(Reuters) Coronavirus pandemic “could be over by June” if countries act, says Chinese adviser. Quoting,

The global coronavirus pandemic could be over by June if countries mobilize to fight it, a senior Chinese medical adviser said on Thursday, as China declared the peak had passed there and new cases in Hubei fell to single digits for the first time.

In the world we live in, this has no chance of happening. Even if everybody rolled up their sleeves and acted correctly within their power, it could not happen. China is unique, the world’s first surveillance state, with capabilities of contact tracing unapproached anywhere else. The acquiescence of China’s citizens to strict measures of control is also unequaled.

The headline of  earlier CNN article, Will the new coronavirus burn out like SARS … or is it here to stay? poses the wrong question. Like many wrong questions, it has no answer:

• SARS did not burn out. It was contained. Containment was feasible because covert infections were not contagious.
• Flu strains, and common colds, for which many viruses are responsible, do burn out, by the development of herd immunity.
• In the absence of public health interventions,  for an historic example, have a look at syphilis. It took about 50 years to convert from a quickly fatal illness to the modern form, which by comparison, is mild.
• COVID-19 will not burn out in a reasonable time frame, unless you consider 65 weeks reasonable.
• Although local containment is possible, COVID-19 cannot be contained globally, because of the prevalence of covert infections, asymptomatic and contagious.
  
• Containment efforts will prolong the time to “burnout.”
• Containment efforts are nevertheless required, so healthcare systems are not overwhelmed, and to preserve the fabric of society.

Mi Feng, the spokesman for the National Health Commission quoted in the Reuters article, was not intentionally misleading. He simply omitted context for the rest of the world. Messages of hope frequently do this; they should not be condemned. It is up to us to supply the context.

The estimate of How Long Will the COVID-19 Epidemic Last? Napkin Calculation,  for true “burnout” is 65 weeks. “Burnout”, a word which tells you nothing, happens when enough herd immunity has developed to change the chain of transmission from growing to shrinking. The estimate is crude, but better than hope.

A painful paradox: Intervention, which presently means quarantine and travel restrictions, without other measures, will prolong the 65 weeks. (You may choose your own number, provided you supply justification other than hope). The fastest way to herd immunity is the cruelest, with unjustifiable loss of human life.

This is the way it will happen in most of the world. Like all the plagues of the past, COVID-19 will “burnout”, with the understanding that plagues end when either

• The concentration of animal vectors has declined.
• Human depopulation has occurred.
• Herd immunity has been acquired.

Since Wuhan bats do not mingle with humans like plague rats, this leaves mostly herd immunity. It would take more than the current lethality of COVID-19 to cause the occurrence of natural selection, the “survival of the fittest.” See COVID-19: A Warning.

Now what about the Third World, when herd immunity is acquired, at the expense of great human suffering? COVID-19 will not vanish. Exiting epidemic, It will go underground, persisting as an endemic, mostly mild disease. The Third World will become a disease reservoir.

This presents a problem for a developed country which has exercised effective measures of travel restrictions and quarantine. It means that the population is “naive” with respect to COVID. Having had no exposure, they are as vulnerable as they were before December 2019. Yet constant vigilance is not feasible with a disease that has covert characteristics.  This is constant, imminent catastrophe.

How can the developed countries acquire herd immunity, while avoiding the suffering of the Third World? There are two ways:

• Spontaneous mutation of COVID-19 to a strain that produces mild disease, which out competes virulent strains. Two strains have already been noted in China. See (Oxford Scientific) On the origin and continuing evolution of SARS-CoV-2. Type L produces severe disease; Type S is comparatively mild.

Although selective pressure towards Type S may have been observed, resulting from stringent quarantine, let’s not rely on it. In fact, it appears that Type L evolved from Type S, in the direction of greater virulence.

• Ignoring luck, vaccination is the alternative. Even if vaccination programs have limited duration, there is a fascinating potential benefit: the COVID-19 virus may change to become less virulent. The result: herd immunity that endures beyond a vaccination campaign.

We’ll explore how this could happen in the next post.

It is disturbing how little of the $8B appropriation is for vaccine development. This must be corrected, stat!

Reference:  (DIVA, pdf) The reproductive number of COVID-19 is higher compared to SARS coronavirus. Contained within the article is a permalink:  http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-168415 . Quoting,

“Teaser:Our review found the average Ro for 2019-nCoV to be 3.28…”

We’re going to do a napkin calculation, closely related to what scientists call a power-of-10 job. There is no claim of accuracy.  Even if we wanted to be sophisticated, there are things in the way of accuracy. The basic reproduction number, R_o, will not be known with any accuracy until this is all history. It’s one of the weaknesses of epidemiology, better at analyzing the past than predicting the future. Nor is there any reason to assume that R_o will be constant with the seasons, and subtle seasonal changes in social behavior.

For this napkin calculation, assume that

•  The number of people in the U.S. who are infected is actually 10 times the reported figure of 700 as of 6 a.m on 3/10/2020. The number is 7000.
• Having COVID-19 confers long lasting immunity.
• R_o, which applies to a population that has never seen COVID-19, is constant.
• The epidemic is not stopped by other means, such as quarantine, drugs, or vaccination.
• R_o = 3.78, a little higher than the reference. It is, after all, an estimate.

We want to know R, which unlike R_o takes into account herd immunity. When a  certain percentage, a majority of the population, has had COVID, with or without symptoms, R drops below 1.  Here we go:

• U.S. population: 327 million
• Percentage of the population to have experienced COVID, for R to drop below 1:  73.5% = 240 million.
• The generation time is the average time it takes an infected individual to infect others. Example: If a person is infected on March  1, and infects 4 more people before recovery, at March 7, 14, 21, and 28, the generation time is 17.5 days.
• If we assume that COVID keeps infecting with R=3.78,  that implies, starting with 7000 infected, 8 generations to reach 240 million.
• The above is not correct; R decreases as time goes on, so more than 8 generations are required. But for simplicity, to keep it a napkin calculation, let’s go with it.
• Assume the generations time is three weeks.
• 8 generations = 24 weeks.
• Now apply a correction for the gradual decrease of R as the number of people who haven’t had it declines: Multiply the above by the magic number e= 2.71828.
• This gives 65 weeks till the reproduction number drops below 1.

In  the world of this very rough estimate, the epidemic takes a downturn 65 weeks from present. It assumes  no modifications by medicine and public health, and a lot of mostly avoidable human suffering.

But there you have it. If this were the pre-scientific world of past plagues, and the pathogen had characteristics similar to COVID-19, it would be close to the truth.

Now you can panic. But do it in style.

(Reuters) Turkey’s Erdogan asks Russia to step aside in Syria.

They will largely do this. The Russians may draw a line on the map, and they may take local action against Turkish deployment beyond that line. If that occurs, it will be the high point of tension, followed by a little freeze, followed by deescalation. This post-conflict pattern has been demonstrated: (BBC) Turkey’s downing of Russian warplane – what we know.

In 2014, when Syria was almost a complete political vacuum, I proposed a reinstatement of the Ottoman Empire, which was dissolved in the aftermath of World War 1, to serve British and French colonial ambitions. Articles: (2014) Turkey & the New Ottoman Empire, and (2016) Turkey in Syria; The New Ottoman Empire; a Brief Note about Cultural Affinity. Additional mentions here.

This colonial redraw is the direct antecedent of today’s map of ethnic conflict, fueled by artificial boundaries that cut across ethnic lines. In some cases, this strategy was intentional, to make these regions more amenable to foreign governance.

Ottoman Syria was a stable component of the empire for 400 years. The semi-representational methods of Ottoman governance, which achieved stability of a multi-ethnic region, remain a marvel to historians, if not a modern aspiration. A reprise in northern Syria, with organic connection to Turkey’s economy, might well have resulted in durable solution. No alternative of the striped-pants brigade has as much life to it.

Turkey’s involvement in Syria reached a high point in the attempt to prevent the recapture of Aleppo. It failed because it was actuated by proxies with insufficient power. Other constraints to greater activity:

• The tatters of the proclaimed “Zero problems with our neighbors” foreign policy.
• Sensitivity to war casualties typical of a modern nation.
• Reluctance or refusal to engage Islamists of any stripe on the battlefield.
• Turkey’s transition from a member of the Western Alliance to an independent, mini “great power”, which requires a state of balance with Russia.

Russian concerns are a delicate balance of:

• Desire to continue peeling Turkey away from the West, with the eventual removal of nuclear weapons from Turkey.
• Reliance on the Bosporus, a choke point for the Black Sea warm-water ports.
• Recognition that Recep Erdoğan was, and is, an Islamist. (Hoover) Erdogan The Nationalist Vs Erdogan The Islamist.

The Russians complain, with justification, that Turkey was not acting with effect against terror groups in the Idlib region. The location of Abu Bakr al-Baghdadi at the time of U.S. action was on the edge of Idlib.

There is a tendency for Islamists to cloak themselves within the current political scene. This was demonstrated by Mohamed Morsi, who came to power by popular election, and proceeded by subtle and then less subtle steps to dismantle Egyptian democracy. (That el-Sisi finished the process is not germane here.)

Erdoğan has also subverted Turkish democracy. He began by showing up to chair meetings he had no standing in, and continued (like el-Sisi), with constitutional change that opens the door to further weakening. The huge number of Gülen movement imprisonments goes beyond the modern meaning of sedition; it is an authoritarian clamp-down. (BBC) Reality Check: The numbers behind the crackdown in Turkey.

Subversion of democracy is not a Russian concern. Erdoğan the crypto-Islamist is.  Since 1991, Turkey and Russia have not shared a border. But the intervening states, Armenia, Azerbaijan, and Georgia, are weak and porous. The recent history of the Middle East suggests that the ambition, and potential for Islamic export and aggression  correlate with national transition from secular to Islamist.

If it were necessary to choose a single word to define U.S. foreign policy, it might be one of “preserve”, ‘protect”, or “defend.” For Russia, it would be “if.” Because Russia is a threatened continental power, this leads to complex constructs, that begin with “If Turkey…”.

At the current level of Erdoğan‘s Islamism, the “if”  still allows accommodation of the Turkish occupation. Provided that the remaining terror pockets of Idlib are eliminated, it offers practical advantages to Russia:

• A reduction of the area of control required of Assad’s overstretched forces.
• Leverage with Turkey. As an arrangement that lacks the pretense of legitimacy, Turkish occupation is a useful pressure point.
• Continuance of a Turkey-Russia alliance, in the context of the Russian “if.”

The era of Ottoman collapse is beautifully depicted in the 1988 movie (Youtube) Pascali’s Island, starring Ben Kingsley. It poses the eternal question of the spy: Is anybody listening?

(CNN) New coronavirus cases in California and Oregon are second and third of unknown origin in U.S. has a video, titled “Doctor says your mask won’t help you against corona virus. Here’s why.” Anderson Cooper interviews a pediatrician, who says as much. This is followed by (CNN) Masks can’t stop the coronavirus in the US, but hysteria has led to bulk-buying, price-gouging and serious fear for the future. Quoting,

“The CDC says that healthy people in the US shouldn’t wear them because they won’t protect them from the novel coronavirus.”

Scarfing up surgical masks when healthcare system has a critical shortage is antisocial. The priority of masks for healthcare workers is for our collective benefit. This does not justify assertion of a fact that does not exist. There is modest evidence that surgical masks offer risk reduction. But there is now a tendency, ranging across the media, and including VP Pence, to manage this subject for the wrong reason, to prevent panic.

The correct statement is that nobody knows for certain whether surgical masks are protective. A study of  mask use by clinicians to protect from general upper respiratory infections, including flu, suggests, with a caveat, that they are. See (NCBI PMC) Effectiveness of N95 respirators versus surgical masks in protecting health care workers from acute respiratory infection: a systematic review and meta-analysis.

This is a meta study, which extracts new information from prior studies by fancy math. The article acknowledges that at the objective level, in the lab, N95 masks filter infectious particles, while surgical masks do not. Yet from the section Interpretation,

“Results of our systematic review and meta-analysis show that there was no significant difference between N95 respirators and surgical masks when used by health care workers to prevent transmission of acute respiratory infections from patients.”

The caveat:  The article authors note that the study has low statistical power, meaning that there is a more than negligible chance that the above conclusion is false.

Follow the logic: If N95 masks protect, and surgical masks work about as well in clinical settings, then surgical masks protect. Remember the caveat. Now translate that into unmanaged news-speak:

Surgical masks might offer some level of protection, but nobody knows for sure.

How do we explain the apparent discrepancy of lab tests versus clinical experience? An easy guess: While the mask doesn’t stop droplets, it changes the physics of the inhaled air stream. It reduces the formation of vortices (rotation in the air stream, see vortex) that rip at the delicate mucous lung lining,  and enhance transport particles deeply into the lungs.

That’s what I would like to see. Treat people like adults, and they are more likely to act as such. Even if you’re into managing, there is another reason to avoid it: If and when the shit hits the fan, they are more likely to follow your lead.

Don’t believe everything a doctor tells you. You just got a second opinion. A surgical mask could also prevent you from being smacked by gobs. I’m not waiting for the study.

An ethical alternative: Wear a scarf. (Oxford Academic, Annals of Work Exposures and Health) Simple Respiratory Protection—Evaluation of the Filtration Performance of Cloth Masks and Common Fabric Materials Against 20–1000 nm Size Particles. From the abstract,

“A shortage of disposable filtering facepiece respirators can be expected during a pandemic respiratory infection such as influenza A. Some individuals may want to use common fabric materials for respiratory protection because of shortage or affordability reasons. To address the filtration performance of common fabric materials against nano-size particles including viruses, five major categories of fabric materials including sweatshirts, T-shirts, towels, scarves, and cloth masks were tested…”

The conclusion is that the performance of improvised filters, such as scarves, overlaps surgical masks. Quoting

“Fabric materials may provide respiratory protection levels (i.e. total inward leakage) similar to the levels obtained using some surgical masks, which have been measured to be <10 (Oberg and Brosseau, 2008)…”

Individual virus particles are too small to be stopped. The authors have a theory complimentary to airflow modification.  They propose that like surgical masks, fabric improvisations are of benefit because much of the virus shed by an infected  individual is bound to larger particles.

Wear a scarf.

(Reuters) U.S. spy agencies monitor coronavirus spread, concerns about India: sources.

If you’re into thought-experiments,  get started with (NCBI PMC) The U.S. Military and the Influenza Pandemic of 1918–1919.  Attend to this question: Are there civil environments in less developed countries that can reprise the process  in those U.S. military camps that  selected for increased virulence?

Modern, urban India is similar in social organization to other modern countries, so propagation is likely to be similar in nature, though greater in scope. Of note, though, India is historically light on  influenza, the closest proxy for experience.

Rural, “Village India”, has different social characteristics:

• Relative immobility.
• Such mobility as there is, is based on kin relationships.
• Likely erection by local authorities of ineffective barriers that actually select for characteristics of virulence.
• General absence of infrastructure to support modern hygiene.
• An incredibly rich microbiota “soup”,  which may promote diverse forms of transmission, including  human-nonhuman-human.
• Lots of opportunities for genetic reassortment.
• By comparison to China, an absence of top-down pervasive social control.

Factors that support rapid mutation might coincide with selection for virulence.

Yet India isn’t much troubled by the flu!

The next article is the promised layman’s intro to epidemiology.

On page 147 of the 1935 printing of Rats, Lice, and History, (pdf Archive.org ) epidemiologist Hans Zinsser writes about the Plague of Justinian,

“It is interesting to note that this epidemic displayed one of the characteristics so often referred to in modern epidemiology — namely, when the outbreaks begin, the number of sick and the mortality were relatively slight, but both rose with appalling violence as the epidemic gathered velocity.”

 It is understood that while worsening conditions of life in an epidemic exact a toll, the primary change is increase in the virulence of the pathogen.

Zinsser had personal experience with the notorious modern example. (NCBI PMC) The U.S. Military and the Influenza Pandemic of 1918–1919 relates the observations of medical officer Alan M. Chesney. Quoting (boldface  mine),

During Chesney’s first documented period, the month of June to July 27, the 5th Artillery Brigade had 77 “relatively mild” cases of influenza. During the second phase, July 27 to August 23, 200 men of the 58th Artillery Brigade became ill, about 6.5%. None of them died, but the outbreak was serious enough that the next brigade cleaned out the barracks, even washing the walls, before they moved in. Despite this precaution, during Chesney’s third phase, August 23 to November 8, more than one-third of the 6th Artillery Brigade, 1,636 soldiers, contracted influenza and 151 died. Chesney concluded that “…these successive outbreaks tended to be progressively more severe both in character and extent, which would speak for an increasing virulence of the causative agent.”¹³

Like the stories of Zinsser’s captivating book,  this factual account omits the mechanics of why virulence can increase. Since that time, epidemiology has evolved from a preponderance of mystery to an inexact science. In the past several months, epidemiologists have used a lot of hopeful words, with reluctance to make predictions. Only within the past week or so has CDC confided that COVID-19 is inescapable.

Like the social sciences, epidemiology lacks the bedrock of hard science master equations. But there is math; it just has to be tweaked to fit the circumstances.  The next article offers an intuitive approach to Zinsser’s assertion and Chesney’s experience. The predator-prey equations, explained in words, are a good place to start. Intuitive epidemiology is accessible to a large audience., including you.

The warning: In large parts of the world, particularly within conflict zones, but also without, conditions exist for an increase in the virulence of COVID-19.

To be continued shortly.

(CNN) First coronavirus death in Europe, with more than 67,000 cases globally,  features an interview with Kent and Rebecca Frasure, quarantined on the  cruise ship Diamond Princess. Print interview at  (Intelligencer) An American on Quarantined Cruise Ship Describes Moment His Wife Was Diagnosed With Coronavirus.

Despite what we expect as intimate contact on the cruise, Kent has not contracted COVID-19.  By itself, this registers as no more than an oddity. With that taken care of, Indonesia’s claim of zero  native cases (ABC, First case of corona virus linked to Bali after report Chinese tourist returned positive test). is no more than carelessness combined with wishful thinking.

But is it? If confirmed by more  instances, the explanations are limited to three:

• Some people are genetically more susceptible than others.
• Some groups have cultural practices that protect.
• There are in circulation, one or more corona viruses with overlapping serotypes.

The serotype is the face the virus presents to the immune system. Viruses can share serotypes, either partly or completely, yet have different characteristics of infection. The common rabies virus is one example. Half a dozen common strains  have different clinical courses, but one vaccine is good for all.

The most famous case is smallpox. In 1796, Edward Jenner, a British physician, et al., promoted the fact that  immunity to smallpox was produced by inoculation with the live cowpox virus.

So there is precedent: a zoonosis immunizes against a human disease.  In Indonesia, a sero-similar virus could be endemic as a local version of the common cold. It could have developed by spontaneous mutation. But are there live animal markets in Indonesia?

Yes, there are. (Animals Asia) Animals Asia Ambassador Peter Egan visits “sickening horrors” of Indonesia’s brutal dog and cat meat markets. But domestic animals are not the historic reservoirs. Bats are more to the point. (ABC Australia) Coronavirus scare prompts call to pause bat meat consumption from Indonesian market.

The picture clarifies. With bats, dogs, and cats, civets and snakes are probably in the mix. A specialty coffee, kopi luwak, is made from beans in civet poop. Human processors of this material are exposed to a constant stream of civet viruses.

So a benign relative of COVID-19 may be present in the Indonesia community. Prior infection may produce the implied  immunity of Indonesians. Immunity caused by a live virus tends to be stronger and last longer than vaccine-induced.

Medical ethics has developed to protect the public from the worst abuses of the past. But it may have taken a turn towards avoiding liability. A simple thought experiment is Jenner’s smallpox vaccine.  Is there a modern path of ethical approval, save from a movie zombie attack, that would allow Jenner’s primitive vaccine, which worked?

It’s not hypothetical. The prospects for third world countries, and war zones, are dismal, unless they have their own fortuitous zoonosis. The analysis problem is not hard. It involves comprehensive sampling of circulating corona viruses in Indonesia, searching for similar serotypes.

There is a preliminary report from China that serum from recovered patients may be useful. A serum from “boosted” Indonesians could be a valuable export.  Or planeloads of sneezy Indonesians could fly to third-world destinations, and meet-and-greet, spreading benign relatives of COVID-19. See (bioRxiv ) Increased frequency of travel may act to decrease the chance of a global pandemic

You may be of conservative mind, rightly observing that you could lose your job with this.  For passive inclinations, there is still work. Detection or absence sero-similar relatives of COVID-19 in world populations offers refined estimates of the ultimate cost.

In (CNN) Coronavirus cases rise to more than 64,000 globally, Anderson Cooper asks Sanjay Gupta whether travel bans make sense. Gupta’s reply seems to be in the negative, with a little vagueness thrown in.

Let’s nail it down. In the short term, travel bans have benefit. The benefit will decrease with time. It will be obvious when the utility of travel bans expires.

If people were like plants, did not travel, and could infect only their nearest neighbors,  an epidemic could be modeled as a pure diffusion process. Drip a drop of ink or food dye in a glass or water. Watch it spread out in the liquid, betraying the invisible currents of water in the glass. This is diffusion. The plume from a smoky fire is another form of diffusion, combined with convection.

The purest diffusion is equalization of temperature, between something which is hot, and something which is cold. But it’s almost always combined with something else. The cooling of your cup of coffee is a combination of diffusion, and air currents.  The currents are analogous to  travelers.

Now pour a fresh glass of water, add a drop of ink, and stir or shake the glass. This adds “travelers”, bulk movement of the water. The ink quickly spreads out through the water in the glass, until it all has the same tint. The ink in the glass will never concentrate again. That’s the past history of the ink, just as the current concentration of COVID-19 around Wuhan will be replaced by general prevalence.

The spread of COVID-19 is by a combination of modes:

• Diffusion, as described above, by which a cluster grows locally.
• Non local processes, which resemble stirring of the glass: an infected, asymptomatic  traveler, the “super spreader”.
• Establishment of new clusters, which spread again by the above, diffusion and travelers.

Diffusion can be modified by sanitation.  Travel bans target the non-local modes. Eventually, COVID-19 will be equally present everywhere, subject only to local factors that have not yet been identified.

Travel bans buy time. The amount of time is impossible to predict.  At some unknown time, asymptomatic “super spreaders” will bypass bans. At that point, travel bans will become useless, but not before.  When is a roll of the dice. Politics will doubtless prolong the bans beyond usefulness, but that is future.

What do we do in the meantime? With a  fully functioning economy, we should be preparing, training, stockpiling, and researching. This is a time to screen small molecule drugs. For inspiration, (Science Daily) Dozens of non-oncology drugs can kill cancer cells. Quoting,

Researchers tested approximately 4,518 drug compounds on 578 human cancer cell lines and found nearly 50 that have previously unrecognized anti-cancer activity. These drugs have been used to treat conditions such as diabetes, inflammation, alcoholism, and even arthritis in dogs…

This kind of information, even in the negative, is vital to stave off quack remedies. From the debatable lore of medieval plagues,

Ring-a-round the rosie,
A pocket full of posies,
Ashes! Ashes!
We all fall down.^[3]

(Reuters) Coronavirus cases outside China may be ‘tip of the iceberg’: WHO. Quoting,

Much remains to be determined about the virus, which has been linked to a market selling animals in Wuhan, the capital of Hubei province, including how easily it spreads and how deadly it is. Chinese researchers found that its incubation period could be up to 24 days….It had been thought to be up to 14 days. 

The maximum incubation period was thought to be a hard number. There may be no such number, invoking the scenario of the “caged virus.”

The caged virus phenomenon was first written about in conjunction with the rabies virus. Typical incubation periods are weeks, extending to months, occasionally up to two years. Then an isolated case of rabies with an apparent incubation period of 37 years was noted (citation missing.) The concept was further developed with the slow virus.

A slow virus replicates without effective immune response. Some trigger,  perhaps environmental, or possibly analogous to the bacterial quorum sensing, causes a switch from slow to fast.

No “slow” corona viruses have been discovered. There is no reason to think 2019-nCoV is the first one. But the 24 day incubation period, which may have measurement difficulties, suggests a gradation into that.

Most of the things epidemiologists are interested in cannot be derived from “first principles.” Observation is used to select a basic statistical model which can be adjusted. For example,

• A uniform statistical distribution distributes the incubation period  evenly distributed up to a fixed limit, say, 14 days.
• A Poisson distribution has an average incubation period, with tails in the direction of less and more.  It’s typical to cheat by chopping off the “more” tail, perhaps at 14 days, or 24. But this may not be valid.
• We could be looking at a distribution without a practical upper limit for incubation. This doesn’t bother statisticians at all. There are many distributions with infinite variance.

It would mean we have blundered into a virus with a highly effective strategy, with widespread infected carriers, undetectable by any simple, practical means.

In 2019 Novel Coronavirus (2019-nCoV), Wuhan, China; Quarantine is Correct Response, I wrote,

Perhaps by tradition rooted in the 1976 swine flu fiasco, the cost of “no vaccine for 2019-nCoV ” is set for typical epidemiology. Yet the 1918 Spanish flu was untypically deadly for an airborne pathogen….The cost/benefit analysis could have an unpleasant surprise.

This could be that surprise.

As evidenced by the cruise ship quarantined in Yokohama, 2019-nCoV  is highly contagious, with no unexpected selectivity. The  lethality of the virus is still a question, which cannot be answered until the actual prevalence of subclinical and missed cases is tallied, which can only be accomplished when test kits are available and cheap.

Two factors may enhance the lethality of nCoV-2019 in China compared to the rest of the developed world, smoking, and genetics.

1. Smoking

In China, 60% of doctors are smokers, with rates in the general population said to be similar. Quoting from (Wikipedia) Smoking in China.

Nearly 60% of male Chinese doctors are smokers, which is the highest proportion in the world.^[4] China does not have laws to punish health care facilities, medical workers and health officials who violate smoking bans, and is instead relying on the Chinese media to act as a watchdog.^[4]

Smoking is a social custom in the PRC,^[1] and giving cigarettes at any social interaction is a sign of respect and friendliness.

Now refer to (PLOS via NCBI) Effect of tobacco smoking on the risk of developing community acquired pneumonia: A systematic review and meta-analysis. From the abstract conclusion (square brackets mine):

Tobacco smoke exposure is significantly associated with the development of CAP [pneumonia acquired outside a hospital] in current smokers and ex-smokers. Adults aged > 65 years who are passive smokers are also at higher risk of CAP. For current smokers, a significant dose-response relationship is evident.

This is a meta-study.  Prior studies with varying endpoints were analyzed via statistical methods to remove confounding factors, isolating the association of smoking with pneumonia. Community acquired is the term for an infectious disease acquired anywhere other than in a hospital.

This study does not examine lethality, probably because statistical techniques  could not dig it out with sufficient confidence levels.  To see the likely connection, consider the structure of the lung. Two parts of the lung come in direct contact with air:

• The bronchioles are air tubes, arranged like an upside down tree, decreasing in diameter the further in you go from the windpipe.
• The alveoli are expandable balloons, attached to the bronchioles like the leaves of a tree. This is where oxygen exchange occurs.
• Both are lined with respiratory epithelium, which is lined with fine motile hairs called cilia, and wet with mucus.

In a healthy nonsmoker, the cilia  “beat” to expel inhaled particles back up the bronchioles to the  throat, where they are expelled or swallowed, usually without notice.

In a nonsmoker, the innate immune system, which requires no prior knowledge of a virus, is active. (NCBI) Innate immunity and mucus structure and function. This is why, in most cases, an individual virus particle cannot cause infection. The number is small, but usually greater than one.

In a smoker, the actions of the cilia, and the innate immune system, are suppressed. Recovery from viral pneumonia is possible due to the adaptive immune system, which requires time to manufacture antibodies specific to the pathogen. It becomes a race in time, between viral load and antibody production.

So it is highly plausible, though missing study results, that a China where most people smoke, including doctors and staff, is likely to experience enhanced lethality due to 2019-nCoV.

2. Genetics

By strict definition, pneumonia is an infection of the alveoli, not the bronchioles which connect. Broadening the definition, it includes bronchiolitis. This is considered  clinically significant primarily with infants. There is an interesting exception, diffuse panbronchiolitis.

Diffuse panbronchiolitis is considered an Asian phenomenon,  which means that the etiology (cause) and prevalence are not nailed down. It is clinically known in Japan and Korea, with suspicion of a genetic influence.  The origins of these groups, like the rest of us, are lost in prehistory. Current theories of origin:

• Koreans have a large genetic representation of tribes from eastern Siberia.
• Japanese contain some of the above, as well as other groups.

This suggests that a genetic bottleneck in eastern Siberia  resulted in the frequency of diffuse panbronchiolitis in both populations.

In prehistory, the Han Chinese were in conflict and competition with every other adjacent group. While they remained culturally distinct, genetic isolation is unlikely. Literature suggests that the prevalence of this disease in China is unknown. A contributor to 2019-nCoV lethality  may lurk within this vacuum.

3. Coincidence of Factors

The combination of a possible genetic factor, and smoking, may be more than additive. It may be multiplicative .

The prevalence of smoking in and near health care facilities may enhance nosocomial (in a hospital) transmission.