveness of masks in preventing infection continues.

Despite the confused messaging, there has been general compliance with stay-at-home orders that has helped flatten the curve. Had the public been less trusting of government directives, the outcome could have been disastrous, as it was in Libera in 2014. After a two-week lockdown was announced, the Liberian army conducted house-to-house sweeps to check for the sick and collect the dead. “It was a draconian method that made people hide the sick and dead in their houses,” Ferme said. People feared their loved ones would be buried without the proper rites. A direct consequence was a staggering number of active cases, and an unknown extent of community transmission. But in the end, the benchmark for the end of Ebola and SARS was the same. The WHO declared victory when the rate of new cases slowed, then stopped. By the same measure, when an entire 14-day quarantine period passes with no new cases of COVID-19, it can be declared over.

It remains possible that even if we manage to end the epidemic, it will return again. Driven by novel zoonotic transmissions, Ebola has flared up every few years. Given the extent of COVID-19’s spread, and the potential for the kind of mutations that allow for re-infection, it may simply become endemic.

Two factors will play into the final outcome of COVID-19 are pathogenicity and virulence. Pathogenicity is the ability of an infectious agent to cause disease in the host, and is measured by R0—the number of new infections each patient can generate. Virulence, on the other hand, is the amount of harm the infectious agent can cause, and is best measured by CFR. While the pathogenicity of Ebola, SARS, and SARS-CoV-2 is on the same order—somewhere between 1 to 3 new infections for each patient, virulence differs greatly between the two SARS viruses and Ebola.

The case fatality rate for an Ebola infection is between 60 to 90 percent. The spread in CFR is due to differences in infection dynamics between strains. The underlying cause of the divergent virulence of Ebola and SARS is largely due to the tropism of the virus, meaning the cells that it attacks. The mechanism by which the Ebola virus gains entry into cells is not fully understood, but it has been shown the virus preferentially targets immune and epithelial cells.5 In other words, the virus first destroys the body’s ability to mount a defense, and then destroys the delicate tissues that line the vascular system. Patients bleed freely and most often succumb to low blood pressure that results from severe fluid loss. However, neither SARS nor SARS-CoV-2 attack the immune system directly. Instead, they enter lung epithelial cells through the ACE2 receptor, which ensures a lower CFR. What is interesting about these coronaviruses is that despite their similar modes of infection, they demonstrate a range of virulence: SARS had a final CFR of 10 percent, while SARS-CoV-2 has a pending CFR of 1.4 percent. Differences in virulence between the 2002 and 2019 SARS outbreaks could be attributed to varying levels of care between countries.

The chart above displays WHO data of the relationship between the total number of cases in a country and the CFR during the 2002-2003 SARS-CoV epidemic. South Africa, on the far right, had only a single case. The patient died, which resulted in a 100 percent CFR. China, on the other hand, had 5,327 cases and 349 deaths, giving a 7 percent CFR. The chart below zooms to the bottom left corner of the graph, so as to better resolve critically affected countries, those with a caseload of less than 1,000, but with a high CFR.

Here is Hong Kong, with 1,755 cases and a 17 percent CFR. There is also Taiwan, with 346 cases and an 11 percent CFR. Finally, nearly tied with Canada is Singapore with 238 cases and a 14 percent CFR.

With COVID-19, it’s apparent that outcome reflects experience. China has 82,747 cases of COVID, but has lowered their CFR to 4 percent. Hong Kong has 1,026 cases and a 0.4 percent CFR. Taiwan has 422 cases at 1.5 percent CFR, and Singapore with 8,014 cases, has a 0.13 percent CFR.

It was the novel coronavirus identification program established in China in the wake of the 2002 SARS epidemic that alerted authorities to SARS-CoV-2 back in November of 2019. The successful responses by Taiwan, Hong Kong, and Singapore can also be attributed to a residual familiarity with the dangers of an unknown virus, and the sorts of interventions that are necessary to prevent a crisis from spiraling out of control.

In West Africa, too, they seem to have learned the value of being prepared. When Ferme returned to Liberia on March 7, she encountered airport staff fully protected with gowns, head covers, face screens, masks, and gloves. By the time she left the country, 10 days later, she said, “Airline personnel were setting up social distancing lines, and [rural vendors] hawking face masks. Motorcycle taxis drivers, the people most at risk after healthcare workers—all had goggles and face masks.”

The sheer number of COVID-19 cases indicates the road to recovery will take some time. Each must be identified, quarantined, and all contacts traced and tested. Countries that failed to act swiftly, which allowed their case numbers to spiral out of control, will pay in lives and dollars. Northwestern University economists Martin Eichenbaum et al. modeled6 the cost of a yearlong shutdown to be $4.2 trillion, a cost that proactive countries will not face. A recent Harvard study7 published in Science suggests the virus will likely make seasonal appearances going forward, potentially requiring new waves of social distancing. In other words, initial hesitancy will have repercussions for years. In the future, smart containment principles,6 where restrictions are applied on the basis of health status, may temper the impact of these measures.

Countries that failed to act swiftly, which allowed their case numbers to spiral out of control, will pay in lives and dollars.

Inaction was initially framed as promoting herd immunity, where spread of the virus is interrupted once everyone has fallen sick with it. This is because getting the virus results in the same antibody production process as getting vaccinated—but doesn’t require the development of a vaccine. The Johns Hopkins Bloomberg School of Public Health estimates that 70 percent of the population will need to be infected with or vaccinated against the virus8 for herd immunity to work. Progress toward it has been slow, and can only be achieved through direct infection with the virus, meaning many will die. A Stanford University study in Santa Clara County9 suggests only 2.5 percent to 4.2 percent of the population have had the virus. Another COVID hotspot in Gangelt, Germany, suggests 15 percent10—higher, but still nowhere near the 70 percent necessary for herd immunity. Given the dangers inherent in waiting on herd immunity, our best hope is a vaccine.

A key concern for effective vaccine development is viral mutation. This is because vaccines train the immune system to recognize specific shapes on the surface of the virus—a composite structure called the antigen. Mutations threaten vaccine development because they can change the shape of the relevant antigen, effectively allowing the pathogen to evade immune surveillance. But, so far, SARS-CoV-2 has been mutating slowly, with only one mutation found in the section most accessible to the immune system, the spike protein. What this suggests is that the viral genome may be sufficiently stable for vaccine development.

What we know, though, is that Ebola was extinguished due to cooperation between public health officials and community leaders. SARS-CoV ended when all cases were identified and quarantined. The Spanish Flu in 1918 vanished after two long, deadly seasons.

The final outcome of COVID-19 is still unclear. It will ultimately be decided by our patience and the financial bottom line. With 26 million unemployed and protests erupting around the country, it seems there are many who would prefer to risk life and limb rather than face financial insolvency. Applying smart containment principles in the aftermath of the shutdown might be the best way to get the economy moving again, while maintaining the safety of those at greatest risk. Going forward, vigilance and preparedness will be the watchwords of the day, and the most efficient way to prevent social and economic ruin.

Anastasia Bendebury and Michael Shilo DeLay did their PhDs at Columbia University. Together they created Demystifying Science, a science literacy organization devoted to providing clear, mechanistic explanations for natural phenomena. Find them on Twitter @DemystifySci.

References

1. Genomic epidemiology of novel coronavirus - Global subsampling. Nextstrain www.nextstrain.org.

2. Covid-19 TrialsTracker. TrialsTracker www.trialstracker.net.

3. Struck, M. Vaccine R&D success rates and development times. Nature Biotechnology 14, 591-593 (1996).

4. Breman, J. & Johnson, K. Ebola then and now. The New England Journal of Medicine 371 1663-1666 (2014).

5. Baseler, L., Chertow, D.S., Johnson, K.M., Feldmann, H., & Morens, D.M. THe pathogenesis of Ebola virus disease. The Annual Review of Pathology 12, 387-418 (2017).

6. Eichenbaum, M., Rebell, S., & Trabandt, M. The macroeconomics of epidemics. The National Bureau of Economic Research Working Paper: 26882 (2020).

7. Kissler, S., Tedijanto, C., Goldstein, E., Grad, Y., & Lipsitch, M. Projecting the transmission dynamics of SARS-CoV-2 through the postpandemic period. Science eabb5793 (2020).

8. D’ Souza, G. & Dowdy, D. What is herd immunity and how can we achieve it with COVID-19? Johns Hopkins COVID-19 School of Public Health Insights www.jhsph.edu (2020).

9. Digitale, E. Test for antibodies against novel coronavirus developed at Stanford Medicine. Stanford Medicine News Center Med.Stanford.edu (2020).

10. Winkler, M. Blood tests show 14%of people are now immune to COVID-19 in one town in Germany. MIT Technology Review (2020).

Lead image: Castleski / Shutterstock

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