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Coronavirus Primer, Part 4: Coronavirus and Society

COVID-19 is much more than a medical issue. The virus, and human response to the virus, have made 2020 feel like a time of war. 1

What is guiding us — the fear of contagion or the contagion of fear?

About This Primer

I am researching and writing this series to take a big-picture look at COVID-19.  I’m taking a step back from the daily news information overload and fact-checking the (even larger) load of misinformation.  I announced this project in June and invited questions from my friends. It is now a series of indefinite duration.  Part 1 covered the basics of viruses and coronaviruses.  Part 2 dealt with SARS-CoV-2 on the level of individual health.  Part 3 discussed the epidemiology.

In today’s installment, I take a turn from the biological to the social realm.  The pandemic is much more than a medical issue.  It has come to define the environment of 2020 in all aspects of our lives.  Part 4 is “Coronavirus and Society.”  I begin with the coronavirus recession.  I then discuss the psychology and politics of how we think, feel, and communicate about this pandemic.  What guides us – the fear of contagion or the contagion of fear?  Why do different segments of society have such divergent outlooks on this event?   

I. The Coronavirus Recession

II. National and Partisan Differences in Attitude

III. The Psychology of Uncertainty

IV. Conclusions

V. Citations

I. The Coronavirus Recession

COVID-19 as a social and economic crisis is arguably more momentous than as a medical crisis.  The only way to slow the contagion for now is to regulate travel and population density.  As you well know, this keeps employees from work, it slows down consumer spending, and it shutters factories – in short, it is an economic wrecking ball.  While the virus itself has harmed about 1% of 1% of us, our response to it has impacted us all.    

A recession is defined as a period of at least two consecutive quarters of economic contraction.  By that standard, the US and 18 other nations were already in recession by the 3rd quarter. 2 The forecast for the year is that the global economy will shrink by 4 – 5%, the deepest plunge since WWII.  This is the first recession to slow down the growth of developing nations.  Some economists predict that over 90% of all national economies will contract this year, a metric that makes this downturn even worse than the Great Depression. 3 The loss of jobs in the second quarter of 2020 alone was equivalent to almost 200 million full-time workers. 4 

When economists describe this recession, a recurring theme is that demand and supply are both down. 5 This double-whammy impact is felt most strongly in travel and inessential establishments like bars and massage parlors.  Not only are these businesses unable to provide their full range of services, but the customers have less discretionary money on hand.  This will make recovery difficult, as there will not be an excess of demand waiting to meet recovering supply or vice versa.   

Another significant effect is a transfer of economic activity from one sector to another.  While restaurant dining is down, food delivery is up; TV on demand has taken over the movie theater industry.  Online shopping has exploded.  Many of today’s hot sectors (like nursing and webcasting) are hiring vigorously.  However, it will take a while for employees to train and find jobs, and by then the short-term surge may have ended.

Some sectors are unequivocally depressed.  Oil prices have tanked as people have driven less and airlines have slashed flights.  This helps consumers but harms many of the poorest countries, which derive a large portion of their income from oil exports. 

In some ways, the coronavirus recession is a tipping point for existing crises.  There was already a major debt crisis in the 2010s.  Now, government spending is breaking records.  There have been numerous high-profile stimulus packages in the US and Europe.  Small governments that are not accustomed to such bailouts are strained to the limits and are borrowing heavily. 6 Lockdowns are also exacerbating famines that were already alarming last year. 7

The two faces of the coronavirus – the disease and the depression – have us between a rock and a hard place.  In the short term, we cannot ameliorate one without aggravating the other.  Concerns about public health and the economy are all legitimate, and it seems politically impossible to find a balance satisfactory to everyone. 

II. National And Partisan Differences In Attitude

An anonymous person on a forum asked,Why do conservatives downplay the pandemic compared to liberals?

A.  Conservative and Liberal Attitudes

B.  Political Parties and Leaders

C.  National Differences

A. Conservative and Liberal Attitudes

The tension between public health and the economy is ages old, and political parties were already positioned on opposite sides of the divide.  Conservatism might be described as an “economy first” philosophy.  Conservatives resist spending money or changing behavior for new or uncertain threats.  Liberal-minded thinkers are more receptive to accepting new problems and solutions, 8 and to paying for those solutions with government funds.  These positions have been consistent at least since the 18th century, when economists sounded alarms about overpopulation.  The same theme has played out with nutritional and medicinal advice, wildlife conservation, pollution, and climate change. 

There is an important commonality to these modern liberal concerns.  They are all “invisible” to the individual.  When it comes to cosmic questions, conservatives feel more comfortable with traditional sources like religion.  Otherwise, reality is conservatively defined by tangible direct personal experience.  The conservative part of our mind is apt to think, “I burn gasoline in my car every day.  My neighborhood is clean, and it snowed here last night.  You can’t tell me that fossil fuels cause pollution or climate change!”  It’s easy to conclude that warnings about fossil fuels are a fiction spun by someone with an agenda. 

The liberal part of our mind may have an easier time seeing, believing, or caring about aggregate effects.  However, liberal parties can take their concerns to extremes that are not clearly necessary.  Public health threats are often detected in their early phases.  We can’t really know the scope of the problem without predicting the future – and predictions often lead to worst-case-scenario anxiety.  Furthermore, aggregate solutions do not always require rapid, radical changes for all persons.   

The political divide is exaggerated by urban / rural differences.  Viral contagion, like many other societal hazards, is most rampant in densely populated cities.  Urban areas also happen to be more liberal in character than small towns and the countryside.  Since ruralites don’t face the same infectious risk as urbanites, they often feel that city-made precautions do not apply to them. 9

B. Political Parties and Leaders

Most people are probably not conscious of why each attitude is associated with a different political party, but it doesn’t matter why.  Once those associations are made, they become self-perpetuating.  Well before the pandemic, the Republican and Democratic parties of the United States had already become hyper-partisan to the point of feeling contemptuous and prejudiced toward each other.  Sociologists actually have a name for this state: affective polarization. 10 It has become more important to each party to defeat the other than to think in terms of a common interest.          

Political leaders and the party rank-and-file reinforce each other.  Politicians know and say what their constituents want to hear.  Their behavior clarifies the party standard, which crystallizes quickly throughout the party.  On the right, presidents such as Trump 11 and Bolsonaro 12 resist wearing masks, downplay the public health threat, and scoff at safety measures.  Trump has said that wearing a mask “would send the wrong message” to his voters by making it seem like he is preoccupied with health instead of the economy. 13 In turn, 84% of Republicans trust the president more than they trust scientists. 14

Political parties can co-exist peacefully even when they have different values.  They may self-segregate or irritate each other.  The differences become more salient when one party imposes its values on the other, or even when one perceives an imposition.  This year, generically speaking, conservatives feel that governments, corporations, and even judgmental neighbors are imposing “liberal” rules and restrictions upon them.  Liberals feel violated when conservatives invade their space without safety precautions.  In this quibble, the stakes are high.   

C. National Differences

Some political leaders feel embarrassed about natural disasters getting out of their control, so they deny the problem or shift blame.  The Chinese and US governments point the finger at each other, sometimes with completely unfounded accusations. 15 President Trump has alternately argued that his opponents are making a mountain out of a molehill 16 or, if it is a bad problem, it’s their fault. 17

The United States and western Europe, the homeland of the 18th century Enlightenment, are unique among the world in their esteem of individual liberty. 18 The rest of the world places higher value on being “protective of the collective” (to coin a phrase) even if it demands personal sacrifice.  As I discussed in Part 3, Asians have a much easier time accepting government recommendations, and they wear face masks in the highest proportions. 

Westerners, on the other extreme, feel threatened when the government tells them what to do, even if it is for the public good.  This sentiment increases toward the right.  Many conservatives deny that there is a public threat at all.  The words that they associate most often with face mask mandates and social lockdowns are not even entirely economical; they include “freedom” and “rights”. 

III. The Psychology of Uncertainty

Karen K. commented, “The speed at which guidance changes based on ‘emerging understanding’ of the virus is enough to make me trust no one.”

Mitzi M-H rhetorized, “How can we possibly know what it’s doing when the numbers are changing or inaccurate to start with?”

William B. rhetorized, “What’s going on with the WHO and the CDC?  Why are there so many disparate studies and conflicting information?”

A. Dealing with Unknowns

B. Whom can we Trust?

C. How Do we Feel?

D. How Should we Feel?

A. Dealing with Unknowns

When it comes to the coronavirus, it’s important to remember a key issue:

There are many unknowns.

This butts heads with a universal law of human nature:

We hate unknowns.

As 21st century web addicts, we demand answers, and we demand them now!  Unfortunately, clear answers are usually hard to find in the early stages of any sudden crisis.  We ask, “How many infections are harmless and undetected?  What causes more harm – the disease or the lockdowns?  Will immunity last forever?  When will vaccines be available?”  We expect textbook right-and-wrong answers.  Although many such questions are mathematically modeled, they usually have answers like, “We don’t know,” or “It depends.” 

These are emotionally unsatisfying answers, especially coming from experts, and doubly so for people who are not accustomed to nuance.  Unresolved anxiety then tempts us to conclude, “There is a simple answer, and someone knows, but they’re not telling me!” Then our imagination fills in the voids.  We are highly prone to believing the next “satisfying” answer that comes along. 1 19

It’s okay to accept that knowledge has boundaries, often blurry ones.  That’s especially true for a moment of panic like this year.  Even honest scientists, doctors, politicians, and public officials don’t have all the answers.  But their bounded answers are much better than conspiratorial guesswork.  Give doubt a chance.

B. Whom can we Trust?

Most Americans say that they trust major health agencies first 20 and that they are skeptical of their social media news feeds. 21 Are these intuitions justified?     

My standard is to consider the sources’ incentives and capabilities: 

Who is most willing and able to find the truth, the whole truth, and nothing but the truth?

By my values, research scientists must be at the top of this list, for at least two reasons.  First, they are the only people with direct first-hand knowledge and expertise in the medical issues.  Second, scientists are judged by how well they find truth, whether it’s beautiful or ugly. 

There is a broad spectrum of media bias and credibility.  I strongly recommend sites such as All Sides and Media Bias / Fact Check , which rank news sources on several criteria.  Still, news outlets produce content for mass consumption, which requires them to simplify and / or sensationalize information.  In an event like this pandemic, most news channels can only present a surface-level account – but it’s an essential first source.   

I do not turn to politics for answers.  This goes somewhat for office holders, but especially for party activists and armchair politicians.  Partisans get emotionally attached to their parties’ preconceived notions.  They then devote most of their time and energy to trash-talking each other and defending themselves.  Truth takes a back seat to “who’s right” or, even more trivially, “who’s righteous”. 

Social media rumors and word of mouth place lowest in my trust hierarchy.  There are large but highly vocal segments of the population that lack the capacity or the incentive to manage voluminous, nuanced, complex information.  Office holders, in turn, must pander to those folks for re-election. 

Unelected government agencies in free countries are generally more trustworthy, as they are ideally sheltered from the partisan winds of emotionality.  Agencies also have money for effective scientific and statistical research.  Unfortunately, there is mounting evidence that President Trump has politicized US agencies like the FDA 22 , CDC 23 , and HHS 24 .  Federal agencies have sent mixed signals as they have vacillated between public health advice and the president’s preferred messaging. 25

C. How Do We Feel?

“People are tired of COVID.  People are saying, ‘Whatever, just leave us alone.‘ ” …

You turn on CNN, that’s all they cover. ‘COVID, COVID, pandemic’ …

People aren’t buying it, CNN, you dumb bastards.”

President Trump, 10/19/20 26

President Trump is describing crisis fatigue, aka chronic stress response.  Whether we are stressed out about the virus itself, the economic impact, impositions on our lifestyle, or simply the unending arguments, most of us have felt stressed all year.  Long-term stress is not natural, and it takes a toll on physical and emotional health.  Nine out of ten Americans reported feeling emotional distress due to the pandemic, and that was already in May. 27

While a crisis can help unite people against a common enemy, in the long term it can aggravate political differences in addressing the problem.  Other effects of chronic stress response include negative emotions and reckless behavior. 28 Substance abuse, crime, and suicide are running high in 2020. 29

Experts advise that knowledge is empowering to cope with stress.  It is easier to confront facts than fears and rumors.  It is also important to be aware of our own feelings.  Only by identifying the sources and nature of our emotions can we ever hope to address them.  Finally, look for solutions when you are in your best state.  Let your “adult self” make your choices, not your “overwhelmed self” or your “survival self”. 30

Historians compare this pandemic to a depression or even a war that has potential to leave lasting changes in society.  We know that billions of people have lived through such crises before – plagues, wars, tyrannies, and more.  Most of us thought that we wouldn’t see such a catastrophe in our own lifetimes, but here we are.  The classic stages of grief are denial, anger, bargaining, depression, and acceptance.  History inspires us by proving that people can get through any tragedy when they learn to accept their new world.     

D. How Should We Feel?

“Nobody panics when things go ‘according to plan’ even if the plan is horrifying! 

Upset the established order, and everything becomes chaos.”

— The Joker, as written by Jonathan and Christopher Nolan, “Dark Knight” (2008)

In the politicized public discourse about coronavirus, one of the major through-lines has been the question, “How serious is this?”  Should we feel afraid of the virus?  Or is it no big deal?  This deceptively simple question is difficult to answer even without the political complications. 

One challenge is that we have to think as individuals and as a society at the same time.  For you, as just one person, chances are slim (so far) that you’ll catch coronavirus, and slimmer still that it will make you seriously ill.  But if we multiplied those small probabilities by the whole human population, we’d end up with tens of millions of preventable deaths.  It comes down to a question of what you care about and what “we” care about. 

Many people illustrate their perspectives by comparing the coronavirus pandemic to other causes of death.  Other respiratory tract infections are a natural comparison.  Diseases like tuberculosis, pneumonia, influenza, and COPD prematurely kill millions of people every year. 31 Why haven’t we been on red alert about them for decades?  This is probably the hardest question I’ve encountered in my research.  I posed this question to my Facebook friends early this year, and I still haven’t found a satisfactory answer. The only explanation I can conjure is the Joker’s principle, a psychological irrationality.  Those diseases have reached equilibrium; they are part of the plan.  They are known background noise, and it is the unknown that we fear.  We don’t know how far or fast coronavirus will spread.  Other dangers that alarm us and boil over in the streets, like terrorism or errant police brutality, kill miniscule numbers compared to any infectious disease.  Our emotions are clearly not linked to the numbers. 

When math nerds like me talk about uncertain events, we describe them with at least three components:  Probability, costs, and benefits.  You have to consider all three to arrive at the most rational way to quantify an event, its “expected value”:

E = P(BC)

In a potentially dangerous situation, sometimes our mind exaggerates the probability P (like plane crashes).  Sometimes we recklessly ignore a high cost or probability because we enjoy the benefit (like drugs).  In the coronavirus situation, some people fixate on probabilities while others focus on the cost of death.  This is why both sides can argue endlessly and both be partly right.  A nuanced understanding must account for the whole formula.

In order to transcend irrational, emotional judgments, most regulatory agencies have adopted numerical limits to acceptable risks.  The value of “one in a million” has become a widely accepted standard. 32 That is, if the probability of death is less than one in a million, a government will usually consider it unnecessary to commit further resources to controlling the risk.  In a world of 8 billion people, this standard would set the acceptable threshold at 8,000 preventable deaths. We reached that point in March, less than a week after COVID-19 was recognized as a pandemic.  

The premise that “coronavirus is just like the flu” is pretty accurate in terms of death toll so far.  It’s the resulting conclusion that’s backward.  This comparison does not demonstrate that the coronavirus is innocuous, but that influenza, like COVID-19, is vastly unacceptable.     

IV. Conclusions

I am finishing this essay in the first week of November 2020, right in the middle of the Biden / Trump presidential election.  I can’t imagine a more apt background.  The coronavirus pandemic has loomed large in this election, both as an issue and as the environment in which we vote.  Each party has a completely different vision of what the problems are and how to address them.  Where Democrats see a serious public health threat, Republicans are not as concerned because it has not affected most of their personal lives.  So far, preventive responses have been much more disruptive than the disease itself.  Then again, it’s impossible to know how much worse the pandemic would have been without such measures. 

Our perception of this pandemic is informed by politics and psychology as much as by facts.  In complex controversies, one side rarely has all the answers.  It’s not a matter of right or wrong but of emotional resonance.  Different groups of people have different cares and concerns.  It’s important to realize this, not only to manage your own thoughts but also to vet information and to understand your neighbors.       

My next article will discuss solutions and a path forward. 

V. Citations

                

  1. Image by Elchinator / CC BY-SA (https://creativecommons.org/licenses/by-sa/4.0), https://pixabay.com/illustrations/recession-economic-crisis-economy-5124813/ (accessed and saved 11/04/20).
  2. Staff writers, “Recession watch: which nations’ GDP is still going down?” The Guardian, https://www.theguardian.com/news/datablog/2009/aug/13/global-economy-globalrecession (updated regularly; accessed and data saved 8/29/20).
  3. M. Ayhan Kose et al., Global Economic Prospects, World Bank (June, 2020), https://www.worldbank.org/en/publication/global-economic-prospects (accessed, saved, and archived 8/28/20).
  4. Staff writers, “COVID-19 and the world of work”, International Labour Organization (2ed, 4/07/2020), https://www.ilo.org/wcmsp5/groups/public/—dgreports/—dcomm/documents/briefingnote/wcms_740877.pdf (accessed, saved, and archived 8/29/20).
  5. See e.g. Peter S. Goodman, “Why the Global Recession Could Last a Long Time”, New York Times (4/01/2020), https://www.nytimes.com/2020/04/01/business/economy/coronavirus-recession.html (accessed, saved, and archived 8/29/20).
  6. Fred Imbert, “Half of the world has asked the IMF for a bailout, chief says”, CNBC (4/15/2020), https://www.cnbc.com/2020/04/15/half-of-the-world-has-asked-the-imf-for-a-bailout-chief-says.html (accessed, saved, and archived 9/11/20).
  7. Staff writers, 2020 – Global Report on Food Crises, UN World Food Programme (4/20/2020), https://www.wfp.org/publications/2020-global-report-food-crises (accessed 9/11/20).
  8. See e.g. Staff writers, “The Politics of Climate”, Pew Research Center (10/04/2016), https://www.pewresearch.org/science/2016/10/04/the-politics-of-climate/ (accessed, saved, and archived 9/23/20).
  9. Sara Burnett and Brian Slodysko, “Pro-Trump protesters push back on stay-at-home orders”, Associated Press (4/17/2020), https://apnews.com/ea4c17f541c7c63fac52941a6f43b885 (accessed, saved, and archived 9/23/20).
  10. Shanto Iyengar et al., “The Origins and Consequences of Affective Polarization in the United States”, Annual Review of Political Science 22:129-146 (May, 2019), https://www.annualreviews.org/doi/full/10.1146/annurev-polisci-051117-073034 (accessed and saved 9/28/20).
  11. Will Steakin and Ben Gittleson, “Trump heads into flu season amid pandemic mocking masks, holding packed campaign rallies”, ABC News (9/11/2020), https://abcnews.go.com/Politics/trump-heads-flu-season-amid-pandemic-mocking-masks/story?id=72950584 (accessed, saved, and archived 9/23/20).
  12. Tom Phillips, “Brazil: Bolsonaro reportedly uses homophobic slur to mock masks”, The Guardian (7/08/2020), https://www.theguardian.com/world/2020/jul/08/bolsonaro-masks-slur-brazil-coronavirus (accessed, saved, and archived 9/23/20).
  13. Will Weissert and Jonathan Lemire, “Face masks make a political statement in era of coronavirus”, Associated Press (5/07/2020),  https://apnews.com/7dce310db6e85b31d735e81d0af6769c (accessed, saved, and archived 9/23/20).
  14. Laura Wronski, “Axios | SurveyMonkey Poll: coronavirus and trust”, Axios (March, 2020), https://www.surveymonkey.com/curiosity/axios-coronavirus-trust/ (accessed, saved, and archived 9/23/20).
  15. Conor Finnegan, “False claims about sources of coronavirus cause spat between the US, China”, ABC News (3/13/2020), https://abcnews.go.com/Politics/false-claims-sources-coronavirus-spat-us-china/story?id=69580990 (accessed, saved, and archived 10/12/20).
  16. Brett Samuels, “Trump hits Democrats over coronavirus criticism: ‘This is their new hoax’”, The Hill (2/28/2020), https://thehill.com/homenews/campaign/485245-trump-hits-democrats-over-coronavirus-criticism-this-is-their-new-hoax (accessed, saved, and archived 10/12/20).
  17. John Fritze and David Jackson, “Trump blames ‘blue states’ for increasing nation’s coronavirus death rates, ignores high rates in red states”, USA Today (9/17/2020), https://www.usatoday.com/story/news/politics/elections/2020/09/16/trump-blames-blue-states-covid-19-death-rates/5819120002/ (accessed, saved, and archived 10/12/20).
  18. Jonathan Haidt, The Righteous Mind: Why Good People are Divided by Politics and Religion, Pantheon (2012), Kindle edition around location 418
  19. See e.g. V. Swami et al., “Putting the stress on conspiracy theories: Examining associations between psychological stress, anxiety, and belief in conspiracy theories”, Personality and Individual Differences vol. 99, pp. 72-76 (Sep., 2016), https://www.sciencedirect.com/science/article/abs/pii/S0191886916303440?via%3Dihub (accessed and saved 9/12/20).
  20. Wronski, op. cit.
  21. Mark Jurkowitz and Amy Mitchell, “An oasis of bipartisanship: Republicans and Democrats distrust social media sites for political and election news”, Pew Research Center (1/29/2020), https://www.journalism.org/2020/01/29/an-oasis-of-bipartisanship-republicans-and-democrats-distrust-social-media-sites-for-political-and-election-news/ (accessed, saved, and archived 9/29/20).
  22. See e.g. The Editors, “Dying in a Leadership Vacuum”, The New England Journal of Medicine 383(15):1479-80 (10/08/2020), https://www.nejm.org/doi/full/10.1056/NEJMe2029812 (accessed and saved 10/10/20).
  23. Brett Murphy and Letitia Stein, “’It is a Slaughter’: Public health champion asks CDC director to expose White House, orchestrate his own firing”, USA Today (10/06/2020), https://www.usatoday.com/story/news/investigations/2020/10/06/expert-cdcs-redfield-should-expose-trump-covid-failures-leave-post/5899724002/ (accessed and saved 10/12/20).  This article includes a link to the letter that former CDC director Foege wrote to current director Redfield.
  24. Staff writers, “Political pressure Inside HHS Policy Shop To Tailor Facts To Fit Trump’s Message Unprecedented, Staffers Say,” Kaiser Family Foundation (7/30/2018), https://khn.org/morning-breakout/political-pressure-inside-hhs-policy-shop-to-tailor-facts-to-fit-trumps-message-unprecedented-staffers-say/ (accessed, saved, and archived 10/12/20); note that this article well predates the pandemic.
  25. Mike Stobbe, “CDC drops controversial testing advice that caused backlash”, Associated Press (9/18/2020), https://apnews.com/article/virus-outbreak-pandemics-public-health-22e7ac15e8d622b12bf784295e4b5266 (accessed, saved, and archived 10/12/20).
  26. Brett Samuels, “Trump calls CNN ‘Dumb bastards’ for covering coronavirus”, The Hill (10/19/2020), https://thehill.com/homenews/administration/521741-trump-calls-cnn-dumb-bastards-for-covering-coronavirus (accessed, saved, and archived 10/22/20).
  27. Olafur S. Palsson, Sarah Ballou, and Sarah Gray, “The U.S. National Pandemic Emotional Impact Report”, UNC and Harvard Schools of Medicine (6/29/2020), http://pandemicimpactreport.com/ (accessed, saved, and archived 11/03/20).
  28. Tony Schwartz and Emily Pines, “Coping with Fatigue, Fear, and Panic During a Crisis”, Harvard Business Review (3/23/2020), https://hbr.org/2020/03/coping-with-fatigue-fear-and-panic-during-a-crisis (accessed, saved, and archived 11/04/20).
  29. Jayne O’Donnell, “’Deaths of despair’: Coronavirus pandemic could push suicide, drug deaths as high as 150K, study says”, USA Today (5/08/20), https://www.usatoday.com/story/news/health/2020/05/08/coronavirus-pandemic-boosts-suicide-alcohol-drug-death-predictions/3081706001/ (accessed, saved, and archived 11/04/20).
  30. Schwartz and Pines, op. cit.
  31. Staff writers, Global Impact of Respiratory Disease, 2ed, Forum of International Respiratory Societies (2017), https://www.who.int/gard/publications/The_Global_Impact_of_Respiratory_Disease.pdf (accessed 10/22/20).
  32. Paul R. Hunter and Lorna Fewtrell, “Ch. 10: Acceptable risk”, Water Quality: Guidelines, Standards, and Health, WHO (London, 2001), https://www.who.int/water_sanitation_health/dwq/iwachap10.pdf?ua=1 (accessed and saved 10/09/20).
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Coronavirus Primer, Part 2: SARS-CoV-2, COVID-19, and the Individual

For most of us, 2020 is a year of masks, gloves, temperature checks, and social distancing. 1

I began this three-part series with background information, zooming in from the domain of viruses to  the genus of coronaviruses.  Today’s post specifically introduces this year’s novel coronavirus.  We’ll cover the topics of the virus’s origins and evolution, its effects, person-to-person transmission, and possibilities for a cure.    

I. Biology

II. Medicine

III. Citations

I. Biology

A. Origins

B. Evolution

A. Origins

The current pandemic is the third wave of deadly human coronavirus infections.  The new virus is officially called SARS-CoV-2, and the disease that it causes is COVID-19.  COVID simply stands for COrona VIrus Disease.

This year’s virus is so closely related to the 2002 SARS virus that virologists classify it as a new strain of the same species. 2 SARS-CoV-2 is not a descendant of SARS-CoV but a “cousin” that shares a recent common ancestor.  Though conspiracy theorists will believe what they will, genetic evidence shows with high confidence that the SARS-CoV-2 virus evolved naturally and was not engineered in a lab. 3 

The path of transmission, from bat to intermediate host to human, is uncertain.  The pangolin or “spiky anteater” was an early prime suspect because pangolins carry a coronavirus similar to SARS-CoV-2.  The current human and pangolin coronaviruses turned out to be, again, only cousins. 4 Nevertheless, they are similar enough to raise concerns about pangolins as potential carriers for future outbreaks, especially since the pangolin is a heavily trafficked wild animal.

The earliest confirmed human case of SARS-CoV-2 was reported on November 17 in Hubei Province, China (where Wuhan is located). 5 Interestingly, traces of the virus have been found in samples collected from Europe in December.  One was in Italian wastewater 6 and another in the bodily fluids of a French man who was tested for pneumonia. 7

The first mass outbreak came in late December.  It was traced to the Huanan Seafood Wholesale Market in Wuhan, China.  Because the market sells exotic animals, and because similar markets had been implicated in zoonotic transmission of SARS, people quickly jumped to the conclusion that Huanan Market was the site where the virus made its first jump into humans.  However, we now know that some early cases were not associated with Huanan Market 8 and that none of the animals at that market were infected. 9 It seems that a person who already had the virus brought it to the market, and it spread simply because of the crowded conditions.  The spike in Wuhan hospitalizations started to make headlines right around the first day of the decade.

B. Evolution

Taletha D. asked:  “How many versions are there? How fast did they mutate?  Why might they have mutated?” 

After SARS-CoV-2 infected people, its evolution was then guided by its human cell environment.  The virus has at least two variants, the “G” and “D” varieties.  They differ by only one “letter” in their RNA code, but the G version is much more effective at latching onto human cells. 10 Hence, the virus has been evolving strongly toward the G variety this year, especially in Europe and the United States.  Unfortunately for us, G’s gain is our loss.  The G virus is ten times as transmissible as D.  In other words, a sneeze requires only 10% as many G viruses as D viruses in order to spread equally to people nearby.  This explains why the epidemic is spreading through the US more rapidly than through China.   

Mutations, or genetic changes, happen randomly.  The G and D varieties might even have existed before human infection.  The part that’s not so random now is the evolution, the competition between G and D in human cells.  Since G is so much more effective, it will come to dominate the viral population. 

II. Medicine

A. Effects

B. Transmission

C. The Race for a Cure

A. Effects

Mitzi M-H. asked about the causes of death

Taletha D. asked:  “Why are some people asymptomatic?”

Karen K. asked, “I’m interested in the research on long-term kidney and lung damage.”

Individuals display a tremendous range of responses to SARS-CoV-2 infection.  The typical manifestation is normal flu-like symptoms.  Some patients experience severe symptoms like shortness of breath, low blood oxygen, or moderate pneumonia. The most critical cases involve respiratory failure, shock, or multiorgan system dysfunction, 11 which can of course be fatal.  Some of the damage comes from the virus itself, and some from cytokine storm, the immune system’s overreaction.  On the other extreme, some cases present no symptoms or signs at all. 12 The percentages of these categories are still in flux, and will be discussed further in Part 3.

The spike protein of SARS-CoV-2, like its cousin SARS-CoV, binds to a protein called ACE2.  ACE2 is distributed unevenly in the human body.  It is present in our lungs, heart, blood vessels, kidneys, liver, GI tract, and the lining of the mouth and nose.  Early COVID-19 reports show that damage to the heart, kidneys, and liver are a serious concern in the worst cases. 13 However, ACE2 is more abundant in the lungs, and that’s where the worst impact will be. 14 Even some asymptomatic carriers get lung damage! 15 The lining of the nose is especially rich with ACE2. 16 That explains those highly invasive nose swabs.  The only true long-term data we have is from SARS-CoV.  A small percentage of SARS survivors suffered long-term lung and kidney damage.  Fortunately, most have recovered completely. 17

The severity of symptoms is correlated to the intensity of viral infection as well as underlying medical factors.  Those with the most critical symptoms tend to be those who had pre-existing conditions commonly associated with old age, obesity, and smoking. 2 18 We still don’t know why some people don’t develop symptoms at all.

The long-term immune response is another great unknown.  We know that the human immune system synthesizes antibodies; almost 30 varieties are currently cataloged. 19 We haven’t had enough time to tell how long a SARS-CoV-2-specific antibody will remain in a survivor’s bloodstream.  As a reasonable comparison, SARS survivors maintained SARS-CoV-1 antibodies in their systems for an average of two years, with significant reduction after three years. 20 Preliminary results seem to show that SARS-CoV-2 exhibits a similar pattern. 21 If so, then we might have to rely on annual shots to avoid getting overwhelmed by future outbreaks.

B. Transmission

Julie W. asked if (and why) food really presents lower risk than surfaces.

SARS-CoV-2 is almost entirely transmitted directly from person to person through exhaled airborne water droplets.  Factors that increase transmissibility include the concentration of virus in a sick person’s system, proximity, crowd density, and duration of contact.  The six-foot rule is based on the distance that the largest cough / sneeze droplets will travel.  This distance is also chosen as a reasonable compromise between medical precaution and social necessities.  However, the dynamics of a sneeze are startlingly effective at spreading germs far and wide, especially because “sneeze clouds” tend to rise and get picked up by ventilation systems. 22

The virus usually incubates in a person for a day to a week before onset of symptoms.  Contagion peaks from two days before to two days after the onset of symptoms. 23 Although we hear a lot of debate about asymptomatic spread, the greater concern is in fact presymptomatic spread.  Of course, someone without symptoms doesn’t know whether she’s uninfected, asymptomatic, or presymptomatic until she starts coming down with symptoms, when it is too late to prevent transmission.  After she develops symptoms, she may be contagious for another week, 24 but by that time she knows she’s sick and is more likely to be quarantined.  The recommended two-week quarantine period comes from adding a week of incubation plus one more week of contagion.              

The makeshift face masks that we ordinary people wear out in public are meant to minimize the spread of water droplets from our own mouths.  These masks protect those around us (in case we are presymptomatic).  No, they are not 100% cough-proof, but they are pretty effective at slowing down water droplets 25 and reducing microbial spread. 26 The respirators reserved for medical workers are engineered for nearly complete two-way filtering; they protect doctors and nurses from infected patients.

We are often warned about touching things – surfaces, other people’s hands, or our own faces.  These are secondary precautions against indirect transmission.  The pathway here is that a sick person coughs or sneezes, his viruses land on a surface (which might be his own hand), a healthy person touches that surface and picks up the virus, and then the healthy person touches her face.  The virus doesn’t penetrate skin, but the eyes, mouth, and nose are vulnerable points of entry.  Since viruses don’t last long on surfaces, they don’t spread as readily this way.  That’s why gloves are not mandated nearly as much as face masks and distancing.   

Best-practice signs in Los Angeles, CA, 6/24/20. 27

The virus can remain on some surfaces for up to three days, though not in great numbers. 28 An exposed surface is not a hospitable place for a virus, so the risk is proportional to how often people touch the surface.  It’s a safe bet that many more people have handled the subway pole than your Subway sandwich! 

Since viruses don’t “eat”, food to them is just another surface.  They could theoretically infect bacteria on the food, but that is not a good route for viral proliferation.  It’s not likely that SARS-CoV-2 would find the right receptors in bacteria cells anyway.  There have been no known reports of people catching COVID-19 through food packaging. 29 Although the virus could theoretically live on produce, that has not been demonstrated as a known vector either. 30

C. The Race for a Cure

1. Vaccine

2. Antiviral

3. Symptomatic treatments

4. Cocktails and computer-aided concoctions

1. Vaccine

Over 40 vaccine trials are in progress. 31 Vaccine development, testing, and approval is an arduous process that normally takes a decade.  Testing occurs in three phases, with a larger and more vulnerable cohort in each phase.  Regulatory agencies are now permitting “fast track” approval processes that could theoretically accelerate the SARS-CoV-2 process to as short as 1 – 2 years.  This would be an unprecedented pace. 

The United States’ Operation Warp Speed is a major collaborative vaccine effort between the federal government and private labs.  OWS has selected three top contenders for Phase 3 testing this summer.  All three teams – Moderna 32 , Oxford / AstraZeneca 33 , and Pfizer / BioNTech 34 – have reported encouraging results in their Phase 1 trials. The Oxford vaccine is especially promising because it stimulates T cells, special white blood cells that would last longer than antibodies.

The road ahead is not guaranteed to be smooth and easy.  Some of the leading competitors in this race, including Moderna and Oxford, have never commercialized a vaccine before.  Proper dosages are still unknown.  The sterile plastic vials that contain vaccine doses will be a major bottleneck in distribution. 35 Nevertheless, these firms continue to speak optimistically of vaccine production beginning this year.

2. Antiviral

There are five or ten viable candidates for anti-coronaviral medications.  Most of them were created years ago for other viruses.  Antivirals are known to have strong side effects, so they are usually reserved for the worst cases until they’ve had adequate testing to prove them safe. 

One of the most promising drugs is called remdesivir, by Gilead.  This was a failed candidate for treatment of Ebola.  One trial has shown that it appreciably reduces the recovery time for surviving patients hospitalized with COVID-19. 36 The FDA has now issued Emergency Use Authorization for remdesivir to treat severe cases. 37

Eli Lilly has taken a new approach to an old remedy, the old “antidote from a survivor’s blood” trick.  After drawing antibodies directly from the blood of a COVID-19 survivor, this company formulated them into a medication called LY-CoV555.  It has been effective in the lab, and is currently being tested on human subjects. 38

3. Symptomatic treatments

The worst cases of COVID-19 result in low blood oxygen and inflamed air passageways.  Ventilators, highly invasive and cumbersome machines, have been the last resort in this fight.  Ventilators present numerous problems of their own.  They can infect patients and damage lungs.  Intubating a patient can eject virus-infected bodily fluid into the air, endangering healthcare workers.  It turns out that COVID-19 patients have surprisingly high tolerance for low blood oxygen.  Researchers now recommend simpler devices such as oxygen tanks and even CPAP machines for patients who have low oxygen as long as they’re still breathing comfortably. 39

Dexamethasone, an anti-inflammatory medication, is the first drug proven to save lives of coronavirus patients.  It was already a well-known pharmaceutical before this pandemic.  Encouragingly, it is also inexpensive.  It has now been shown to reduce the death rate of critically ill patients by 20 – 30%. 40 However, it has not been properly vetted for side effects, and is not recommended for mild cases.  Researchers are cautiously optimistic.

Hydroxychloroquine is a 1950s medicine made controversial when touted by President Trump.  It has been effective against malaria and lupus, neither one of which is caused by a virus.  It also has anti-inflammatory benefits for treating arthritis.  It showed early promise at reducing SARS-CoV-2 in petri dishes (though nobody knew why).  Clinical trials in humans have been inconsistent. 41 Hydroxychloroquine actually appears to suppress the initial immune response against SARS-CoV-2 42 , and it can be harmful to vital organs. 43 The FDA and WHO have dropped it from consideration.

4. Cocktails and computer-aided concoctions

Why choose just one?  The strongest remedies could turn out to be hybrids or pharmaceutical “cocktails”, as for AIDS.  Roche and Gilead are conducting a trial to combine remdesivir with an anti-inflammatory; expect Phase 3 results this summer. 44 Carprofen and Celecoxib are anti-inflammatories that also appear to slightly inhibit replication of SARS-CoV-2. 45

The latter two drugs were identified by computerized analysis of pharmaceutical databanks.  A crowdsourcing project is underway to identify, synthesize, and test more super-candidates like these.  The world’s top chemists are submitting their ideas, and new supercomputer lab PostEra is running simulations to see if and how they can be made.  PostEra has pledged to release any winning chemical formulas into the public domain.  When I first read about this, I called it a “global brainstorm.”  PostEra has a better name for it: “COVID Moonshot”. 46

🦠🌒

Continue to Coronavirus Primer Part 3: Epidemiology

III. Citations

  1. U.S. Air Force photo by Tech. Sgt. Anthony Nelson Jr., in the public domain as the creative work of a US federal agency. https://www.kunsan.af.mil/News/Article/2134889/sky-warriors-covid-19-response/, Photo 1
  2. Alexandar E. Gorbalenya, “The species Severe acute respiratory syndrome-related coronavirus: classifying 2019-nCoV and naming it SARS-CoV-2”, Nature Microbiology 5, 536-544 (3/02/2020), https://www.nature.com/articles/s41564-020-0695-z (accessed and saved 7/23/20).
  3. Kristian G. Andersen et al., “The proximal origin of SARS-CoV-2”, Nature Medicine 26, 450-452 (3/17/2020), https://www.nature.com/articles/s41591-020-0820-9 (accessed and saved 7/03/20).
  4. Kangpeng Xiao et al., “Isolation of SARS-CoV-2-related coronavirus from Malayan pangolins”, Nature (5/07/2020), https://www.nature.com/articles/s41586-020-2313-x (accessed and saved 7/03/20).
  5. Josephine Ma, “Coronavirus: China’s first confirmed Covid-19 case traced back to November 17”, South China Morning Post (3/13/2020), https://www.scmp.com/news/china/society/article/3074991/coronavirus-chinas-first-confirmed-covid-19-case-traced-back (accessed and saved 7/03/20).
  6. Kate Kelland, “Italy sewage study suggests COVID-19 was there in December 2019”, Reuters (6/19/2020), https://www.reuters.com/article/us-health-coronavirus-italy-sewage/italy-sewage-study-suggests-covid-19-was-there-in-december-2019-idUSKBN23Q1J9 (accessed 7/03/20).
  7. “Coronaviruses as early as December?  Diagnosis of French patient shakes up pandemic chronology,”  KHN Morning Briefing (5/06/2020), https://khn.org/morning-breakout/coronavirus-cases-as-early-as-december-diagnosis-of-french-patient-shakes-up-pandemic-chronology/ (accessed 7/03/20).
  8. Xiaonan Zhang et al., “Viral and host factors related to the clinical outcome of COVID-19”, Nature (5/20/2020), https://www.nature.com/articles/s41586-020-2355-0 (accessed and saved 7/03/20).
  9. From a sample of animal tissues at the market by the Chinese CDC and / or Wuhan Institute of Virology.  I have not yet seen the original report, but it was published shortly before 5/26, when the Wall Street Journal reported on it. The Chinese report was vetted by American scientist Colin Carlson, who finds its results credible.  Carlson communicated the report to LiveScience.  See excellent summary at Rafi Letzter, “The coronavirus didn’t really start at that Wuhan ‘wet market’”, LiveScience (5/28/2020), https://www.livescience.com/covid-19-did-not-start-at-wuhan-wet-market.html (accessed 7/03/20).
  10. Lizhou Zhang et al., “The D614G mutation in the SARS-CoV-2 spike protein reduces S1 shedding and increases infectivity”, Scripps Research Institute (June, 2020; not sure if it’s peer-reviewed yet), https://www.scripps.edu/news-and-events/press-room/2020/20200611-choe-farzan-sars-cov-2-spike-protein.html (accessed and saved 7/03/20).
  11. WHO-China Joint Mission on Coronavirus Disease 2019 (COVID-19), Report (2/24/2020), p. 12, https://www.who.int/docs/default-source/coronaviruse/who-china-joint-mission-on-covid-19-final-report.pdf (accessed and saved 7/14/20).
  12. Paul Sax, “What We Know – And What We Don’t – About ‘Asymptomatic COVID-19’”, WBUR (6/26/2020), https://www.wbur.org/commonhealth/2020/06/26/asymptomatic-covid-faq-what-we-know (accessed, saved, and archived 7/19/20).
  13. Tamar Lapin, “Coronavirus may Damage your Kidneys, Heart and Liver”, New York Post (4/15/2020), https://nypost.com/2020/04/15/coronavirus-reportedly-damages-patients-kidneys-heart-liver/ (accessed 7/04/20).
  14. Krishna Sriram, Paul Insel, and Rohit Loomba, “What is the ACE2 receptor, how is it connected to the coronavirus and why might it be key to treating COVID-19?  The experts explain”, The Conversation (5/14/2020), https://theconversation.com/what-is-the-ace2-receptor-how-is-it-connected-to-coronavirus-and-why-might-it-be-key-to-treating-covid-19-the-experts-explain-136928 (accessed and saved 6/26/20).
  15. Heng Meng et al., “CT imaging and clinical course of asymptomatic cases with COVID-19 pneumonia at admission in Wuhan, China”, J. Infect. 81(1):e33-39 (4/12/2020), https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7152865/ (accessed and saved 7/04/20).
  16. Waradon Sungnak et al., “SARS-CoV-2 entry factors are highly expressed in nasal epithelial cells together with innate immune genes”, Nature Medicine 26, 681-687 (4/23/2020), https://www.nature.com/articles/s41591-020-0868-6#Fig1 (accessed and saved 7/14/20).
  17. Staff writer, “Severe Acute Respiratory Syndrome (SARS)”, American Lung Association, https://www.lung.org/lung-health-diseases/lung-disease-lookup/severe-acute-respiratory-syndrome-sars (accessed and saved 7/04/20).
  18. Staff writer, “People with Certain Medical Conditions”, CDC (7/17/2020), https://www.cdc.gov/coronavirus/2019-ncov/need-extra-precautions/people-with-medical-conditions.html (accessed, saved, and archived 7/22/20).
  19. Staff writer, “SARS-CoV-2 Antibodies”, Sino Biological (apparently continuously updated), https://www.sinobiological.com/research/virus/sars-cov-2-antibody (accessed, saved, and archived 7/19/20).
  20. Li-Ping Wu et al., “Duration of Antibody Responses after Severe Acute Respiratory Syndrome”, Emerging Infectious Diseases 13(10):1562-4 (Oct., 2007), https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2851497/ (accessed and saved 7/19/20).
  21. Quan-Xin Long et al., “Clinical and immunological assessment of asymptomatic SARS-CoV-2 infections”, Nature Medicine (6/18/2020), https://www.nature.com/articles/s41591-020-0965-6 (accessed and saved 7/21/20).
  22. Lydia Bourouiba, Eline Dehandschoewercker, and John W. M. Bush, “Violent expiratory events: on coughing and sneezing”, Journal of Fluid Mechanics 745:537-563 (4/25/2014), https://www.cambridge.org/core/journals/journal-of-fluid-mechanics/article/violent-expiratory-events-on-coughing-and-sneezing/475FCFCBD32C7DB6C1E49476DB7A7446 (accessed and saved 7/19/20).
  23. The facts about incubation and contagion are taken from Xi He et al., “Temporal dynamics in viral shedding and transmissibility of COVID-19”, Nature Medicine (4/15/2020), https://www.nature.com/articles/s41591-020-0869-5 (accessed and saved 7/19/20).  See esp. fig. 1c.
  24. Sax, op. cit.
  25. Matthew E. Staymates, “My Stay-at-Home Lab Shows How Face Coverings Can Slow the Spread of Disease”, NIST (6/11/2020), https://www.nist.gov/blogs/taking-measure/my-stay-home-lab-shows-how-face-coverings-can-slow-spread-disease (accessed, saved, and archived 7/19/20).
  26. Rich van Wyk, “Do face masks really slow the spread of COVID-19?” WTHR (7/07/2020), https://www.wthr.com/article/news/investigations/13-investigates/do-face-masks-slow-the-spread-of-covid-19/531-96479b50-7041-4f95-a88c-e33e2355fa37 (accessed and archived 7/19/20).
  27. Photo by Scot Fagerland
  28. Neeltje van Doremalen et al., “Aerosol and Surface Stability of SARS-CoV-2 as Compared with SARS-CoV-1”, New England Journal of Medicine 382:1564-1567 (3/17/2020), https://www.nejm.org/doi/full/10.1056/nejmc2004973 (accessed and saved 7/14/20).
  29. Staff writer, “Food and Coronavirus Disease 2019 (COVID-19)”, Nat’l Center for Immunization and Respiratory Diseases, Div. of Viral Diseases, US CDC (6/25/2020), https://www.cdc.gov/coronavirus/2019-ncov/daily-life-coping/food-and-COVID-19.html (accessed, saved, and archived 7/14/20).
  30. William F. Marshall III, M.D., “Can COVID-19 (coronavirus) spread through food, water, surfaces and pets?” Mayo Clinic (2020), https://www.mayoclinic.org/diseases-conditions/coronavirus/expert-answers/can-coronavirus-spread-food-water/faq-20485479 (accessed, saved, and archived 7/14/20).
  31. The full list is updated at Jeff Craven, “COVID-19 vaccine tracker”, Regulatory Focus (updated regularly since March, 2020), https://www.raps.org/news-and-articles/news-articles/2020/3/covid-19-vaccine-tracker (accessed 7/19/20).  
  32. Lisa A. Jackson et al., “An mRNA Vaccine against SARS-CoV-2 – Preliminary Report”, New England Journal of Medicine (7/14/2020), https://www.nejm.org/doi/full/10.1056/NEJMoa2022483 (accessed and saved 7/20/20).
  33. Pedro M. Folegatti et al., “Safety and immunogenicity of the ChAdOx1 nCoV-19 vaccine against SARS-CoV-2: a preliminary report of a phase ½, single-blind, randomized controlled trial”, The Lancet (7/20/2020), https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)31604-4/fulltext (accessed and saved 7/21/20).
  34. Amy Rose et al., “Pfizer and BioNTech Announce Early Positive Data from an Ongoing Phase ½ study of mRNA-based Vaccine Candidate Against SARS-CoV-2”, Business Wire (7/01/2020), https://www.businesswire.com/news/home/20200701005576/en/ (accessed, saved, and archived 7/20/20).
  35. Ciaran Lawlor et al., “The Timelines and Expectations for COVID-19 Vaccines”, BCG (5/14/2020), https://www.bcg.com/en-us/publications/2020/covid-vaccines-timelines-implications (accessed 7/20/20).
  36. Staff writer, “NIH Clinical Trial Shows Remdesivir Accelerates Recovery from Advanced COVID-19”, NIH-NIAID (4/29/2020), https://www.niaid.nih.gov/news-events/nih-clinical-trial-shows-remdesivir-accelerates-recovery-advanced-covid-19 (accessed, saved, and archived 7/21/20).
  37. Staff writer, “Coronavirus (COVID-19) Update:  FDA Issues Emergency Use Authorization for Potential COVID-19 Treatment”, FDA (5/01/20), https://www.fda.gov/news-events/press-announcements/coronavirus-covid-19-update-fda-issues-emergency-use-authorization-potential-covid-19-treatment (accessed, saved, and archived 7/21/20).
  38. Staff writer, “Lilly Begins World’s First Study of a Potential COVID-19 Antibody Treatment in Humans”, Eli Lilly (6/01/2020), https://investor.lilly.com/news-releases/news-release-details/lilly-begins-worlds-first-study-potential-covid-19-antibody (accessed, saved, and archived 7/21/20).
  39. Ardan M. Dondorp et al., “Respiratory Support in COVID-19 Patients, with a Focus on Resource-Limited Settings”, Am. J. Tropical Medicine & Hygiene 102(6):1191-7 (6/03/2020), https://www.ajtmh.org/content/journals/10.4269/ajtmh.20-0283 (accessed and saved 7/21/20).
  40. Peter Horby et al., “Effect of Dexamethasone in Hospitalized Patients with COVID-19 – Preliminary Report”, medRxiv (6/22/2020), https://www.medrxiv.org/content/10.1101/2020.06.22.20137273v1 (accessed and saved 7/22/20).
  41. Jennifer Tran, “Can Hydroxychloroquine and Chloroquine Be Used to Treat Coronavirus (COVID-19)?” GoodRx (7/08/2020), https://www.goodrx.com/blog/coronavirus-medicine-chloroquine-hydroxychloroquine-as-covid19-treatment/ (accessed, saved, and archived 7/21/20).
  42. Nils Rother et al., “Hydroxychloroquine inhibits trained immunity – implications for COVID-19”, medRXiv (6/09/2020, peer review in progress), https://www.medrxiv.org/content/10.1101/2020.06.08.20122143v1 (accessed and saved 7/21/20).
  43. Staff writer, “FDA cautions against use of hydroxychloroquine or chloroquine for COVID-19 outside of the hospital setting or a clinical trial due to risk of heart rhythm problems”, FDA (7/01/20), https://www.fda.gov/drugs/drug-safety-and-availability/fda-cautions-against-use-hydroxychloroquine-or-chloroquine-covid-19-outside-hospital-setting-or (accessed, saved, and archived 7/21/20).
  44. Nicholas Dunant et al., “Roche initiates phase III clinical trial of Actemra/RoActemra plus remdesivir in hospitalized patients with severe COVID-19 pneumonia”, Roche (5/28/2020), https://www.roche.com/media/releases/med-cor-2020-05-28.htm (saved, accessed, and archived 7/22/20).
  45. Aleix Gimeno et al., “Prediction of Novel Inhibitors of the Main Protease (M-pro) of SARS-CoV-2 through Consensus Docking and Drug Reposition”, Int’l Journal Molecular Sciences 21(11):3793 (5/27/2020), https://www.mdpi.com/1422-0067/21/11/3793 (accessed and saved 7/22/20).
  46. Alpha Lee et al., “COVID Moonshot:  Help Us Fight Coronavirus”, PostEra, https://postera.ai/covid (accessed, saved, and archived 7/22/20).
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Coronavirus Primer, Part 1: Background

Color-enhanced but real image of viruses (green) infecting a human cell (blue) 1
 

I. About This Primer

II. Viruses

III. Coronaviruses

IV. Citations

I. About This Primer

Without a doubt, the biggest story of 2020 is the coronavirus epidemic. 2 By the middle of the year, I, like many others out there, felt overwhelmed in a muddle of fragmented news and science, misinformation, and general confusion.  I announced on Facebook that I wanted to “digest it all” and assemble the best known information into one primer.  “Any questions you’d like me to research?” I asked, and a few friends immediately chimed in with requests.  Hopefully, this will help us understand coronavirus basics from the ground up.  I will begin this primer with the big picture and then gradually zoom in from viruses to coronaviruses to this year’s unwanted pests.  There is far too much ground to cover in one article, so I’m breaking it into multiple parts.  Today’s post is Part 1:  Background.  This article discusses viruses and coronaviruses in general. 

II. Viruses

A. Square One: What is a Virus, Anyway?

B. Infection, Immunity, Inoculation

C. Human Viral Diseases

D. Measuring Epidemics

E. Treatment Options

A. Square One: What is a Virus, Anyway?

Viruses occupy one of the most intriguing positions in the whole grand scheme of things.  They are microbes right at the boundary of life and non-living chemistry.  This makes them primary subjects of interest for scientists studying the origins of life.      

You are made of about 30 trillion cells. 2 We call a cell the smallest unit of life because it performs all the functions that we expect of a living thing.  A cell grows, responds to stimuli, metabolizes, heals, sustains and defends itself, reproduces, and dies.  However, it is not a unitary blob of spittle.  A cell is a complex system with hundreds of interacting parts, with names like macromolecules and organelles.  Most of those parts specialize in just one life function, so by themselves they are not fully alive.  If I could compare a virus to anything else, I’d say it’s like a cell organelle that specializes in reproduction. 

Viruses are like living things in numerous ways.  They are made of the same basic macromolecules as us:  nucleic acids, proteins, lipids, and carbohydrates.  At the core of every virus is a bundle of DNA or RNA comprising a few genes.  Viruses reproduce and evolve / speciate.  Biologists classify them and give them Latinesque scientific names.  Viruses can be “killed” by heat, chemicals, or radiation.             

However, viruses are like lifeless chemicals in that they don’t metabolize, respond, heal, change, or grow.  Nor are they able to protect themselves from the environment.  And although viruses specialize in just one thing – reproduction – they can’t even do that by themselves.  A virus is an absolute parasite.  In order to function, it must inhabit a living cell.  The “life” cycle of a virus is to invade a cell and exploit the cell’s resources to make dozens of copies of itself, which then burst forth to invade other cells.  Viruses infect the cells of all living things, from bacteria to whales.  They kill more life forms, and more humans, than any other force of nature.

B. Infection, Immunity, Inoculation

While some viruses are harmless or even beneficial, most of them cause irreparable or fatal damage to their host cells.  Rapidly reproducing viruses consume a cell completely and then burst out like a battalion of creepy little microscopic robots.  Since they are vulnerable outside of cells, they must pass quickly from dying cell to living cell.  They can pass from one person to another through skin, body fluids, or air currents.

Viral infection involves proteins on the surfaces of viruses and cells.  Proteins have complex three-dimensional shapes like locks and keys.  If a virus has the protein “key” to a cell’s outer “lock”, it will latch on and inject its genes inside.

In a human or animal body, fragments of viruses called antigens react with our white blood cells, aka our immune system.  In lucky cases, the immune system produces a protein called an antibody, a natural defense.  An antibody latches onto the antigen that stimulated it.  Sometimes, the antibody disfigures the virus’s “key” so that the virus can no longer penetrate cells.  Other antibodies “flag” a virus so that white blood cells can easily identify and destroy it.  While a person has an antibody in his blood, he is immune to that virus.  The next time the virus comes along, his antibodies will latch onto the virus’s antigens and slow it down or stop it.  Some antibodies last a lifetime, while others disappear from the bloodstream in a few years.  A vaccine is a human-made, finely tuned dose of antigens – just enough to stimulate an immune response without a full-blown infection.  If enough people in a community become immune to the virus, whether through natural immunity or vaccine inoculation, the virus begins to die out and can even go extinct.             

It’s important to note that viruses evolve quickly.  This is especially true of RNA viruses, which most human viruses are.  When a virus evolves, its proteins can change shape.  That is a headache for us; we are forced to keep reinventing new locks to morphing viral keys.  Occasionally, a virus that infects one animal will evolve to a new form that infects another animal, including humans.  A virus that jumps ship from one species of host to another is called zoonotic.

C. Human Viral Diseases

A viral disease is not quite the same as the virus that causes it.  A disease is the physical manifestation of the virus, its effects on the person.  Sometimes a virus and its disease have different names, as HIV (Human Immunodeficiency Virus) causes AIDS (Acquired Immuno-Deficiency Syndrome).  In other cases, we use a single term, like “Ebola”, to name both the virus and its disease.  There are too many human disease-causing viruses to list here.  Examples include adenoviruses, astroviruses, encephalitis, enteroviruses, hepatitis, herpes, HPV, influenza, measles, meningitis, mumps, noroviruses, parainfluenza, polio, pox, rabies, rhinoviruses (which cause colds), roseola, rotaviruses, rubella, West Nile, Zika, … you get the picture.

D. Measuring Epidemics

Viruses are inherently public health threats.  Human viruses would quickly die out if they did not have lots and lots of people to infect. Viral infections can be quantified in numerous ways. The three most fundamental independent metrics are reproduction number, transmission time, and infection-fatality rate.

Reproduction number is commonly abbreviated as R.  It measures the average number of healthy persons who catch the virus from each infected person.  For example, if each sick person makes four other people sick, then R = 4. 

Transmission time is the average time it takes a virus to spread from one person to another.  I don’t see this factor discussed very often, but it makes a big difference whether a sick person infects others in a matter of hours (like an airborne virus in a mall) or years (like a sexually transmitted virus). 

Finally, the infection-fatality rate is the most morbid statistic of them all: the percentage of infected persons who die.  The number of serious illnesses or hospitalizations may be measured as well; they will be closely correlated to the fatality rate.

Unfortunately, the fundamental metrics above are difficult to measure.  We can’t measure them all in a lab because they are not entirely intrinsic to the virus.  They depend on human activity too.  It’s hard to know how many people are infected when not everyone is tested and / or exhibiting symptoms. We reserve the word “case” for a known infection. That is, if 100 people carry the virus but only 60 of them have been tested and confirmed, then there are 100 infections but only 60 cases. In some epidemics (especially new ones) there can be quite a gap between actual infections and known cases. 

The easiest way to measure the severity of an epidemic is with the number of deaths and / or hospitalizations.  These numbers are documented well.  There will still always be some over-reporting (deaths attributed to the virus that were really due to something else) and under-reporting (deaths due to the virus that weren’t counted).  On a societal level, sheer numbers are more important than rates.  It doesn’t really matter if there are 1,000 infections that are 10% fatal or 10,000 infections that are 1% fatal.  Both scenarios will result in 100 deaths and should be considered equally dangerous.  Of course, if you get infected, you sure will be interested in knowing if you have a 1% or 10% chance of dying!

Taken together, the reproduction number and transmission time determine the doubling time, or the amount of time it takes for the prevalence of infections to double in the population.  The pattern characterized by a constant doubling time is called exponential growth.  In real life, exponential growth never lasts long, because it runs up against limitations like immunity or finite populations.  Doubling time is the metric we hear most on the news, because it is easy to calculate by simply counting cases.  Breaking it down offers slightly more insight, if only theoretically.  When doubling time increases, it demonstrates that each sick person is infecting fewer healthy people and / or she’s doing so more slowly, which are the intended effects of social distancing.

When doubling time slows down (as it always must) the simplest model for epidemic growth is the logistic formula.  This S-shaped curve represents the all-time number of infections “flattening” as it reaches its maximum and stops growing.  The point where the number of daily infections starts to decrease is the point of inflection.  I hear some people using the term “inflection point” as if it means the point where a virus “really takes off”.  That’s the opposite of the correct meaning, and there is no well-defined point of acceleration on the curve.

Real epidemiologists use sophisticated numerical algorithms that model the interactions among Susceptible, Immune, and Recovered people.  These SIR  or compartmentalized models are run on supercomputers.

The logistic curve, unlike exponential growth, models the “flattening” or maxing out that must eventually occur.  The inflection point is where growth starts to slow down; it is shown at (5, 50) on this example. 3

E. Treatment Options

Besides vaccines, there are at least two medical options for some viral infections.

Antiviral drugs kill viruses after infection.  Antiviral pharmacology is recent technology.  It is more sophisticated than vaccinations.  To produce an antiviral medicine, researchers sequence the virus’s RNA and proteins and then engineer molecules to target the virus’s vulnerable points.  This highly advanced research developed in response to the AIDS pandemic. 

Each vaccine or antiviral medication is engineered specifically for one strain of virus.  Though the vaccines for polio and smallpox were “miracle cures” that drove their viruses to extinction, they are useless against other viruses.  Medical labs are experienced and pretty effective at making influenza vaccines.  On the other hand, centuries of effort have still yielded no rhinovirus vaccines.

Because vaccines and antivirals are not always available, hospitals must also rely on symptomatic treatments, which only mitigate the disease without managing the virus.  Some drugs treat symptoms such as inflammation (also known as cytokine storm).  In extreme cases, medical equipment like ventilators assist with breathing while the virus passes.

III. Coronaviruses

A. What Coronaviruses Are

B. The First Two Killer Coronaviruses

A. What Coronaviruses Are

Coronaviruses are classified as the family Coronaviridae in the virus family tree.  They get their name from the “spike” proteins, also known as S proteins, embedded in their fatty envelope.  The spikes look like the corona (crown) of the sun, and they are the killer proteins involved in latching onto host cell membranes. 

Coronaviruses have infected bats and birds for tens or hundreds of millions of years. 4 They are occasionally transmitted to other mammalian species that come into contact with bats.  There are now five genera of coronaviruses.  Two of them, Alphacoronavirus and Betacoronavirus, include species that infect humans.  Today’s living alpha- and beta-coronaviruses descend from a common ancestor four or five millennia ago. 5

Some animal diseases that are now recognized as coronavirus infections came to veterinary attention in the early 20th century.  The viruses themselves were only observed and named in the 1960s.  Since then, the medical community has identified seven coronaviruses that infect humans.  Four of them only cause colds.  The three most recent strains, all beta-coronaviruses that evolved in the 21st century, are much more severe.  There are no known treatments for any of them. 

B. The First Two Killer Coronaviruses

The first alarming coronavirus outbreak was the SARS epidemic of 2002 – ’04.  SARS stands for Severe Acute Respiratory Syndrome. 2 The virus that caused it was named SARS-CoV.  The SARS coronavirus originated in horseshoe bats in southern China. 6 It was then apparently transmitted to intermediary species that were sold in exotic animal markets: the palm civet (a wild cat), the raccoon dog (a wild dog), and / or the ferret badger.  All of these species carried SARS-CoV-like viruses.  The exact pathway from bat to carrier to human has not yet been solved.   

SARS had a high infection-fatality rate, about 10%.  It was easy to detect infected people, though, because almost everybody who caught it broke out into fever and coughs within 2 – 3 days.  The sick were quickly quarantined and questioned about their most recent contacts, who were also isolated.  Local governments also ordered a mass killing of palm civets. 7 Even without a vaccine or anti-viral remedy, the anti-SARS campaign was a complete success.  Only 8,000 people ever caught this disease.  Canada was the only non-Asian country with more than one death.  Curiously, just like COVID-19, SARS barely touched Africa.  The peak of the outbreak lasted just a few months, February – July 2003.  The onset of summer weather slowed it down.  By 2004, SARS-CoV was extinct. 

Living in a world city, Los Angeles, I have long noticed Chinese nationals wearing face masks all the time, and I always wondered why.  It’s the SARS outbreak that got them in the habit, and many have worn masks routinely ever since 2003.  It doesn’t seem so unusual anymore!

The next major coronavirus outbreak was called MERS (Middle East Respiratory Syndrome) because it was concentrated in Saudi Arabia and neighboring countries.  The MERS virus passed from bats to camels in the 1990s and then to people who made close contact with camels in 2012.  This virus had a distinct profile.  MERS had an even higher infection-fatality ratio.  30 – 35% of the patients who caught it died!  Fortunately, it did not easily pass from one person to another.  The MERS virus still exists, but it has only killed 900 people, just a few each year now. 

In 2017, the scientists who traced SARS-CoV to a bat cave in Yunnan Province observed that the viruses were recombining (intermixing) to form myriad new combinations.  Their discussion included this prophetic warning:

“We have also revealed that various SARSr-CoVs … are still circulating among bats in this region.  Thus, the risk of spillover into people and emergence of a disease similar to SARS is possible.” 8

Ben Hu (2017)

Continue to Coronavirus Primer Part 2: SARS-CoV-2, COVID-19, and the Individual

IV. Citations

  1. Photo Credit: C. GoldsmithContent Providers: CDC/ C. Goldsmith, P. Feorino, E. L. Palmer, W. R. McManus / Public domain.  https://commons.wikimedia.org/wiki/File:HIV-budding-Color.jpg (accessed and saved 6/23/20).
  2. Ron Sender, Shai Fuchs, and Ron Milo, “Revised Estimates for the Number of Human and Bacteria Cells in the Body”, PLOS Biology (8/19/2016), https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.1002533 (accessed 7/06/20).
  3. Logistic curve by Yapparina / CC0, https://commons.wikimedia.org/wiki/File:Logistic_curve,_r%3D1,_K%3D100,_N0%3D1.png (accessed 7/07/20).
  4. Joel O. Wertheim et al., “A Case for the Ancient Origin of Coronaviruses”, Journal of Virology 87(12):7039-45 (June, 2013), https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3676139/ (accessed and saved 6/25/20).
  5. Patrick C.Y. Woo et al., “Discovery of Seven Novel Mammalian and Avian Coronaviruses in the Genus Deltacoronavirus Supports Bat Coronaviruses as the Gene Source of Alphacoronavirus and Betacoronavirus and Avian Coronaviruses as the Gene Source of Gammacoronavirus and Deltacoronavirus”, Journal of Virology 86(7):3995-4008 (Apr., 2012), https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3302495/ (accessed and saved 6/25/20).
  6. Ben Hu et al., “Discovery of a rich gene pool of bat SARS-related coronaviruses provides new insight into the origin of SARS coronavirus”, PLOS Pathogens 13(11):e1006698 (11/30/2017), https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1006698 (accessed and saved 6/25/20).
  7. Jane Parry, “WHO queries culling of civet cats”, BMJ 328(7432):128 (1/17/2004), https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1150312/ (accessed and saved 7/03/20).
  8. Hu (2017), op. cit., “Discussion”, last paragraph.
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