Back to Work? Not so Fast!

For brief descriptions of and links to recent posts, click here. For an inverse-chronological list with links to all posts after January 23, 2017, click here. For a subject-matter index to posts before that date, click here.

For discussion of the fact, and its consequences, that viruses are not alive, click here. For the principal post, click here.

Improvised PPE

The economic pundit Farhad Manjoo has described the cascade of interlocking blunders and stupidities that made the richest country in the world unable to fight a pandemic for want of 75-cent masks. He aptly terms these fiascos “capitalist pathologies”—the relentless search for lowest cost and higher profit, no matter what the item is, or how vital it might be in a pandemic like the present one. It will be weeks, maybe months, before we Americans undo the stupidity of letting China make 80% of the world’s masks and Malaysia most of our medical gloves. In the meantime, maybe we can do what Americans are supposed to do best: improvise in times of need. Here are some ideas how similar products created for distinct purposes might be recruited to serve our first-line medical defenders as personal protective equipment (PPE) in this pandemic war: 1. Non-“Medical” Gloves. There are gloves and there are gloves. They come in latex, vinyl and nitrile. I use a lot in my work around the garden and house, to protect myself from harsh chemicals, paint, stain, glue and occasionally possible pathogens in disposing of dead mice (hantavirus) or bats (rabies). The ones I buy seem indistinguishable from the medical ones but are about $2 cheaper per box of 100 pairs. Their makers mark them conspicuously with the words “NOT STERILE,” and they’re probably excluded from hospitals’ procurement lists for that reason. But put them on, do the normal hand-washing routine and/or swab them with disinfectants, and voilà! You have a sterile pair of gloves. Probably no one produces these hobbyists’ gloves in anywhere near the same volume as medical gloves, but they could at least provide a supplementary supply while we ramp up production. All that’s needed is a little flexibility in procurement. 2. Face shields. Many, if not most, machinists and shop workers wear face shields to protect themselves from flying bits of material and broken tools in their shops. I have one in my home workshop. By and large, machinists’ face shields are bigger, heavier and more robust than those worn by health-care workers. But they are strong enough to be repeatedly washed and sterilized, perhaps even autoclaved. With machine shops all across American locked down due to the pandemic, why not collect both new and used machinists’ face shields and put them on health-care providers? These face shields are mostly open, not closed like some of the medical-workers shields. But together with masks and gowns with hoods, they could provide substantial protection against the projectile force of coughs and sneezes from patients in close proximity. The same probably holds true for diving masks and goggles, perhaps even with snorkels whose open ends are stuffed with cotton or gauze for protected breathing. 3. Impermeable gowns from thunderstorm “parkas.” Hikers and outdoor folk are familiar with plastic “parkas” that you can buy for a couple of bucks in stores like REI. They come in small plastic pouches that can fit in pockets, but they fold out into a complete knee-length waterproof parka with hoodie. The idea is to provide quick, cheap emergency protection from getting saturated by a thunderstorm. With a face shield and mask, or with goggles and a cotton-or-gauze-stuffed snorkel, this cheap and simple device could provide significant protection for front-line medical workers facing seriously sick patients. Their only obvious drawback is that most of their sleeves are short, so these plastic parkas would have to be supplemented with normal hospital gowns having full-length sleeves. * * * The word “scandal” is far too weak a word to describe the cascade of criminal negligence in our government that left our health-care heroes so vulnerable to a pandemic that everyone knew was coming someday. But now is not the time for blame and recrimination. It’s the time to pull out all the stops to protect the people who protect us. If I had a loved one on the front lines of this pandemic, I know I would be buying, begging, borrowing, stealing and improvising whatever PPE I could, making whatever mods and improvements I could, and putting it in his or her hands before work every day. And if I were a hospital administrator watching improvised PPE in action, I would wink and smile and be glad that health-care providers were protecting our most precious resource: themselves.

The principal post follows:

Is our president’s mouth an instrument of mass destruction? It certainly seems so.

In the last few weeks, he has discouraged crash programs to make more tests, masks, ventilators and personal protective equipment (PPE) by saying or implying that we already have plenty available. Just in the last fews days, he caused a run on the malaria drug chloroquine by suggesting that it might cure Covid-19. Not only did that run deprive people of the drug who really need it for malaria; it also inducing at least one true believer to kill himself with it. Meanwhile, there is absolutely no scientific evidence that chloroquine works for Covid-19.

The president’s recent suggestion that nonessential workers begin to go back to work in two or three weeks could have a much wider and more devastating effect. There is absolutely no evidence that their doing so would help people or lower the sickness and death rate, and no expert in the field is recommending that course of action.

On the contrary, going back to nonessential work in numbers would have all the terrible effects that competent epidemiologists have been valiantly trying to avoid in “flattening the curve.” It would explode the ranks of sick people, including those seriously ill. It would rapidly exhaust our dwindling supplies of tests, masks, PPE, hospital beds, ICU beds and ventilators. In so doing, it would put our health-care providers at risk, get more of them sick, and reduce our capacity to deal with the spike in cases it would cause, not to mention any second wave or possible follow-on pandemic.

In other words, the president’s “back to work” suggestion is precisely the wrong advice. It would countermand the social distancing and lockdowns now in place, replacing them with nothing but hope and a prayer. Most of all, it would elevate profit over people, putting at risk the people (aka “workers”) who produce the profit, not to mention those who are trying valiantly to keep them healthy.

It’s possible—although not likely—that we could be ready to start putting nonessential workers back to work in a few months. But a lot of things would have to fall into place before that would be a good idea. We would have to develop a new kind of test, different from the one being used now to tell whether people are infected. We would have to develop antibody tests. Here’s the theory.

That vast majority of people who catch Covid-19 will recover. Once they have recovered fully, chances are good that they will be: (1) immune to further sickness from the same virus and (2) no longer carriers. Once properly identified, recovered nonessential workers could go back to work without endangering themselves or others, as least insofar as concerns Covid-19.

The problem is, we don’t yet know precisely how this theory works in practice for Covid-19. We don’t know how strong is the immunity in recovered patients, or whether it varies with the patient and the severity of the sickness overcome. We don’t know how long it lasts. And we don’t know at what point they are no longer carriers of the virus. There is some evidence that recovering patients can be infectious for longer than the now-presumed quarantine period, i.e., fourteen days.

Enter the antibody test. When a person’s immune system overcomes an infectious disease, it does so in part by producing antibodies to the infectious agent. The antibodies circulate in the patient’s blood. Generally speaking, the more antibodies there are, i.e., the higher their chemical concentration in the blood, the better the immune response. So the first step in being able to tell whether recovered patients are (1) immune and (2) no longer carriers involves being able to measure the levels of antibodies to SARS-CoV-2 (the Covid-19 virus) in their blood.

Blood tests for this purpose are separate and distinct from the nasal-swab tests that detect active viruses in a patient’s airways. Antibody tests cannot be used to detect initial infection because it takes time for patients to develop and multiply antibodies. For example, flu vaccinations require from 14 to 20 days to produce enough of an antibody response in those vaccinated to confer a reliable level of immunity. But once patients have developed their own antibodies after recovering from infection, they can be as if vaccinated, i.e., both immune and “clean.”

Unfortunately, I have not seen any public report that we have such antibody tests, or that anyone is now working on them. The virus is too new. Anyway, at this initial stage of the pandemic, the focus must be on identifying people who have been infected but who have not had a chance to develop antibodies. Hence the active-virus nose swabs. But work on antibody tests should begin forthwith, and Congress should appropriate money for their research and development now.

That work will have to answer a lot of questions. What kinds of antibodies do recovered patients produce, and how much immunity do they confer? (There may be several kinds of antibodies, which target various portions of the SARS-CoV-2 virus’ biochemistry.) Can you tell whether a person is immune and not a carrier from the type and levels of antibodies in his or her blood? How long does the immunity last, and is it correlated with blood antibody levels?

Only when we’ve answered those questions, and only if the answers are promising, can we know how to identify people who’ve recovered, are immune, and are no longer carriers. Then we can send them back to non-essential work, confident that we are not endangering them, their families, health-care workers, or others.

Not only that. Once recovered patients had been “cleared” by antibody testing, they could be trained to replace health-care workers who had fallen ill, at least those not requiring extensive education. Having natural immunity, the recovered patients wouldn’t even require PPE; they could just take very thorough showers at the end of each work day to avoid infecting their families and others.

With a little clever science and chemical engineering—and a little luck—antibody tests can be made simple and cheap. Because antibodies populate blood at relatively high levels, tests for them are not nearly as complex and expensive as the tests for active viruses in the nose, which rely on sequencing whole or partial RNA strands. Some antibody tests can be as simple as an over-the-counter kit that lets a patient prick his finger, put some blood on a reagent stick, and watch for a change in color.

But a whole lot of research and study has to precede the happy day when such tests are available, over the counter, by the millions in drug stores nationwide. So shouldn’t we get started now?

Viruses are Not Alive

SARS-CoV-2 is the virus that causes Covid-19, our current pandemic. As I talk with friends and family and read news articles about it, I find a repeated misconception. Neither SARS-CoV-2 nor any other virus is alive. That simple fact makes the viruses both more and less fearsome than bacteria, amoebae, and other protozoa, which are alive, and which also can cause disease.

(Sometimes you will hear lay people or even doctors speak of “live viruses” or “killed virus vaccines.” But that terminology is a holdover from the past, when truly live microorganisms were the principal focus of infectious medicine. Human language develops by analogy and becomes more precise only with time.)

High-school biology teaches the seven signs of “life.” Three of them are respiration (breathing), alimentation (feeding) and locomotion (moving). Viruses don’t do any of these things. Unlike bacteria, they have no “organelles,” or microscopic organs, capable of processing oxygen or food, and no appendages or other organs capable of moving.

Viruses are simple biochemical structures that must physically contact a target cell, more or less by accident, in order to infect it. Their receptors (the red structures in the ubiquitous electron micrographs of SARS-CoV-2) must contact a cell surface with the requisite biochemical structure. When they do, the receptors force their way into the cell and insert the viral DNA or RNA messengers, which then force the cell’s own DNA or RNA to reproduce more of the virus. (With SARS-CoV-2, the inserted stuff is RNA.)

The whole process is a delicate chemical takeover, which can be stopped at any of its three stages. But the virus doesn’t “eat” the cell in any recognizable way. It commandeers the cell’s own reproductive machinery by a simple biochemical process and causes the cell to make thousands of copies of the virus itself.

In this way, viruses are like minute “zombies.” They’re not alive and not dead. Yet they can make us sick and even kill us. But unlike Hollywood zombies, viruses are real. They are even more more fearsome because we can’t even see them without expensive scientific equipment.

You can think of a coronavirus as a tiny landmine, with its protruding red receptors as its “triggers.” What the receptors trigger is not an explosion, but a delicate and precise biochemical forced entry into the cell and a takeover of its reproductive machinery.

For us humans who suffer from viral diseases, these facts have both good news and bad news. The good news is that viruses don’t move on their own. They can’t crawl up your arm or even your nose. They don’t have any means of doing so.

In fact, SARS-CoV-2 has a tough time getting up your nose to where it can do damage. It must avoid somehow getting stuck in your mucus and expelled by a cough, sneeze or even heavy breathing. It must evade your tiny cilia (minute hairs) that are constantly in motion, expelling foreign particles from your airways. Then it must contact a fresh, vulnerable cell capsule and begin to do its dirty work.

That’s why masks are helpful, both to protect you and others (from your coughs and sneezes). That’s why netipots and saline-solution squeeze bottles might help avoid infection, by washing away the viruses before they can get a foothold. That’s why smoking lowers your protection; it slows or stops the cilia that are otherwise constantly expelling foreign matter from your airways. That’s why coughing and sneezing can (at the very early stages) help you avoid infection while, at the same time, increasing the risk to others around you. That’s why our bodies evolved the ability to cough and sneeze in the first place.

The downside of these facts is that viruses are hard to “kill.” They have no heart, stomach or vital organs to target. They don’t need food or air. To “kill” them—i.e., render them non-infectious—you have to cap or remove their receptors, burst their capsules and take the virus appart, or somehow destroy or disable their patiently waiting interior reproductive machinery. That’s what medicines and the antibodies that vaccines trigger try to do.

So when scientists tell you that SARS-CoV-2 can remain active and dangerous on hard surfaces such as plastic and metal for up to nine days, you should pay attention. They don’t “live” there. They just exist. As long as they maintain their original form and can be detached from the surface, they remain infectious if you should, for example, pick them up on a finger and insert that finger in your nose. So it’s best to wash possibly infected surfaces with soap and water, which can also disrupt the viral capsules, or to destroy their receptors and maybe disrupt their capsules with things like household disinfectants and ultraviolet light, including strong, direct sunlight.

Now that viruses have established themselves in our biosphere, they will probably be with us as long as our species survives. They have co-evolved with us and with our fellow creatures. The only way they increase their numbers and geographical scope is by infecting us and other similar organisms.

But viral evolution has some interesting and hopeful twists. Like all evolution, it proceeds by mutation and the natural selection that follows mutation.

Suppose that a virus mutated to cause violent convulsions in its victims and kill them in as little as five minutes. It wouldn’t spread very far, would it? Even primitive human societies would have shunned, burned, and buried the victims’ bodies as riven by “evil spirits.” Today, all remains would be quickly cremated or carefully sequestered as medical waste. Unable to move and “chase” its victims, the virus would probably find no further hosts after its first dozen or so victims had been disposed of.

The most “successful” viruses, from an evolutionary point of view, are those that spread far and wide by making their hosts sick but not killing them. As long as hosts are well enough to stay out of bed and out of the hospital, and to spread the viruses by sneezing or coughing on others, the virus can expand its human and geographical reach. High mortality is therefore a negative adaptation for viruses; that’s why non-lethal viruses such as the “common cold” have some 250 variant strains.

So we can expect our war with viruses to continue for a long, long time. With each new mutation, our bodies must adapt by getting sick and getting well, thereby “training” our immune systems to fight the new threat. Medical science must develop new medicines to cap or remove the new viral receptors, destroy the capsule or defeat the internal reproductive machinery. We must develop new vaccines to train our immune systems to fight the new virus before we feel sick.

Some day, we may have cheap and simple masks, or even nose inserts, that can filter out viruses at the nanoparticle level. Some day we may automate the tedious processes of developing medicines and vaccines and testing them for safety and effectiveness. Some day, we may find a universal or near-universal antibody for most or all or our respiratory viruses.

But in the meantime, our exploding global population, densely packed cities, and even more densely packed modes of transportation (including elevators), provide fertile ground for even the wimpiest viruses to infect us and spread among us by means of our own social movement, and then to mutate and spread some more.

That’s why isolation, keeping our distance, wearing masks, not touching our faces, washing our hands, washing our faces, cleaning possibly infected surfaces, irrigating our noses and sinuses, quitting smoking, and changing our social behavior during epidemics will be with us as far forward as anyone can see.

Asian cultures, which have long dealt with greater human density, are ahead of us Westerners in this regard. It has been customary in Asia for people not feeling well to protect others by wearing masks when in public, at least since the mid-eighties when I first visited Japan.

As viruses proliferate and take advantage of greater human density and more frequent travel, the rest of the world is going to have to catch up with Asia in simple precautions and mechanical means of control, as well as in making social changes in times of epidemics. The days of supposed isolation of man from man are gone even in the “Wild West,” when a cowboy in Montana might have gotten off a plane from Paris or Beijing only a day or two ago.

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