Tag Archives: Covid-19

How an epidemic (or pandemic) starts

Years ago Ebola made itself known to scientists, when it appeared simultaneously in the Sudan and Zaire. The two events were a very long way from each other. It happens that I am very familiar with that part of the map, and I’m certain that any attempt to go from Nzara, Sudan, to Yambuku Zaire on land would take several weeks and, actually, be impossible. It could not happen casually. For a while, experts thought a particular person who was probably patient zero at Yambuku had made the trip, despite no evidence for him having done so. In the end, most ebola experts simply stopped thinking about this conundrum. A few of us working in the area, though, had a different idea. Animal-born (we thought fruit bat) ebola spread in the animal first, and conditions emerged that heightened the chance of a jump to humans also spread, so there were two separate jumps. Likely, this could happen now and then, with several jumps within a few weeks time, but only during those few weeks time when conditions were just right. The trick to managing future ebola outbreaks might be to figure out what those conditions might be, and at least, set up a warning system. But, since epidemiology worked at the time entirely on the pump model, one source, one initial spread, that sort of thinking never happened.

If that is typical for zoonotic diseases (even if not inevitable in every case) it presents a slightly different view than what one usually conjures up. It is not the case that an animal sneezes or bleeds (or whatever) on a human, then that humna, patient zero spreads the disease to other humans. Rather, the condition of transfer from an animal reservoir becomes temporarily highly likely insead of almost impossible, and perhaps dozens of transfers happen, of which, one or two or three, perhaps, are traced to eventually by epidemiologists.

Turns out that is what probably happened with Covid-19. The transfer happened twice, over just a few weeks time. The best explanation for this is that some animal species (could be more than one) had their own epidemic of this particular coronavirus strain going on, and there happen to be a big market with this animal species (or species) on sale, and the rest is history.

There are two studies, this one and this one, seem to support this idea. When the disease experts are done being incredibly busy with Covid, maybe they can go back to Sudan/Congo and rethink the initial appearance of Ebola with this model, now no longer just some zany idea a few of us had years ago, in mind.

Everyone in the US will be vaccinated by early August.

Everyone eligible and who wants to, that is.

Have a look at this line. I call it “line going up.” Feel free to download it and use it for your own purposes.

This line. It is going up.

I ask you to consider the following questions. Assume the vertical scale on the y-axis is 10:

1) What is the average value of this line?

2) What is the average value of the last 20% of the line, over to the left?

3) Assume the “line going up” is in fact upward-going indefinitely. This is the first ten units of time. What will be the average value of the second ten units of time?

4) Given the same assumption, what is the average value of all 20 units of time?

5) If you were asked to predict the total magnitude (all the areas under the curve) for all of the curve, for the next 10 units of time only, what would it be?

Answers:
1: about 5.
2: About 8
3: About 15
4: About 10
5: A lot, but it runs from about 10 to about 20, so if it is that many units per day, about 150 (the average of 10 and 20 times 10).

I know you got all those questions right. So, now that we can do baby analytical geometry and statistics, have a look at this:

This graph shows an upward trend. We know the trend is somewhat open-ended up to about 7 million a day, with new vaccines coming on line. The drop before the recent mode, which casues an average that would have been about 2.0 million per day, was caused by a preternatural natural disaster (Texas). So, the best estimate of curent production is much closer to 2.5, not 1.7, and that rate will continue to go up so in about four weeks it will be closer to 4 million a day. This is not just based on me looking at the graph and sucking my thumb. This is what the experts are saying. April through July would be 600 million doses, many of which would be one shot doses of the newest vaccines. In other words, every eligible person in the US will be vaccinated by the end of July, comfortably.

That is a very conservative estimate.

Why to people take perfectly good data combined with clear projections from the health experts and turn them into bald face lies? Oh, it is not a lie you say, just a mistake. No, I reply, it is impossible to make a mistake like this and publish it in bloomberg. This is a lie, designed to get a rise out of the readership, and that lie regardless of its intent will contribute to the gloom and doom and that has consequences.

Everything is as expected, even the Covid-19 pandemic

When I was in graduate school, four things happened at almost the same time (probably within a three year time frame, but who’s counting?) 1) The publication of The Coming Plague: Newly Emerging Diseases in a World Out of Balance by Laurie Garrett (well, and my reading of the book); 2) the cultural phenomenon of “hot zone” movies and books, of which the most memorable is probably Outbreak starting Dustin Hoffman; and 3) the realization that a good part of the archaeology I was doing in the Congo was of villages that had been abandoned because a plague of some kind came along and killed enough people that everyone moved elsewhere, which is apparently a tradition in that area; and 4) the Zaire Ebola outbreak in Kikwit. Since I had been working in the area, I got involved, in a minor way, with some of the Ebola research, and I produced evidence for a model for the virus jumping from fuit bats to humans that turned out to be exactly what had happened about ten years later when the West African Ebola epidemic occurred. Continue reading Everything is as expected, even the Covid-19 pandemic

Widespread Rejection of a Covid-19 Stick is a Click-Baiting Falsehood

A high percentage of people are going to get the Covid-19 vaccine that is available to them, because they are going to be choosing between two clearly labeled doors. One door says “Look like you believe science has something to offer.” The other doors says, “Maybe you die!”

I have the impression that people who have been taken in by anti-vax thinking, but only to some degree, who are not acolytes of that cult, get the stick when push comes to shove. They think about their health, their children, and they make the right choice. Certainly, it does not go the other way. Add this to the fact that a) the most refusing population out there is the US population, and in the US the refusal (as well as the acceptance, by the way) of the vaccine is almost entirely political, and we can guess that much of the “no, no” really means “ok, whatever.”

Yet another factor is the reporting. Whenever a poll has an undecided middle, or a weak “yes” or “no” element, it is possible to report the poll in a biased matter, even if the poll itself isn’t biased. This is clearly what happens when we see “X% say nope” without mentioning that a number equal to a third or fourth of that said “I don’t know, whatever.”

Here are some data for three polls that address this topic.

An April 2020 survey in seven European countries, with 7,662 respondents showed that 81.1% of the population were indifferent or willing to be vaccinated. (73.9 were explicitly willing.)

A Pew Research Center poll in mid September of Americans compared May and September. This September poll was taken at the height of cynicism about the Trump regime’s handling of Coronavirus, just before Trump himself got the virus. In this poll, 49% of all respondents said “no” (to some degree) to the vaccine (“I don’t know” was not a choice in this survey), with 56% of Republicans preferring to not be vaccinated, and 42% of Democrats preferring not.

The May survey showed those numbers at 27% for the whole survey, and 34% and 21% for Republicans vs. Democrats, respectively.

The September poll is probably the one most cited by those who prefer to be alarmed, but it actually underscores the likelihood that people will get the the shot at much higher numbers. A waft from 27% to 49% over four months indicates that the pollsters are not sampling what the questions indicate they are sampling. There is a huge amount of elasticity in what people say. Also, the fact that this survey had no room for “I don’t really have an opinion” forced people into a category. Given the high degree of politicization of the disease, which mainly consists of many Republicans preferring to appear to be reject science (in order to make lefty big city elite academics cringe) or Democrats rejecting a vaccine they see likely to be yet another Jared Kushner scam, the best numbers, among these, in my opinion are optimistic. In May, before the politicization occurred to a great degree, 72% of Americans said yes to the disease, but only 11% felt strongly about no. That conforms with the other surveys.

A survey reported in late October and published in Nature, across 19 countries, showed that 82% were indifferent or preferred the shot (61.4% were willing, the rest indifferent). Of those who seemed not to want the shot, only 9.8% felt strongly that way.

My friend, scientist Roderiko Kampen, recently suggesting, while agreeing that resistance to the vaccine will diminish over time, to “never underestimate human stupidity. Nothing is stable or ‘normal’ now, every single day some butterfly may flap the global hurricane. Humanity has thoroughly outlived its stay and is now beginning to meet that cool adversary – i.e. my great friend – called reality.” I agree. There will be pockets of resistance that will prove troublesome, and lives will be taken and illness spread because of resistance to science. But, ultimately, most people are going to get the shot, and at some point, schools are going require Covid-19 vaccination alongside the already required vaccinations in order to attend.

Look, people endlessly complain about TSA, and they complain more about TSA and the equivilant agencies around the world, the modern security systems at airports, even more than they complained about the totally fake ineffective security that was prevalent before 9/11, especially in the US. But they still get on the plane with a some sense of security. Covid-19 is worse than terrorism, by the numbers. We are having, in the US, a 9/11 level event every single day as I write this. The vaccine is the way out of this plague. People are going to get vaccinated. I would even go one step further. Anti-vax will always be with us. It is an industry, and anti-anti-vax is also an industry. But a movement (or, really, scam) designed to hamper the fight against this pandemic will get weaker, not stronger, over the next year.

Covid-19 Update: Vaccines, Airborne, Seasonality, Irony

A tale of two vaccines

Two vaccines are racing to the finish line. We can’t say which one will arrive first, because they each have a different finish line.

The good vaccine, the one likely to be safe (though not necessarily without some side effects) and effective (though you may need two doses, which is normal for vaccines so don’t panic about that) had this deadline: When it is ready, as in, finished with Phase 3 trials. My money is still on the Oxford Jenner vaccine. If that is the first one ready, don’t expect to see it in the US because a) Jared Kushner does not have any ownership in it and b) Jared’s F-I-L is the corrupt leader of the formerly Democratic Republic of the United States. We’ll get it after Joe and Kamala, if they are not killed by Putin, are in the White House.

What? You think we are going to let you have a vaccine that I don’t make money off of? Nope, not going to happen as long as the Trump Crime Family is in charge!
The bad vaccine is whatever vaccine the Trump Crime Family has decided they can sell us. The deadline for that is November 3rd, but really, earlier, because of early voting. FDA Commissioner Stephen Hahn, a member of the Trump Crime Family has started to say, “Oh, no, if we approve a vaccine early, and that is possible, then it will be a great vaccine, a really great vaccine, don’t worry, we are not going to play political games here. Nope. No October Surprise from the FDA, no sir.” Meanwhile all of the senior actual scientists in the government that have anything to do with this have warned Hahn, uselessly, that he should not do this, because they expect him to do this.

I’m fine with this. The fake vaccine might actually work. It will be distributed among Republicans first, and they will blindly take it because they are morons and the head of the Trump Crime Family will order them to do it. If the vaccine turns out to be dangerous, it will be they that suffer, deservedly for the adults (sorry, kids, your parents are dangerous assholes) and it will be they that later sue (if they live) Hahn and Trump over the damage done. If, on the other hand, the fake vaccine is actually a good vaccine, an emergency use authorization by Hahn will certainly speed up data collection, owing to the additional rats, er, lab rats.

See “Here’s how the U.S. could release a COVID-19 vaccine before the election—and why that scares some

The Second Coming

Never mind what you may have heard about Covid-19’s virus not being seasonal. The assertions that it is not were falsehoods, mostly generated by the press misunderstanding what this all means, spread by people who, amazingly, are not actual epidemiologists, on Facebook. OK, admittedly, I am not actually an epidemiologist either, though back in Grad school when I discovered it exists, I almost jumped ship. And, I do play one in the classroom in the class I co-teach on immunology and epidemiology. Point is, I know a little better than the average person when I’m about to say something stupid. Usually, I then shut up. But not always, so beware.

Anyway, for all the various scientific reasons, it might be seasonal. Consider group of immunologists and epidemiologist siting around having a beer, and someone asks the question, “Is Covid-19 seasonal?” you’d get a lot of hemming and hawing. Then, the inquisitor says, “OK, fine. Each of you take this slip of paper and pencil, and write down “yes” if you think it will turn out to be seasonal, and “no” if you don’t think so. Don’t share your work. If you all turn out to say the same answer, then the beer is free for the rest of the night.”

I strongly suspect they would all write down a non-committal but educated “yes.”

The thing is, an outbreak has its own momentum. Some of the worse influenza outbreaks violated the seasonal pattern we know influenza has. All the Covid-19 outbreaks we have been having have masked any possible obvious seasonality for Covid, though one study that looked at underlying factors linked to seasonality concluded that there is a pretty good chance Covid-19 is seasonal.

On top of that, we have another (not unrelated) set of seasonal factors. No matter what you do to mitigate against spread of the disease in a school, going back to school, even in some sort of limited “hybrid” pattern, WILL result in increased spread. This is not an uncertainty. And, we are starting that now, and as you probably know, it is happening. Between back to school and climate related seasonal effects, we are looking at a long hard winter.

Related: COVID-19 rising in 26 states as US hits 6 million cases

Covid-19 is probably not mainly airborne.

But it is totally airborne as well.

I think it is funny (as in “funny, holy crap, how stupid can people be????”) that once news came out that Covid-19 is very likely airbonre, that many people actually then asserted that it was NOT spread hand to object to hand. It still is folks! KEEP WASHING YOUR DAMN HANDS PEOPLE. Jeesh.

But anyway, the evidence of airborne transmission builds and our understanding of that phenomenon deepens.

COVID-19 patients in earlier stages exhaled millions of SARS-CoV-2 per hour

Exhaled breath samples had the highest positive rate (26.9%, n=52), followed by surface swabs (5.4%, n=242), and air samples (3.8%, n=26). COVID-19 patients recruited in Beijing exhaled millions of SARS-CoV-2 RNA copies into the air per hour. Exhaled breath emission may play an important role in the COVID-19 transmission.

For refernece, this is the very rough not yet accepted article that started this whole thing: Outbreak of COVID-19 in a nursing home associated with aerosol transmission as a result of inadequate ventilation

See this for a very current summary on the airborne situation.

Or, maybe you are just on your own

The latest plan from the Trump administration, other than faking a new vaccine to make money somehow, is the do nothing and wait for herd immunity to “kick in.”

New Trump pandemic adviser pushes controversial ‘herd immunity’ strategy, worrying public health officials

One of President Trump’s top medical advisers is urging the White House to embrace a controversial “herd immunity” strategy to combat the pandemic, which would entail allowing the coronavirus to spread through most of the population to quickly build resistance to the virus, while taking steps to protect those in nursing homes and other vulnerable populations, according to five people familiar with the discussions.

The administration has already begun to implement some policies along these lines, according to current and former officials as well as experts, particularly with regard to testing.

The approach’s chief proponent is Scott Atlas, a neuroradiologist and fellow at Stanford’s conservative Hoover Institution, who joined the White House in August as a pandemic adviser. …

Irony

Yes, I am aware that the picture at the top of the post is an example of irony. That is why it is there.

Our social distancing guidelines are underthought

Seriously under-thought.

One way Covid-19 spread is you shove your hand in your mouth, then you use your hand to gob onto a door knob, then the next person to come along licks the door knob. So don’t do that!

If you think I’m being silly, watch some pre-schoolers for a while.

But even adults, at a somewhat lower rate, continuously shed their sheddable viruses a little at a time onto every surface, where the viruses either die over a period of a few hours or get picked up by the next person.

So imagine a scenario in which a person is sitting in a room and a stream of people come in, one at a time, to socially distance at 6 feet away, masked, to have a conversation with that person. Further, imagine the person sitting in place is a teacher, and the visitors are little kids getting to meet their teacher before a semester of distance learning.

Sounds totally safe. Indoors, six foot distance, masks. Nothing can possibly go wrong.

OK, now lets backtrack and find the student in the parking lot. The student and her brother and two parents have just parked. They are coming from a sports event they’ve been attending weekly for a month, at which everyone is shouting and no one is wearing a mask. The are all infected but don’t know it yet. The family heads for the school, and let themselves in the front door. Four people have now touched the doorknob. They are now in the lobby and a school employee, masked and with a face shield, stops them and says, “OK, you’all stay here in the lobby but six feet away from the other families, and I’ll walk little sally to see Mr. Scary the teacher.”

While the student is away, the family gravitates over to some people they know, and start a conversation at what they think is a safe 6 foot distance, but they forget, don’t pay attention, whatever, and pretty soon they are closing in and talking around their masks at each other. Family 2 is now exposed, and has, say, a 1 in 30 chance of getting the virus. This scenario is, of course, playing out hundreds of times across the school district, so there will be some transmission at the door knobs and in the lobby. In the parking lot outside, even.

Little Sally is now being accompanied down an empty hallway by a person she does not know wearing a face shield and a mask, and she starts to cry (= major shedding) on the way down the hall and needs to have her hand held for the last few meters going into the room. While talking to her teacher she is overwrought being away from her parents in this strange place so she throws up breakfast. But that’s OK, the teacher and a para clean it up. But, remember, Little Sally is a carrier, so there is now a thin film of Covid-19 kooties from the lobby to the classroom, even where the hasty cleanup (everyone is behind schedule) happens. This is the first of a four day meet and greet, with two days this week, and two days next week. So this gives Mr. Scary and the para plenty of time to become contagious. So, on week two, one in 100 kids that come in to meet their teacher picks up Covid-19. That is’t many. But the school district has 10 elementary schools, and this scenario is happening in all of them, for a total of 3,000 kiddos. So there are now 30 sick and shedding elementary students mostly doing distance learning at home and, slowly, one by one, killing off the grandparents.

If you don’t like that scenario, make up your own. The point is, masking up and staying 6 feet apart slows, but does not eliminate, infection. As we return to schools, even with precautions, this is going to happen. Everywhere.

And now there is new research that gives us a better idea of how a 6 foot social distance is an oversimplified concept that provides a false, and in this case, deadly, sense of security. More to the point: People think that if everyone “wears” a “mask” (did you notice the scare quotes there?) and stays “six feet” away from each other, than the chance of infection is zero. It isn’t. It never was.

The following nuance inducing graphic is from “Two metres or one: what is the evidence for physical distancing in covid-19?” by Jones, Qureshi, et all, just published.

Risk of SARS-CoV-2 transmission from asymptomatic people in different settings and for different occupation times, venting, and crowding levels (ignoring variation in susceptibility and viral shedding rates). Face covering refers to those for the general population and not high grade respirators. The grades are indicative of qualitative relative risk and do not represent a quantitative measure. Other factors not presented in these tables may also need to be taken into account when considering transmission risk, including viral load of an infected person and people’s susceptibility to infection. Coughing or sneezing, even if these are due to irritation or allergies while asymptomatic, would exacerbate risk of exposure across an indoor space, regardless of ventilation

I’m not going to provide much of a summary of the article. It is very readable and clear. Just click here and find it, read it yourself.

“Instead of single, fixed physical distance rules, we propose graded recommendations that better reflect the multiple factors that combine to determine risk. This would provide greater protection in the highest risk settings but also greater freedom in lower risk settings, potentially enabling a return towards normality in some aspects of social and economic life.

Key messages:

  • Current rules on safe physical distancing are based on outdated science
  • Distribution of viral particles is affected by numerous factors, including air flow
  • Evidence suggests SARS-CoV-2 may travel more than 2 m through activities such as coughing and shouting
  • Rules on distancing should reflect the multiple factors that affect risk, including ventilation, occupancy, and exposure time

Teachers: This one neat trick could save your life

This is for all teachers, but only some of you will be able to do this. Depends on your topic. This may pertain mostly to biology teachers, maybe stats or math, but by extension, any science or empirical topic including history.

Never mind that the first thing bio students to know is about Hydrogen bonds, or that the first thing stats students need to know is basic probability theory. You already probably do some sort of introduction thing that gets the students oriented to your subject, with a “get to know you” component, etc.

Replace that with this. The first thing the students should encounter in your classroom is some sort of topic appropriate, level and age appropriate, encounter with pandemic reality. Many of your students are not taking this pandemic seriously. They’ve been hanging round mask-less and in close quarters with their friends all summer, maybe practicing on a team, whatever. They are not going to properly manage their own viral shed or the possibility of someone else’s pathogenic effluence. They are going to be gobbing all over each other, their desks, and you.

Now is the time to use your mad teaching skills to push at least some of your students in the direction of being more careful, and possibly, slowing the spread of the Covid-19 causing disease.

I know, I know, you are saying “we are doing distance learning, this does not matter.” But it does matter. The back to school outbreak is going to happen whether or not you, or your school, is doing distance learning, and your small part of the learning community overlaps with the rest of it. And, you never know when your college, HS administration, or school district is going to send the students back into your room. This is your chance. Take it.

Can’t think of an example of a lesson that would smart up your students, to enhance the behavioral part of their innate immune system? Don’t give me that! Of course you can, you are a great teacher! In face, once you’ve thought about it, I want to hear your ideas. Let’s get moving on this!

Before the Covid-19 Vaccine, This.

Antibodies may precede vaccines in fighting Covid-19. Antibody treatments involve producing antibodies against a disease, either by harvesting them from previously infected individuals or, better, making them using some sort of scientific magic (aka technology that is hard to explain). An antibody treatment can fight an existing virus, and avoid infection short term. Eventually the antibodies go away, so this does not confer immediate immunity.

This is not an uncommon situations. Lots of diseases appeared out of nowhere, and were initially treated this way until other longer term solutions could be developed. But many of those diseases were rare to begin with and remained rare, so the antibody treatment was not scaled up. Just read all those books and stories about “emerging diseases” from back in the “Hot Zone” literature days and you’ll see these stories played out.

Anyway, here is what some experts say quoted in a recent Science coverage by Jon Cohen:

“If you were going to put your money down, you would bet that you get the answer with the monoclonal before you get the answer with a vaccine,” says Anthony Fauci, head of the National Institute of Allergy and Infectious Diseases (NIAID).

and

“Antibodies have the potential to be an important bridge until the vaccine is available,” says Ajay Nirula, a vice president at Eli Lilly, one of several large companies investing in them. Likely to be more effective than remdesivir and dexamethasone, the repurposed drugs shown to help against COVID-19, antibodies could protect the highest risk health care workers from becoming infected while also lessening the severity of the disease in hospitalized patients. But producing monoclonals involves using bioreactors to grow lines of B cells that make the proteins, raising concerns they could be scarce and expensive. On 15 July, Lilly, AbCellera, AstraZeneca, GlaxoSmithKline, Genentech, and Amgen jointly asked the U.S. Department of Justice (DOJ) whether they could share information about manufacturing their monoclonals without violating antitrust laws “to expand and expedite production.”

Antibody expert Amy Jenkins (Pandemic Prevention Platform (P3) program at the Defense Advanced Research Projects Agency) suggests a N ovember-December time line for seeing this technology in the field is not unrealistic.

Opening the schools, Plan B

This should really be Plan A but no school district is going to adopt this plan until after just the right cute little kid or beloved teacher dies of Covid-19 on a news day with few other distractions. This plan pertains to High Schools only. Perhaps later we can extend a version of this to other grades.

Here’s the plan.

1) Admit there is a deadly pandemic and that we need to not feed the virus. Also recognize that a realistic estimate of when a vaccine starts to be available is during the school year after the upcoming one, and that it will take a year or so to fully deploy it in the US. The plan for starting school should not be, as it is now, “we’ll do this for the first week then… who knows?” The plan should be one that will flexible but outlined for a two or three year time range, because that is the time range over which this pandemic is going to play out.

2) Change the requirements for graduating from high school. Henceforth, students must meet the core* class requirements, and do not need to meet total credit requirements. All students who have met these requirements are graduated instantly. That would instantly reduce the number of students in the schools by a few percent.

4) Add one year to the high school plan. Call it “Covid-Extention-Year.” (Why? See below.)

3) Identify (mainly) Seniors and Juniors who have only a few core class requirements to finish. Spread those required classes over the next two years (some Seniors will thus be extending their school time into CEY). Many students in most schools will in this manner only have one class at a time, at most, with many semesters/quarters not having to attend school at all.

4) Restrict all other teaching to core requirements only. So, no electives. All teachers are switched to core requirements, all students are taking core requirements.

Suddenly, 3-4% of students would be gone. Within one semester, another 10-15% of students would be graduated, while another 20% of students would be committed to attending school for only one or two classes over about a year and a half. These first four changes simply thin out the herd gracefully and without killing anyone, as opposed to the current approach, which will thin out the herd the hard way.

5) Do as much distance learning as possible, but if classes are required…

6) Revise the one room schoolhouse model.

  • Students stay in one room.
  • Passing time and bathroom access is set up to minimize hallway contact.
  • Teachers move from room to room (teaching core classes only) and wear hazmat
  • Very few students in each room so when an infection pops up the total number of students removed from school is small. They can come back in a few weeks.
  • Since teachers are suited up they do not have to be quarantined when a student in their room tests positive.

It is essential to keep the teaching staff intact. There will be more needed than usual because several will be out sick for more time than usual. Classes, both distant and in person, should have smaller class size (for most classes, some distant learning classes may not need that). The one room schoolhouse method not only reduces infection, but serves another goal: Relationship building will be easier and more solid in mostly distance learning settings.

*Many schools use the term “core” to refer to a specific subset of academics. What I mean here is different, and includes more. Think of it this way: Look at a set of class records for a sample of seniors. Consider the total number of classes, and the types of classes, that make those students viable HS graduates, and cut out everything else. In other words, pare down. Most students manage to get what we think of as a full on high school degree with a few classes extra. Some students do everything in three years, and earn a year of college. This does not mean removing art or music. It means paring down the individual student’s total work, and probably, the full range of options.

By reducing the number of students and keeping the number of teachers the same, and simplifying the offerings, it is easier to have smaller one-room learning units. While distance learning is ongoing the one-room learning units are not necessary, but they are ready to go when the students and teachers are called back into the classroom. This might be after a vaccine is available, but is still being deployed, and the virus is in smaller numbers but still a threat, which one might estimate to be some time during the 2021-2022 school year.

Understating Airborne Covid-19

My title is slightly misleading but meant to tell you what this essay is about. I want to talk about recent reports that SARS-CoV-2, the virus that causes Covid-19, is airborne.

The concept of airborne in thinking about pathogens is probably the single most misunderstood thing in epidemiology, not by epidemiologists but by regular people. It is also probably the most evocative, and stupifying. Recently, the word “airborne” has been used in discussions of Covid-19, and this led to many extreme reactions. Like this:

Input: Bla bla bla Covid-19 bla bla bla airborne.

Output: All the credible experts have agreed that Covid is airbone! it is no longer spread by contact, but now it is airborne! The Fauci mutation probably made it airborne! And so on!

SARS-CoV-2 is spread by shedding from an infected person’s respiratory system and getting into a new host’s respiratory system via droplets of mucus that go from hand to hand, hand to mouth, mouth to hand, mouth or nose to surface, surface to hand then hand to mouth, etc. Human upper respiratory bodily fluids (snot, etc.) get on stuff and then people touch stuff and then it get into their respiratory system. This is how most cold and flu infections are passed on, generally. That is not airborne spread.

Among all the many viruses that give us colds or the flu — the many strains of influenza, rhinovirus, coronaviruses other than SARS-CoV-2, etc. — this is how infection happens.

Again, this is not airborne spread. It might be airborne in your head, because you imagine someone sneezing, into the air, droplets of virus-containing spittle and snot flying around in the air, and since that stuff flies through the air it must therefore airborne. But that is not what airborne means, and the distinction is important.

There is probably a certain amount of true airborne transmission in any of the above mentioned categories of virus, including the flu and more common colds. But it is rare enough that these diseases are not said to be airborne.

So what is airborne then, if it is not simply flying snot particles?

Airborne spread requires several things to be true often enough that an observable number of cases were spread in this way. First, the virus must be aerosolized. This means that the virus is embedded in a very small gobs of snot, perhaps near 5 microns, droplets that are small enough to be suspended in the air. Larger drops will fall out of the air, these smaller drops will float in the air like they were part of the air. They act like a gas in the air.

The droplets also have to be small enough to get into the parts of the respiratory system that the virus targets, which for SARS-CoV-2 is not too much of a limiting factor since it likes to inhabit the upper respiratory tract. But, since it also can invade the lungs, there would be the possibility that airborne transmission would be more associated with a more serious infection, if and when it happens.

Airborne spread also requires that the virus can live in the air long enough to get to its target. The longer the virus can live in the air, the worse of a problem it is because it can travel farther, through ventilation systems, down hallways, etc. There is no evidence that SARS-CoV-2 does that like, say measles, the king of airborne infection does it. Whatever environmental conditions are experienced by this suspended droplet have to NOT kill the virus. IV light kills SARS-CoV-2, so it is not going to get far during the day, outside, when the sun is out. SARS-CoV-2 might like certain humidity levels. None of this is really known for SARS-CoV-2, but it is a virus of type that we generally know about. Other forms of coronavirus are known to survive a while in the air, so that may pertain here. Be cautious in reacting to what you hear though. Detecting a virus some distance away from a sneeze does not mean that the virus is viable or capable of infection

Also, the virus has to be out there in the air in sufficient numbers to actually cause an infection. One would think that it only takes one single virus to infect someone, but generally it takes a much larger number. There seems to be a threshold for most viruses. The body dispenses of the first N viruses, then after that it gets harder, and eventually the system is overwhelmed. Maybe. The point is, virus experts will tell you that is has to be a large number for most viruses, and this is certainly true for SARS-CoV-2.

Truly aerosolized, viable, in sufficient numbers.

Finally, note that if SARS-CoV-2 was mainly airborne, we would know it by now. You can look at it, epidemiologically, and say, no, the main form of transmission is not airborne. That does not mean that there is not an airborne component, but it means that airborne is not the major way of spread. That has not changed.

What does the new research tell us?

Well, by the standards of peer reviewed scientific research, pretty much nothing, because that research is still in its infancy. But here is what happened. Several cases of infection have been reported that can be best explained by airborne infection. How many? So few that some would interpret that as potentially useless data. These may be cases that are simply misreported. Somebody licked someone else’s tongue and refuses to admit it. Does that really happen? Well, ask any expert on the epidemiology of sexually transmitted diseases about it. Of course it can. Most rare cases can be explained away or ignored.

But in this case, a large number of experts have settled on a provisional consensus: They see enough cases of possible airborne transmission of SARS-CoV-2 to ask the overarching institutional authorities like the CDC to seriously consider it and look into it. Yeah, that is it. Important, concerning, should shape policy modestly for now, requires more consideration. The smart money is on SARS-CoV-2 being transmittable via aerosol, though that will probably not be the main modality of transmission in most settings. That is my bet. Airborne transmission can happen, and will happen in some cases. More on that below. But, this is provisional.

What this does not mean.

This does not mean that there is a new mutation. Repeat: this is not a new mutation. This has been there all along, and the fact that it has not been obvious since the beginning means, as stated, this is not the new mode of transmission. This does not mean that the virus has changed. Probably.

This also has no impact on mask wearing. Airborne transmission will go right around the masks most people wear, but we already know that if airborne transmission is happening, it is not the main way the virus is spread. This is NOT AN ARGUMENT TO NOT WEAR MASKS so don’t go making that argument or you are a full-on jerk. Ignorant jerk. I know you won’t, but if you see that argument being made by others, that is what you are seeing. That argument is so stupid, you can expect Trump to make it soon.

What this might mean.

This is the important part of all this, worthy of careful consideration. Assume that normal near-distance non airborne transmission is the normal and most common form of transmission by a large margin. We assume that if people are kept a minimum of 6 feet away from each other (or 10 if you like) and do not share objects with their hands and faces, i.e, social distancing, that transmission will be minimized. This works for social gatherings, according to some, especially if masks are worn.

However, over longer term, while people are avoiding infecting each other by keeping their mucus to themselves, a low level background transmission via the air could be happening at a small level.

It would be rare. Say one hour of exposure within a single medium size room with modest air circulation has a one in a thousand chance of one infected person giving the disease to one other person in the room. (I am totally making up all these numbers, but just bear with me.)

But now, we take that room and put between zero and three infected people in it, and 30 target non infected people. But we put then in that room for 8 hours, and do that for 185 days. This configuration of people might sound familiar to you.

This is a classroom full of students social distancing. But wait, you say, if they are social distancing, they can’t fit 30 people in the room. But you would be wrong in some cases. Elementary schools with the pod system have four classes of 30 (including teachers) in the room. They will get their social distancing by spreading out into larger rooms in closed high schools or other places (gyms, etc.), so the main class of about 30 is still in one room. Maybe not. The point is, in the worst case scenario, we divide 1,000 by 8 (hours) then again by 185 (days) to get a baseline on transmission probability (though the math is slightly more complex than that) to arrive at this conclusion: Transmission within the classroom where there are one or two virus shedding individuals on any given day is nearly inevitable if there is a low probability of airborne transmission. Most classrooms may have zero infected people most of the time, but in a given school there would be several classes. In a given school system, maybe dozens and dozens.

If the air circulation does not remove the viruses, maybe they are being spread across the school. Students passing in halls, or any classes where the kids are reshuffled add to the dynamic, families with multiple kids (or both kids and staff) in the same school, etc. add to the dynamic.

You can do a similar calculation for restaurants and bars. Regular inside dining and bar hopping even with social distancing and mask wearing is probably not recommended if there is a low level of airborne transmission. More limitations on how retail shopping happens may be recommended. Certainly, unnecessary retail shopping maybe an unnecessary danger.

The final meaning of it all: When it comes to basic day to day life, under the current conditions of caution and distancing, this airborne problem would not have that much of an effect because it has to be rare. We know it is rare (if it is real) because if it was common we would see it. But, under school or large workplace reopening conditions, or reopening of indoor dining and shopping, etc., it may be a factor that causes two really bad problems.

1) More outbreaks, and some insidious ones. The school children, some getting very sick and maybe dying, others never becoming ill, passing the disease on to their families. Ignoring the airborne problem may involve asking our children to kill their grandparents, then live with that for the rest of their lives. You might get sick because you needed to shop for a new comic book or try out the headphones at the electronic store instead of ordering on line.

2) Not discussed anywhere else as far as I know, but I would think obvious: if we set up a situation where the rare airborne transmission has a better chance of actually transmitting the disease, we may also be setting up a positive selective environment for that. In other words, we may help make SARS-CoV-2 more airborne by giving it this chance. That is pure speculation on my part, but speculation based on some damn powerful theory (Darwinian evolution). It is not a chance I’d like to take.

How The Pandemic Ends

The gold standard, the ones to beat, the top dog, brain trust magnate, 800 pound gorilla, paragon, cream of the crop, and the one head and shoulders above all others, in the matter of a Covid-19 vaccine, is Oxford.

The group at Oxford already made a Coronavirus vaccine, for MERS, but it never underwent final testing and deployment. Not enough people were getting sick from MERS, and it was under control.

This group is optimistic about having a vaccine in September of this year. Give them a month leeway, a few months for emergency intensified field testing, and some extra time to ramp up production and negotiate liability issues, and we could have a world wide vaccination program well under way by the end of January.

Between now and, say, August 15th, the medicos will have developed and deployed a half dozen nursing, ER, and IC procedures that drop the death rate of the most severely ill well below its near 90% level, to maybe half, and various treatments, therapies, and all will drop the number who go from diagnosed to severe down by a double digit percent.

Although natural herd immunity would take multiple waves and years, a certain reduction of infection rate happens at any percentage. New normal practices will have adapted to slow the disease. By mid September there will be parts of the US, and various smaller sized countries, where COVID-19 will become rare or nearly non existent, even as new hotspots emerge. But even those hotspots will be dealt with better than the US addressed this disaster in the early week.

But the flareups will be severe, and in most cases, caused by politically driven Republican strategies cheered on by Trump and sullenly overseen by Pence. The carnage will continue to be so bad, and the response to it by Trump and his gang of Republicans so inept and inextricably linked to nefarious side bets and deals, that there is a non-zero chance his administration will not still be in place on election day, November 3rd. Either way, Trump will be voted out of office on November 3rd, and probably dragged from the White House and impaled with a broom stick well before inauguration day by angry tourists and DC residents after he attempts to annul the election results. There is a non-zero chance that the 46th President of the United States will be Speaker Pelozi, for the several days between Trump and Pence’s awkward and painful departure (captured on hundreds of cell phones) and the inauguration of President Joe Biden.

There will be no Biden Inaugural Ball and his Inauguration speech will be on Zoom, But his first act will be to sign the 2021 Rapid Immunization Order, speeding up the delivery of the vaccine already developed by Oxford and manufactured everywhere but the United States even as Jared Kushner tries to get his vaccine (which is fatal to 1 in 200 who are injected with it, and does not actually protect against COVID-19) to be the legally required stick.

But I digress.

Schools will not reopen in the Fall, but by Spring it will be possible to have limited activities, as vaccination spreads faster than COVID-19 itself ever did. Kids who come from anti-Vax families will be shunned, and hate their parents forever, because they won’t be allowed to go to the 2021 proms and graduation ceremonies, which will be endlessly televised and smeared across social media until we are giddily sick of them.

By the end of 2021, the virus will be history (except in the Congo, where all diseases go to retire securely), social distancing will be a fond memory (for everyone with sensory processing disorder), and our new society, led by science and reason, will begin the process of building windmills instead of tilting at them.

Problems conceptualizing Covid

The Covid-19 pandemic is serious, scary, real, and kills. And there is a fair amount we don’t know about it.

There I said it. You don’t have to worry about me thinking Covid-19 isn’t serious. That happens to me a lot. Someone says “OMG, the COVID-19 is just like a grizzly bear eating your face off!” and I point out that a virus and a face-eating grizzly bear present distinctly different problems. Then the person gets all pissy and mad because I did not share their specific horror. Generally, I prefer it if people do not shove their fears in my face at the expense of reason. We have real fears, we don’t need to add on the ones that are bogus, unsupported, panicked, or untethered from reality.

You might say, jeezh, Greg, what harm does it do if people don’t understand every little thing about COVID-19 and, in their conceptualizing this disease, stray away from actual science and reality and stuff? Most of the time it probably does’t matter. But people make decisions on the basis of what they think they know. If you think the SARS-CoV2 virus doesn’t really live on surfaces, you won’t be careful about door knobs and push plates in heavily used public places, and you may thus contribute to the spread of this disease. If you think COVID-19 can be spread by eating food from a can, you might waste your energy, my energy, everybody’s energy, by campaigning against canned food. And so on.

So what kinds of things are people getting wrong? Here’s a sampling.

COVID-19 is caused by a virus. Most life lessons about pathogens are not transferable across types of pathogens. A coronavirus can’t be compared usefully to malaria or sleeping sickness because those are single celled eukaryotes. COVID-19 can’t be compared to bacterial infections. All these different kinds of pathogens have different effects, do different things, act in different ways, and need to be dealt with using specific actions (or avoiding specific actions).

COVID-19 is caused by a particular type of virus. There are many kinds of viruses, and the different kinds have distinctly different biologies. Comparing the behavior of SARS-CoV2, the virus that causes COVID-19, to the influenza virus, is like comparing the behavior of eels to eagles. How they reproduce inside a cell, how they avoid a body’s immune response, how much they mutate, and how a vaccine might work for each type of virus, are really very different, in fact, astonishingly different. Comparisons are not helpful at all.

Immunity is a tricky concept to understand. I wrote about it here. I think immunity (to a pathogen) is often viewed as an absolute, and as a somewhat magical thing. If I’m immune to a particular pathogen, that pathogen can not infect me, right? If I’m walking down the street, and a pathogen is coming the other way and I’m immune to it, it crosses the street to not get anywhere near me, right?

No. If I’m what we call “immune” to a pathogen, that means that the pathogen still goes inside me. It starts to do whatever that pathogen normally does in a human body. It is, in fact, infecting me. Then, because I’m “immune” a particular part of my immune system quickly responds to that pathogen’s presence, because I’ve acquired an immunity to it either by prior infection or by vaccination. Other parts of my immune system also work against a pathogen whether I was previously vaccinated or exposed or not.

The acquired immunity that comes with vaccination or prior exposure causes my body to respond more quickly. The best kind of immunity is where my body responds well within the time period where the pathogen hasn’t made me sick yet, attacks the pathogen, and kicks the crap out of it before it can do anything. I don’t get “sick” from the pathogen not because it did not infect me — it did infect me — but because the illness that pathogen typically causes never got of the ground. The natural biological course of the pathogen did not advance sufficiently to either make me feel bad or to be passed on to another person. Or, in a less ideal immunity, common with many pathogens, I do actually get somewhat sick, and maybe I can even pass the disease on, but acquired immunity makes me much less sick and much less contagious.

And as noted, a person who is “not immune” is typically a little immune anyway. That is because the immune system has several parts that try to stop a pathogen, and because the above mentioned acquired immunity is still an immunity before it is trained up in your body. It just takes longer.

The difference between a typical “non-immune” person and a typical “immune” person, as the term is usually applied, is this and only this: For the immune person, the adaptive immune system (only one part of the immune system) acts faster because it is trained by prior infection or a vaccine (which simulates a prior infection) so the body is prepared.

Indeed, a normal immune response to a pathogen is often to get sick and seem not very immune at all. Little kids get colds all the time, and they can last a long time. It seems like from a certain young age until a few years later, still at a young age, a kid is sick all the time. Adults go around bragging about how they haven’t lost a day of work in 20 years. (Not all adults, but some.) This is largely because kids don’t have a very strong immunity to the handful of different viruses that give us regular colds. But over time, a human will typically develop a stronger and stronger immunity. All these humans are immune to those viruses to some degree, just not perfectly and totally immune.

With COVID-19, we hear stories of “reinfection” and this has led many people to believe that humans do not develop an immunity. The numbers of possible re-infections is very very small compared to the number of people infected, and it is highly likely that those instances are bad reports, or individuals who never really got rid of the disease to begin with. Of the remaining, much smaller number of individuals, re-infections may have happened because that person’s immune system just didn’t produce a strong immunity in that person. A very small number of possible re-infections is expected for any disease and isn’t alarming.

Usually, an exposure to a pathogen that we can develop an immunity to results in an immunity that lasts for a while. Usually, years.Sometimes enough years that it seems like a life long immunity, or close to it. In other cases, you get a modest immunity that gets better with more exposure. Remember, SARS-CoV2 is a particular virus, and should not be compared willy nilly to other viruses. HIV gets around the human immune system, but it is a very different virus. Not a valid comparison at all.

Sometimes our immunity does not help us much with a later infection, or so it seems. You get a Yellow Fever shot and later they tell you you need another one. Or, the flu shot from last year isn’t helpful this year. This might be a linguistic matter. We call the pathogen by a certain name, but underlying that name is a wide range of different species or strains of that pathogen. We use the word “flu” for “influenza” but there are many different major types of influenza. If influenza was a “canid” then there would be foxes, wolves, coyotes, and domestic dogs. All in the same family but not really the same.

Alternatively, later infection could be the result of a particular strain mutating enough to side step our immunity, somewhat. Or, it could be that our immunity wore off.

A common misconception about mutations is that they make a pathogen worse. Well, they can, but they usually don’t. We hear “COVID has had 29 mutations! Aieeeee!!!” I assure you that SARS-CoV2 has had many many more mutations than that. If you get COVID-19, the SARS-CoV2 inside you probably mutates hundreds or thousands of times as it replicates using your cellular machinery, as viruses do. But, the vast majority of mutations cause a viral strain to become broken, or to not change at all. A small number may make the virus a little better at what it does, or a little less good at what it does. From our point of view as the host of the virus, a small number of mutations might make it harder to pass it on, or easier to pass it on, or liable to make a person a little more sick or a little less sick. That any one of these mutations occurs in your body does not mean that that mutation will now be part of the general population of SARS-CoV2 viruses. The vast majority of mutations that both happen in an infected individual and that do not produce a dead-end variant will not be passed on to the next person. You will just sneeze them out and they will be killed by ultraviolet light, hand sanitizer, or the main thing that kills most individual virus particles: Time.

We hear a lot now about rare and scary things. Twenty-three year olds dropping dead of a stroke, or other odd blood clotting things, and so on. Those may be real or they may not be real. If tens of millions of people get a disease, there will be situations where a cluster of individuals were going to also have some other thing happen to them medically, and they happen to have this thing occur while they have COVID-19. Coincidence. Or, a disease like this might really have some other effect that is very rare, but that thing is, well, very rare. After the discovery of some possible odd effects on blood clotting, people started to say things like “it kills young people in this strange way and we didn’t know it until now! Aieeeee!!!!” but at the same time, the death-over-age statistics did not change. We did not find 300,000 dead 23 year olds. The strange new thing remained rare, and enigmatic. Important, interesting, something we must find out about. But still very rare.

I’ll end here with a dirty little secret of the immune system: Of all the different biological systems that make up the typical animal (including humans) it is with the immune system that the gap between all that can be known and what we confidently know is largest and deepest. We know a lot, but we also don’t know a lot. And, it is so damn complicated that it is impossible to expect the average non-expert to not make the sorts of mistakes mentioned above. I can add this: I’m heavily revising what I cover in my course on the immune system, to help future generations of pandemic victims have an easier time parsing what is happening around them. Assuming I can get back into a classroom with them!

How To Think About Immunity to COVID-19

This is what immunity is not: You are an organism walking down the street, and you are immune to the rare virus squirrelpox. A squirrelpox virus is walking on the same sidewalk towards you. It sees you, and goes, “that one’s immune to me,” and quickly crosses the street, going nowhere near you. Beause you are immune.

This is what immunity often is: You have built up an immunity to a common cold virus. Somebody infected with that virus sneezes on you and now that virus is in you. It begins to reproduce and do its thing, and you develop cold symptoms. However, your adaptive immune system has seen this virus before, so it quickly mounts a defense, so even though you do get a cold, you fight it off quickly and in five days you feel fine.

Lots of times, though, immunity works like this: You have an immunity to a certain disease. Perhaps you had that disease earlier in your life and your adaptive immune system developed a strategy to attack this pathogen next time it comes around. Perhaps you got a vaccine that prompted your adaptive immune system to develop a strategy to attack this pathogen next time it comes around. The virus goes in you — the virus does in fact infect you, it does not “cross the street” to avoid you. But your body is so ready for it that the counter attack is fast and effective, and before you can either develop symptoms or start passing the disease on to someone else, your body’s immune system has literally killed it.

An acquired or induced immunity can be called “100%” and it can be “life long” but it is never able to actually keep the disease out, and it is likely that few, if any, adaptive immune system build-ups last for the entire life of a person who lives a long time. Some immunity does not stop you from getting sick but does cause you to get better faster, and some immunity doesn’t last that long.

Much of the misunderstanding about immunity comes from the fact that our understanding of immunity comes from two distinct diseases: Polio and influenza. Polio vaccine is famous because its invention and deployment was historic and significant. Polio vaccine confers a strong immunity, one that is seen as life long and complete. Even this is not so simple, but if you believe what I just said about polio vaccination and immunity you would be in the ballpark. Influenza immunity is often discussed because it is at the center of the anti-vax debate, everyone gets the flu now and then (or so it seems) and the so-called “flu vaccine” is supposedly only “60% effective” or thereabouts, and thus, being imperfect, is the focus of rage on the internet as though it was a candidate for office.

If polio is an outlaw gunslinger in the old west, and the polio vaccine is Marshal Dillon, then influenza is all the underground crime organizations imagined in fiction and the flu vaccine is a competent but underfunded police agency.

When we say that the influenza vaccine is 50% effective in a give year in the US, as an example, what that can mean is that there are five kinds of flu circulating at various proportions in the population, and there are three kinds of vaccine in the shot you get; maybe two of those vaccines are nearly 100% effective in immunizing a person against two of the circulating influenza viruses, one of the viruses is untouched by the vaccine but doesn’t get you that sick, and one of the vaccines is for a virus that never really showed up, and the leftover viruses are the ones doing most of the damage. Or something along those lines. The outcome is, across the population, that the average vaccinated person in the population under consideration would have their chance of getting the flu if exposed is half what it would have been were they not vaccinated. So, 50% effective that year. Some other year these parameters may be very different, and the “vaccine” (a mix of different vaccines in one shot) is different. And, each vaccine may itself have a higher or lower level of effectiveness.

And that is the simple version of the story.

Immunity is not a folk concept. It is a medical concept. The fact that many people believe that immunity is the inability of a disease to affect a person, which is 100% wrong in every way, is not relevant to anything but people’s misunderstanding of the concept.

When we hear that there is a certain possible reinfection rate of COVID-19 in China or Japan, this does not mean that people don’t get immunity once they have the disease, or that COVID-19 has special powers. One health expert misstated that since we don’t know for sure what acquired immunity to COVID-19 looks like, we can’t assume that it is long term. That is balderdash. It is very likely long term (if “long” is years) because that is what normally happens. This statement is like looking at the first new car off the line of a new make and model and saying, “since we’ve never actually seen one of the drive, we have to assume there is a good chance none of these cars will work.” There may be a few recalls in the future of this make and model car, but it will work.

We can assume normalcy, we can assume biology to do what biology does. Bill O’Reilly does not know how tides work, but someone else does. Normally, adaptive immunity occurs, and lasts for a good time. Normally, immunity to certain kinds of viruses can be less than 100%, so there is some getting sick, and normally, a subset of people don’t develop much of an immunity because their own immune system simply fails at that task. COVID-19 will ultimately be found to match normal biological expectations, though we don’t know the details yet, and we won’t for some time. The fact that normal biological expectations do not form the basis of folk thinking about this disease, or pathogens and immunity in general, does not make Covid-19 a preternatural force, or an unknowable thing.

Still, remain hiding in your house until the all clear.

There is another level of thinking about immunity that I won’t go into detail about right now, but I’ll mention. We often, rightly, think of immunity at the population level, even though it does, truly, work at the individual and molecular level. Assume a particular vaccine, or exposure, typically provides ~100%) immunity in individuals. If 10% of the population have that immunity at the start, the disease will act like nobody is immune, as far as we’d be able to see. Often, natural (genetic?) immunity at low levels exist in a population, and can only be discovered by intensive research over a long time. If, on the other hand, 90% of the people in a population are ~100% immune, the disease may be so unable to get a foothold that it is like it isn’t there. The point is, the appearance of a diseases behavior seems to range from 0% (there ain’t none) to 100% (it’s everywhere!) on the surface, but this outcome is a function of a much smaller range of actual immunity values, like the 10-90% just noted, or more likely, closer to 0-70%. Putting this another way, a population gets very close to “immune” at the population level as the proportion of individuals who can’t get and pass on the pathogen rises over about half. This is called herd immunity. It will take several cycles of COVID-19 infection to achieve natural herd immunity, most likely, unless a vaccine is found. But once that happens, the disease is likely to stay around at low levels then occasionally come back and be menacing, but not as bad as it is now, on occasion.

So, let’s get that vaccine going!

The Complete Scientific Guide to COVID-19

… will be written in about three years from now. Meanwhile …

We labor under a number of falsehoods about how science works. Even scientists do. There are considerable differences among the panoply of scientific disciplines, and these are important enough that I would never trust the practitioners of one scientific discipline to, say, review research procedures or grant proposals from another discipline, by default.

These differences are even more significant outside of science itself. A common example is this one. A lay person evaluating peer reviewed research claims that a certain scientific conclusion can not be supported because there have been no double blind studies. That person may be unaware of the fact that almost no science uses double blind studies. This is a methodology used only in some areas of research. A study of earthquake hazards, genetic phylogeny of chickadees, or how long a particular virus lingers on a surface will not have a double blind methodology.

In some fields of study, a single idea will often be represented by a single major publication (sometimes a book) and will not be seen elsewhere unless it is being criticized. This is not common in the true sciences, per se, but this does happen in the peer reviewed literature. In other fields of study, a single idea may be addressed in hundreds of peer reviewed papers. In some fields of study, if a published peer reviewed paper presents a conclusion that is thought to be wrong, because of some flaw, the scholars in that field are expected to learn of this problem and thereafter avoid citing that paper. In other fields, when this happens, the paper is withdrawn from the literature after the invocation of complex rituals that might or might not involve the sounding of trumpets.

There seems to be two falsehoods affecting some of our thinking about COVID-19. One is the idea that a “study” or “publication” about some detail of the disease tells us something that we can take as fact. Yes, Covid-19 stays on a certain kind of surface for N days, therefore we can’t do X! That sort of thing. However, this research is, firstly, not peer reviewed. There may very well be no peer reviewed papers on COVID-19 at this time. This Pandemic has lasted less time that the typical peer review process takes. Maybe there are a few out there, but mostly, we are dealing with non-reviewed work, or work in review. This is good work, and important work, but it is more like a set of “emergency results” that address specific pressing questions in a provisional way.

It has been important to decide which of a small number of broad categories COVID-19 can be placed in, and the work on persistence on various surfaces has provided that rough and ready guide. There are pathogens that can find their way out of an exam room, go 20 feet down the hall, and infect a person sitting in a different exam room. There are pathogens that are so unlikely to infect another person that you practically have to lick the inside of their mouth five times to catch the disease. COVID-19 is in the in between category, where it sheds into the air and hangs around on surfaces for long enough that surfaces are found to have the virus on them. Is COVID-19 more or less surface-contaminating than, say, norovirus? Rotavirus? Nobody knows, because the research to determine that, and the publication array that would be necessary to lead to policy and recommendations about that, will take time. Someday there will be a study that looks at how much of the virus persists for how long on various surfaces, integrated with the other important question of how can the virus on a given surface actually infect a human, in order to allow for a realistic and useful statement about how to go about keeping a home, and ICU, an examining room, or a school relatively safe. COVID-19 has the potential to be the most studied pathogen in recent history, but not today.

So, that is the first fallacy: that a handful of quick and dirty, rough and ready, studies designed to get a clue about this disease constitute a well tempered and developed peer reviewed literature from which we can glean an accurate characterization of most o fhte important details of this disease. Nope.

One cost of this fallacy is the second fallacy, that we can evaluate models of either COVID-19’s behavior, or the efficacy of our reaction to it, based on a solid knowledge of the disease. That is backwards. We will eventually be able to evaluate ideas like “curve flattening” by understanding a lot about COVID-19, but that will happen after we have actually seen what various curve flattening efforts have done. A recent proposal that certain areas of the world may have seen a prior passage of COVID-19, causing some local immunity. One well meaning expert (not an actual expert) on social media responded that given the way COVID-19 operates, this is simply impossible. But that is backwards. The way we will eventually be able to describe how COVID-19 actually works is by observing it, measuring it, developing good explanations for what we see, strengthening and tempering those explanations by further hypothesis testing, replication, critique in the formal peer review process as well as the less formal but sometimes more important conversations at the conference-bar setting, and time. Time to just think. Then, we will be able to say things like “X is pretty much impossible because this is how COVID-19 works.” Now, we have an expansive void where some good theory and data will eventually reside, and the job of the scientists focused on this problem is to carefully and thoughtfully fill that void with what they come to know. To get a sense of how this works, read up on the literature that came out of the 2013 Ebola epidemic. Many key known things about the pathogen and its effects were not nailed down until months or years after the last patient was identified. These things take time.

I’m not an epidemiologist, but I play one in the classroom. Amanda and I teach a class on the immune system and epidemiology. Had I not gone into palaeoanthropology, I might have gone into this field. Excellent books on the topic include The Coming Plague: Newly Emerging Diseases in a World Out of Balance by Laurie Garrett (not current but mind-changing and foundational, includes some important forgotten history), Epidemics and Society: From the Black Death to the Present (Open Yale Courses) by Frank Snowden, and for a good textbook, Gordis Epidemiology.