Blog, Reports

How A Virus Can Shake The World

by Edward Dutton and Richard Spencer

It has happened before. It can happen again. And it can happen here.

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Introduction

The novel Coronavirus has already changed the world.

As of this writing, some 1.6 million Covid-19 infections have been recorded worldwide. More than 100,000 people have died total: 18,000 in the United States and 6,000 in New York City alone.[1]

Economies have screeched to a halt. Stock markets have crashed. Borders have been sealed. The Prime Minister of Great Britain was put into intensive care due to a Coronavirus infection; he thankfully recovered, but the ordeal foretells the destabilization of societies from top to bottom. Henry Kissinger has warned that the geopolitical order has been disrupted permanently.[2]

Average citizens are engaging in behaviors, like “social distancing,” self-quarantining, and wearing masks in public, that would have been unimaginable merely a month ago. Cities have become surreally abandoned as citizens are holed up inside their apartments. Unemployment is skyrocketing, and rent is not being paid en masse. Trends that were underway before the crisis—like streaming entertainment, work-at-home, and delivery of groceries—are now the only option, and the old norms may never return.

Major League baseball has been suspended. And the latest James Bond film is delayed for months, as if caught up in plot by an international mastermind.

All of this because of a little virus.

Photo: SkyNews

The corona crisis may emerge as a singular event—like the fall of the Berlin Wall, 9/11, and the 2008 financial crisis—after which nothing can be the same, as it informs and inflects, not just politics, but the deepest levels of culture and human psychology.

This essay is an attempt to take the Coronavirus seriously and adumbrate its potential social and demographic impact. This is not an exercise in “doomsaying,” though it might be read as such. There is never any shortage of Cassandras or “conspiracy theorists,” particularly on the Internet, but lately the more dangerous phenomenon has been wishful-thinking.

Up until mid-March, President Donald Trump and his allies referred to the viral outbreak as “just the flu” or some variation thereof. This talking-point was recklessly naïve about the Coronovirus—and doubly so, considering that a hundred years ago an influenza outbreak led to the deaths of 1-3 percent of the global population, as we discuss below.

We shouldn’t exaggerate the potential consequences of the Coronavirus, but we should avoid minimizing them. Ultimately, comparisons between the death tolls of the World Wars and the potential devastation of Coviod-19 are not without merit.

The wishful-thinking among politicians and the media had its obvious motivations, and perhaps it represents a failing of human nature. But it also derived from a simple lack of understanding about the biological nature of a virus, the power of exponential growth, and the tremendous demographic impact that can be wrought by a pandemic.

This has all happened before. And an advanced industrial economy has the power to severely mitigate, if not quite prevent, pandemics and eradicate viruses. But none of that is possible if we are not willing to face what we are up against.

What is a Virus?

These days, it’s difficult to read a newspaper or check your Twitter feed without encountering the word “virus.” But what exactly is one?

Throughout human history, we have been surrounded by microscopic viruses. We ingest millions of them every second. We have co-evolved with them, such that the vast majority of organisms have viruses that are specifically designed to infect them. We have become resistant to most, so long as we have a reasonably healthy immune system to fight them off. Viruses are so common that bacteria and even other viruses can be subject to viral infection.

Viruses are not living beings in the strict sense of the term. Rather, they are complex collections of matter that are able to self-replicate. In many ways, they blur the line between what is alive and what is not. Viruses undergo evolution by natural selection, and they have “interests” in the metaphorical sense that they pursue strategies to expand, dominate their environments, and pass on their genetic material.

Viruses are constructed of a shell containing enzymes for the replication of either their DNA or RNA—the virus’s essential genetic information, its genome. It uses this, with the help of various molecular techniques, to replicate itself. However, unlike most organisms, and even bacteria, a virus cannot replicate itself on its own. It is a kind of parasite, needing to take control of a host, which it infects in order to replicate. Specifically, it must infect a cell belonging to that host.

Photo: The Mayo Clinic

The cell is the fundamental building block of any organism. Cells manufacture proteins, replicate DNA, and store important resources. Cells perform their function for a period of time, divide (manufacturing their own replacement in the process), and die. The organism’s entire genetic code—its genes, composed of DNA—reside in each cell’s nucleus. These genes tell each cell what its function is and, thus, which parts of the DNA code they should use. In each cell, the relevant part of the DNA code is transcribed by its RNA. With this accomplished, the cell can produce a protein that permits it to affect its ordained role in the overall functioning of the organism.

These functions make a cell a wonderful host for a virus. The virus infects them and transforms them into virus-producing zombies. The virus’s shell is covered in receptors. It uses these to bind itself to the outer membrane of a cell. Once it has done this, the virus forces the cell to either accept its genetic material or accept it—the virus—in its entirety.

Once inside, the virus hijacks the cell’s protein-manufacturing systems and DNA-replication mechanism. In so doing, it forces the cell to make copies of the virus. Eventually, the cell is full to capacity with viruses, resulting in the viruses bursting out of the cell in search of new hosts in which to replicate. Through this process, they infect more and more of the organism, preventing the infected cells from doing their job properly.

If a virus infects too many cells in the lungs, for example, then the organism will not be able to breathe properly, ultimately leading to death. In the meantime, that organism will have transmitted the virus to other members of its own species.

This is, in fact, the great danger of a Coronavirus infection, which is an acute respiratory disorder. We can live with some viruses. The chickenpox virus, for example, resides, mostly inactive, in the nervous system of billions of humans. But the Coronavirus, if not defeated by a healthy immune system, will attack the lungs and can kill the host.

The Parasite’s Dilemma

All life—or, in the case of viruses, all quasi-life—seeks to reproduce itself. And as mentioned, viruses pursue “strategies” for expansion. Specifically, they engage in an evolutionary trade-off in relation to the speed at which they replicate and highjack cells.

Viruses are not like other parasites in nature, which exploit their hosts but not to the point of destroying him. Tapeworms, fleas, and barnacles on whales are examples of such creatures. Viruses, by their very nature, undermine and destroy whatever system they enter. But through evolution, they “learn” not to do this too quickly.

If viruses replicate extremely fast, then they may overwhelm their host before he can spread them to another. And if viruses cannot continually find new hosts, they will eventually die out. If, on the other hand, viruses replicate slowly—and don’t kill or severely undermine their host—they will have a greater opportunity to spread. The host will interact with other members of his species and infect them, too. But this also means that the host’s immune system will have greater time and energy to destroy the viruses, or the infection could be treated medically.

Successful viruses develop a balanced strategy—not too quick, not too slow.
Covid-19’s long dormancy period—10-20 days, from what we know—is key to its potency and danger. A Coronavirus victim might not show symptoms for weeks—or even not at all—while he interacts with potential new hosts, and they interact with him. In this regard, Donald Trump’s description of Coronavirus is apt—an “invisible enemy.”[3]

How to Measure Contagion

The number of people that an individual carrier is expected to infect with his virus is called its R0 (“R-Naught”). The common flu has an R0 around 1.3. In other words, if you are infected, you will likely pass it the virus to one other person—a co-worker, family member, a random person on the bus, etc. This person will, in turn, pass the virus along to someone else, who will also pass it along, and so on. The flu virus will thus steadily expand, even if it never generates explosive outbreaks like measles, whose R0 is between 12-18.[4] If the R0 of a virus is under 1, that means that, more likely than not, an infected person will not spread the virus to another, and it will gradually disappear.

At this point, we can only make an educated guess regarding the R0 of Covid-19, because we do not know how many people have been infected, as so many experience few or or no symptoms. The general estimate is that Covid-19’s R0 is 2.6—or somewhere between 2 and 3 new infections each round.[5] Coronavirus is thus on par with the deadly Spanish Flu, whose R0 was around 3. If this is true, then Covid-19’s potential to expand throughout the population should not be underestimated.[6]

Vaccinations, hygeine, and other advancements can significantly reduce a virus’s R0. For instance, when H1N1 virus (the basic structure of the Spanish Flu) returned in 2009, its R0 was down to 1.6.[7] As of this writing, there is reason to believe that social distancing is working, and the Coronavirus’s expansion is beginning to slow.[8]

The Power of Exponential Growth

The human mind tends to comprehend matters linearly. If a ball is rolled down a sidewalk, we can quickly gauge its speed, perhaps factor in friction, and predict where it will end up. Our minds are wired to think in terms of constant, predictable growth—what happened then is happening now and will happen in the future. It is much more difficult for us to imagine exponential growth, that is, something that “breeds like rabbits” and can compound from 1 to 2 to 4 to 8 . . . to 512 to 1,024 . . . and, in a few more rounds, to 1,048,576.

If Covid-19 does, in fact, have an R0 of 2.6, then on the first round of infection, “Patient 0” will pass the virus on to two-to-three people. This new group of infected will pass it along to six-to-eight people, and then 17-18. By the fifth round, more than 118 will be infected. By the 10th round, more than 14,000. And by the 20th, around 200 million!

Our inability to get our minds around such growth was behind some of the naively optimistic comments from politicians at the start of the Covid-19 outbreak: “We only have a few cases here . . . no need to panic . . . we’re going to be okay” was a frequent refrain. A few weeks later, these same politicians were contemplating scenarios in which two-thirds of the population would be infected, and hundreds of thousands would die.

The difference between an R0 of 1.3 (common flu) and 2.6 (coronavirus) might seem slight, but it is tremendous in effect. In the United States, between 10 and 35 million catch the common flu each year (3-to-10 percent of the population).[9] With Coronavirus and its R0 of 2.6, after around 21 rounds of reproduction, some half a billion infections would take place—meaning the entire population of North America.

There are, however, natural barriers to exponential growth. A virus cannot reproduce exponentially ad infinitum for the simple fact that potential new hosts will have already been infected. Once roughly 60-70 percent of the population is infected, the Coronavirus will begin to encounter more infected people than uninfected, and its R0 will gradually collapse. This natural barrier is the basis of so-called “herd immunity,” which in March was the strategy of the British government; put simply, do nothing and allow the virus to burn through the population.[10]

On the other hand, if national leaders attempt to reduce the virus’s R0 directly through medical and social actions, then some two-thirds of the infections that would have taken place need to be prevented for the strategy to be effective.[11] This is the concept behind obligatory quarantines, social distancing, and “flattening the curve.”[12] Such a strategy, of course, comes with a major economic cost. And for it to work, the politicians and nations have to go “all in.” Half-measures accrue costs without addressing the real issue.

Why is Covid-19 So Deadly?

With most forms of flu, tiny particles that include the virus are inhaled, meaning that the virus will enter cells in your nose and throat. From these, it will enter saliva and mucus. And the body will expel these, potentially passing on the virus in the process. The virus can also be expelled from the body via the air and, thus, from breathing on somebody else or talking to them at close range. The nose produces mucus and the mouth produces saliva. These are both critical for body functioning. Mucus also captures air-born viruses and thus protects the body against them. If the body doesn’t do anything about this river of fluid, then it will be carried towards the lungs, filling them and causing you to develop pneumonia. In healthy people, however, this doesn’t happen. Healthy people transport this fluid back up the windpipe and swallow it where it will be digested and destroyed. Accordingly, they are less likely to develop pneumonia. If people have damaged lungs, then they will be less able to transport this fluid back up the windpipe.

Covid-19 is more serious than normal flu because it appears to specifically attack cells in the lungs, meaning that the sufferer is less able to expel fluid and more likely to develop pneumonia.[13] At the same time, if the host’s immune system is weak, then the virus is more likely to successfully make its way to the lungs, causing serious complications.

This dimension of Covid-19 is one of the reasons why the fatality rate is so high. The fatality rate of seasonal flu is approximately 0.1 percent of patients.[14] In general, victims die because seasonal flu develops into pneumonia. These deaths are heavily skewed towards the elderly, because they tend to have weaker immune systems, worse general health, and more underlying conditions that render catching even a mild flu dangerous. The father of modern medicine, Sir William Osler (1849-1919), referred to pneumonia as the “old man’s friend” because it often was a painless way of putting an elderly man out of his misery. Osler would himself die of an underlying health condition exacerbated by the Spanish Flu.

It is unclear what the precise mortality of Covid-19 is, because, it being novel, there are far fewer detailed studies on it than the seasonal flu. It has been estimated by the World Health Organization that the mortality is between 2 and 3.5 percent.[15] The recorded fatality rate in Northern Italy was high (12 percent), while in Germany, remarkably low (1.6 percent).[16] As of early April, the fatality rate in the United States was around the WHO’s estimate, and ranging between one and seven percent, according to data compiled by Johns Hopkins University.[17] Obviously, the infection rate will vary significantly due to factors such as the sample size and the quality of the testing regime, as well as the underlying health of the population. Covid-19 is far less serious among young people and far graver among the old. For those over 80 in China, the mortality rate was reported as high as 14 percent.[18]

Across all age groups, Covid-19 seems to be 10-35 times more deadly than everyday flu, and possibly 100 times more deadly in certain contexts.

The virus has thus achieved a dangerously balanced strategy for its reproduction. Its long dormancy and asymptomatic period accelerates its spread. Its low mortality rate, particularly among the younger and healthier people, has led to widespread complacency and even denial among Western governments and populations. It is an “invisible enemy”—and one whose potency might only be properly understood after it has struck.

The Spanish Flu

During the final months of the First World War, an influenza pandemic erupted across the globe, which came to be known as the Spanish Flu. In America, the epidemic was articulated in three great waves during the spring, fall, and winter of 1918.

The “Spanish” Flu probably originated in New York City and was, in fact, an outbreak of the H1N1 virus.[19] Spain was neutral during the war, and its media was actively reporting on the severity of the epidemic, while the antagonistic parties sought to keep their outbreaks secret, so as to project national strength and resolve.[20] Whatever the case, the name stuck.

The Spanish Flu, it is thought, had an R0 of 3 and morality rate of 2.5 percent, some 25 times that of the common flu.[21] This high death rate was due, in large part, to the close crowding of individuals during wartime and the limited development of antibiotics and personal hygiene. Most deaths were due to secondary bacterial infections, not the H1N1 virus itself.[22]

The outbreak proved to be nothing short of a planetary disaster. Long before commercial air travel, the virus expanded across Asia, Europe, Africa, and into the wilds of Alaska. The victims of the Spanish Flu would ultimately outnumber those of the World War.

By 1920, it is estimated that some 500 million people had been infected worldwide.[23] Global fatality estimates range from 17.4 million[24] to as high as 24.7, 39.3,[25] and even 50 million.[26] Between 500,000 and 1 million people died of the virus in the United States alone.

Unlike Covid-19, which is fatal mostly among the elderly and those with pre-existing conditions, deaths due to the Spanish Flu were pronounced among infants and people between the ages of 20 and 40, especially young men. The average age of those who succumbed was 28.[27]

To put the Spanish Flu into perspective, the H1N1 virus was able to expand and ultimately infect around 30 percent of the global population. And somewhere between 1 and 3 percent died of the virus or resulting complications.

Comparisons to the other global catastrophe of that period—the Great War—leap to mind. Around 0.13 percent of the U.S population died in W.W.I. Thus, for Americans, who joined the war late and whose participation was more limited than that of the European powers, the Spanish Flu was significantly more devastating. And even for the European powers, the death toll from Spanish Flu was not much less than that of the Great War. Just over 2 percent of the British population died in World War I, only slightly higher than its death rate from the Spanish Flu.[28]

Across the last 150 years, life expectancy in America and Europe has doubled, from roughly 40 to 80 years. This is, of course, due to the major advancements of the industrial revolution, modern medicine, and the exploitation of fossil fuels. Compiling data from multiple countries, Max Roser has demonstrated that this gradual push upwards in life expectancy was dramatically interrupted during the 1918-20 period, in which it dropped some 10-15 years in the United States and across Europe.

Those born in the last 20 years of the 19th century reached adulthood during the horrors of the Great War, the Spanish Flu, the Russian Revolution and Civil War, and more. The shared experience of the “Lost Generation,” as Hemingway named them, was nothing short of demographic decimation.

Potential Demographic Impact of Covid-19

The world, and the West in particular, is getting older. And one of the chief reasons why Covid-19 could devastate populations to a war-like extent is that it particularly affects the elderly.

During the Spanish Flu crisis, the average age of death in the United States was 55 (which partly reflected the higher child mortality at the time). Today, the average age of death among Americans was 78. The most common age of a U.S. citizen is now 27, with a median of 38. But these seemingly low figures obscures the demographic structure of a rapidly aging country, particularly for non-Hispanic Whites. The most common age among Whites is 58 (30 years higher than that of ethnic minorities); 10 percent of Whites are over the age of 73 (Silent Generation) and 26 percent, over 54 (Baby Boomers). As a comparison, 60 percent of non-White minorities are under the age of 37, and only 20 percent are over the age of 54.[29]

Recent reports have suggested that Coronavirus is spiraling out of control in ethnic-minority neighborhoods. In Chicago, for example, African-Americans make up 68 percent of the city’s 118 deaths due to Coronavirus.[30] In New York, Rockland County, home to many Hasidic Jewish communities, has the highest per capita rate of infection.[31] These numbers seem to be the result of behavior, not genetics; African-Americans and Jews are ignoring calls for self-quarantining and social distancing, and sadly paying a price.

The fact remains that, if Coronavirus is to spread as widely as feared, White Americans are unquestionably the most vulnerable group, precisely because they are the oldest.

There are, we should point out, many differences between the situation in 1918 and that of 2020 that could make Covid-19 less catastrophic than the Spanish Flu. Science and medicine are vastly improved; we have better sanitation; health agencies can more immediately communicate with the public; and the population is, overall, better nourished.

On the other hand, the world of 2020 has a plethora of “First World Problems,” such as obesity and diabetes, which make people more vulnerable to fatal infections.[32] We are also more interconnected, and our transportation systems allow the virus to spread with much greater ease. Put bluntly, we live in a more crowded, fatter, busier, more interconnected—and perhaps more fragile—world.  

Postmodern America is not immune to the shocks of history. And there is ultimately nothing new under the sun. It has happened before. It can happen again. And it can happen here.



References

  1. See United States Covid-19 Statistics, https://covidusa.net (accessed April 6, 2020); Johns Hopkins University and Medicine, “Coronavirus COVID-19 Global Cases,” https://coronavirus.jhu.edu/map.html (accessed April 6, 2020).↩︎
  2. Henry Kissinger, “The Coronavirus Pandemic Will Forever Alter the World Order,” Wall Street Journal, https://www.wsj.com/articles/the-coronavirus-pandemic-will-forever-alter-the-world-order-11585953005 (accessed April 6, 2020). ↩︎
  3. Donald J. Trump, Twitter Post, 1:14 PM, March 18, 2020, https://twitter.com/realDonaldTrump/status/1240355985673392128?s=20 (accessed April 6, 2020). ↩︎
  4. Fiona Guerra, Shelly Bolotin, Gillian Lim, Jane Heffernan, Shelley Deeks, Ye Li, and Natasha Crowcroft, “The Basic Reproduction Number (R0) of Measles: A Systematic Review, The Lancet: Infectious Diseases (2017). ↩︎
  5. Rachael Rettner, “How does the new coronavirus compare with the flu?” Science Live, https://www.livescience.com/new-coronavirus-compare-with-flu.html (accessed April 6, 2020). ↩︎
  6. Holly Yan and Scott Andrew, “You Asked, We’re Answering: Your Top Coronavirus Questions,” March 31, 2020, https://edition.cnn.com/interactive/2020/health/coronavirus-questions-answers/ (accessed April 6, 2020). ↩︎
  7. Vanessa Bates Ramirez, “What Is R0?: Gauging Contagious Infections,” Healthline, June 24, 2016, https://www.healthline.com/health/r-nought-reproduction-number (accessed April 6, 2020). ↩︎
  8. Dan Barry, “Optimism is Less Distant As Global Coronavirus Wages On,” New York Times, https://www.nytimes.com/2020/04/08/us/coronavirus-global-progress.html (accessed April 6, 2020). ↩︎
  9. Centers for Disease Control and Prevention, “Disease Burden of Influenza,” January 10, 2020, https://www.cdc.gov/flu/about/burden/index.html (accessed April 6, 2020). ↩︎
  10. See Neil M Ferguson et al., “Impact of non-pharmaceutical interventions (NPIs) to Reduce COVID- 19 Mortality and Healthcare Demand,” Imperial College Covid-19 Response Team, https://www.imperial.ac.uk/media/imperial-college/medicine/sph/ide/gida-fellowships/Imperial-College-COVID19-NPI-modelling-16-03-2020.pdf (accessed April 6, 2020). It’s worth noting that, reportedly, 70 percent of blood donors in the Italian region of Castiglione d’Adda have traces of Coronavirus in their bloodstreams, meaning that some kind of collective immunity might have been achieved. See Anatoly Karlin, “The Cost of Herd Immunity,” Unz.com, April 4, 2020, https://www.unz.com/akarlin/cost-of-herd-immunity/ (accessed April 6, 2020). ↩
  11. See Anna Carthaus, “Corona confusion: How to Make Sense of the Numbers and Terminology,” Deutsche Welle, March 20, 2020, https://www.dw.com/en/corona-confusion-how-to-make-sense-of-the-numbers-and-terminology/a-52825433 (accessed April 6, 2020). ↩︎
  12. See Brandon Specktor, “Coronavirus: What is ‘Flattening the Curve,’ and Will It Work?” Live Science, https://www.livescience.com/coronavirus-flatten-the-curve.html (accessed April 6, 2020). ↩︎
  13. Bruce L. Davidson, “Doctor: How to Reduce Your Vulnerability to Coronavirus—When sleeping,” CNN News, March 13, 2020, https://edition.cnn.com/2020/03/12/opinions/coronavirus-vulnerability-while-sleeping-bruce-davidson/index.html (accessed April 6, 2020). ↩︎
  14. Centers for Disease Control and Prevention, “Disease Burden of Influenza,” op cit. ↩︎
  15. World Health Organization, “Coronavirus disease 2019 (Covid-19) Situation Report – 46,” March 6, 2020, https://www.who.int/docs/default-source/coronaviruse/situation-reports/20200306-sitrep-46-covid-19.pdf?sfvrsn=96b04adf_2 (accessed April 6, 2020). ↩︎
  16. Katrin Bennhold, “A German Exception? Why the Country’s Coronavirus Death Rate Is Low,” New York Times, April 4, 2020, https://www.nytimes.com/2020/04/04/world/europe/germany-coronavirus-death-rate.html (accessed April 6, 2020). ↩︎
  17. See United States Covid-19 Statistics, op cit. ↩︎
  18. AFP, “No, Coronavirus Isn’t ‘Just Like the Flu’. Here Are the Very Important Differences,” Science Alert, March 14, 2020, https://www.sciencealert.com/the-new-coronavirus-isn-t-like-the-flu-but-they-have-one-big-thing-in-common (accessed April 6, 2020). ↩︎
  19. Donald R. Olson, Lone Simonsen, Paul J. Edelson, and Stephen S. Morse, “Epidemiological Evidence of an Early Wave of the 1918 influenza Pandemic in New York City, Proc. Natl. Acad. Sci. U.S.A. 102, 11059–11063, https://www.pnas.org/content/pnas/102/31/11059.full.pdf (accessed April 6, 2020). ↩︎
  20. Max Roser, “The Spanish Flu (1918-20): The Global Impact of the Largest Influenza Pandemic in History,” Our World in Data, March 4, 2020, https://ourworldindata.org/spanish-flu-largest-influenza-pandemic-in-history (accessed April 6, 2020).
    ↩︎
  21. Molly Billings, “The Influenza Pandemic of 1918,” Stanford University, June 1997, https://virus.stanford.edu/uda/ (accessed April 6, 2020). ↩︎
  22. Roser, “The Spanish Flu,” op cit. ↩︎
  23. Centers for Disease Control and Prevention, “1918 Pandemic (H1N1 virus),” https://www.cdc.gov/flu/pandemic-resources/1918-pandemic-h1n1.html (accessed April 6, 2020). ↩︎
  24. Peter Spreeuwenberg, Madelon Kroneman, John Paget, “Reassessing the Global Mortality Burden of the 1918 Influenza Pandemic,” American Journal of Epidemiology, https://academic.oup.com/aje/article/187/12/2561/5092383 (accessed April 6, 2020). ↩︎
  25. K.D. Patterson and G.F. Pyle, “The Geography and Mortality of the 1918 Influenza Pandemic,” Bulletin of the History of Medicine (1991), 65(1), 4. ↩︎
  26. Niall P.A.S. Johnson and Juergen Mueller, “Updating the Accounts: Global Mortality of the 1918-1920 “Spanish” Influenza Pandemic,” Bulletin of the History of Medicine Vol. 76, No. 1 (Spring 2002), 105-115. ↩︎
  27. Centers for Disease Control and Prevention, “The 1918 Flu Pandemic: Why It Matters 100 Years Later,” https://blogs.cdc.gov/publichealthmatters/2018/05/1918-flu/ (accessed April 6, 2020).
    ↩︎
  28. Reperes, “World War I Casulties,” http://www.centre-robert-schuman.org/userfiles/files/REPERES%20–%20module%201-1-1%20-%20explanatory%20notes%20–%20World%20War%20I%20casualties%20–%20EN.pdf (accessed April 6, 2020).
    ↩︎
  29. Katherine Schaeffer, “The most common age among whites in U.S. is 58—more than double that of racial and ethnic minorities,” Pew Research, https://www.pewresearch.org/fact-tank/2019/07/30/most-common-age-among-us-racial-ethnic-groups/ (accessed April 6, 2020). ↩︎
  30. Meagan Flynn, “‘Those numbers take your breath away’: Covid-19 is hitting Chicago’s black neighborhoods much harder than others, officials say,” Washington Post, https://www.washingtonpost.com/nation/2020/04/07/chicago-racial-disparity-coronavirus/ (accessed April 6, 2020). ↩︎
  31. Jesse McKinley and Nate Schweber, “Fear and Frustration Rise as Virus Spikes in Jewish Enclaves,” New York Times, https://www.nytimes.com/2020/04/08/nyregion/coronavirus-rockland-monsey-jews.html (accessed April 6, 2020). ↩︎
  32. Alex Morales, “U.K. May Warn the Obese They’re More Vulnerable to Coronavirus,” Bloomberg, https://www.bloomberg.com/news/articles/2020-04-09/u-k-may-warn-the-obese-they-re-more-vulnerable-to-coronavirus (accessed April 10, 2020). ↩︎