Category: pandemic

Why we shouldn’t be worried (yet) about the new strain of Covid-19

December 23, 2020 • 10:30 am

Reader Jim Batterson sent me this 25-minute video with the comment:

I know you prefer to read rather than watch a video, but I wanted to make you aware of a 24-minute YouTube video from Vince Racaniello, a virologist at Columbia University who leads a cast of virology geezers and one younger immunologist in a weekly zoomcast production of “This Week in Virology”.  He did this standalone presentation to rant a bit on the way that this latest variant in the UK is being hyped to the world. I think he does a pretty good job for any viewer who has had a biology course in the past five or so years.
The point is that viruses are mutating constantly, and yet none the coronavirus mutations have yielded a new “strain”—that is, a mutant type that has new biological properties. The property touted for the new virus is its purportedly increased “spreadability”, but, as Racaniello notes repeatedly, that simply hasn’t been demonstrated. As he shows, you can get some variants spreading more widely than others simply by accident: the variant may not have any effect on spreadability itself but can increase in frequency as a byproduct of “superspreader events”—the main way the virus spreads—because only a small subset of all viruses get passed to other humans.

Racaniello then shows the changes in the new mutant “strain”, noting that only one of the several mutants in the spike protein is even a candidate for a change in spreadability, but there is not an iota of evidence that any of those mutations actually make the strain more spreadable.  Nevertheless, all of us are inundated with media scare stories about this “superspreader virus”.

Racaniello’s point is that though there are epidemiological data showing a correlation between the presence of the mutant in some areas and a greater spread of the virus, that’s just  a correlation without evidence of causation. And there could be several causes, including accidents. To show this mutant is a “super virus”, you simply have to do lab experiments; epidemiological correlations show nothing.

Racaniello doesn’t rule out that this mutant spreads faster than its ancestors, but he’s not convinced it is, and doesn’t think that we yet have a reason to be concerned. In fact, he suggests that the changes in the new strain may make it less spreadable. Let me add that Racaniello knows what he’s talking about, as he’s co-author on a well known textbook of virology.

Like all good scientists, Racaniello isn’t declaring that this virus is “neutral” compared to its competitors—he’s simply saying that we don’t have any data suggesting it’s more nefarious. In fact, the same story happened earlier with a different mutant that spread widely, but nothing ever came of that.  We need experimental cell-culture data from the lab on viral shedding, and that doesn’t exist.

His final comment:

“We should move on from the scary headlines, and get ahead with vaccination programs, which are underway—and that is going to be the way we get away from this pandemic.”

Anyway, this is a good and clear mini-lecture, and listening to it should calm you down a bit if the media have gotten you worried.

Dr. Lickerman on the Moderna vaccine

December 22, 2020 • 10:30 am

My GP has written another post on vaccines, this time on the new Moderna vaccine, which has just been approved by the FDA.  Click on the screenshot to read it, or you’ll likely be satisfied with the conclusions and unanswered questions below, which were remarkably similar to his take on the Pfizer vaccine.

That’s because, except for a difference in storage conditions (the Moderna vaccine requires far less cold than does the Pfizer one), the trials show both are about equally effective (94.1% for Pfizer, 95% for Moderna, which are probably not statistically significant. Both are also mRNA vaccines that inject the code for making part of the virus’s spike protein into the body, where part of the protein is made, activating antiviral antibodies, and then the mRNA is degraded. (See below for an article about how these vaccines work.) There’s a slightly higher incidents of side effects with the Moderna vaccine as well: muscle pain and joint pain after the jabs are about 20% higher for Moderna’s vaccine (an incidence of around 40%) than for Pfizer’s (incidence about 20%). But these aren’t severe side effects.

The Pfizer vaccine was tested on individuals older than 16, while Moderna’s on individuals older than 18, so efficacy in that two-year age range remains an unanswered question for Moderna.

Finally, the two doses of Moderna’s vaccine were spaced 28 days apart rather than Pfizer’s 21, but this may not be important since there seems to be a leeway of a few days. Consult your doctor.

The overall take (these quoted from the post):

  1. The vaccine is highly effective in preventing symptomatic COVID-19 infection.
  2. The vaccine is safe. Adverse reactions, both local and systemic, are mostly minor. Though the study hasn’t yet gone on long enough to prove there are no serious long-term adverse affects, such adverse affects, if they exist, are likely to be rare and non-life-threatening based on other Phase I and II studies of other RNA vaccines.
  3. We recommend everyone who is eligible to receive the vaccine should receive it when it becomes available to them.
  4. It very well may take all of 2021 to get everyone who’s willing to be vaccinated to receive the shots, which means it likely won’t be until early 2022 that life returns to pre-pandemic normal. In the meantime, continue to wear a mask when indoors with anyone you don’t live with, wash your hands frequently, and refrain from dining indoors at restaurants.

And the unanswered questions:

  1. While suggested by the study, still left unproven is whether BNT162b2 prevents severe COVID-19 infection, whether it prevents COVID-19 infection after just one dose, and whether it prevents COVID-19 infection in subjects who’ve already had COVID-19.
  2. The study didn’t look to see if the vaccine prevents asymptomatic infection. Nor did it assess whether subjects who developed COVID-19 despite vaccination are less likely to transmit the virus. Thus, it’s not yet clear how effective the vaccine will be in containing the spread of the infection.
  3. The study hasn’t gone on long enough to tell if subjects who were vaccinated yet still contracted COVID-19 have a lower risk of long-term effects of COVID-19.
  4. We don’t yet know if the vaccine reduces the risk of dying from COVID-19.
  5. There was insufficient data to draw conclusions about safety and efficacy of the vaccine in children younger than 18, pregnant or lactating women, and patients who are immunocompromised.
  6. We don’t yet know how long immunity lasts and whether or not booster shots will be necessary.

As far as which one you should take, I think Alex’s recommendation would be to take whichever one is offered to you. The news last night said that big pharmacies like CVS may well stock both types, in which case you should consult your doctor.

Here’s a new NYT article by Jonathan Corum and Carl Zimmer about how Moderna’s vaccine works (click on the screenshot; I think the article is free for all). It’s a comic-book-like series of graphics which are very good, and I’ve put a summary at the bottom.

You’ll have to click on the screenshot below, perhaps twice, if you want the whole story in one place.

Guest post: The New Yorker suggests that “other ways of knowing” can cure Covid-19

December 17, 2020 • 9:15 am

A few years ago I got an email from a colleague who was disturbed about the anti-science attitudes of the New Yorker, which include an emphasis on “other ways of knowing” —often through the arts and literature. But first I’ll repeat my colleague’s analysis:

The New Yorker is fine with science that either serves a literary purpose (doctors’ portraits of interesting patients) or a political purpose (environmental writing with its implicit critique of modern technology and capitalism). But the subtext of most of its coverage (there are exceptions) is that scientists are just a self-interested tribe with their own narrative and no claim to finding the truth, and that science must concede the supremacy of literary culture when it comes to anything human, and never try to submit human affairs to quantification or consilience with biology. Because the magazine is undoubtedly sophisticated in its writing and editing they don’t flaunt their postmodernism or their literary-intellectual proprietariness, but once you notice it you can make sense of a lot of their material.

. . . Obviously there are exceptions – Atul Gawande is consistently superb – but as soon as you notice it, their guild war on behalf of cultural critics and literary intellectuals against scientists, technologists, and analytic scholars becomes apparent.

Today’s topic, though, is “other ways of knowing through folk wisdom“. In particular: ways of healing used by indigenous people. Now this shouldn’t be rejected out of hand; after all, many modern remedies, like quinine, derive from plants used by locals. But that doesn’t imply a wholesale endorsement of “the collective lived experience” touted in this video about plant-based healing. For the “collective lived experience”, after all, sometimes includes shamanism and, in the example below, “spiritual elements” as a way of curing disease. And here the disease that “lived experience” tackles is something the Siekipai of Ecuador have never experienced: Covid-19.

Reader Jeff Gawthorpe saw a New Yorker video at the link below; I’m not sure whether you’ll have free access, but you will using the yahoo! finance link at the bottom, where the video was republished.

Jeff is about as distressed as I by the fulminating wokeness of the magazine and delivered his critical “review” of the video, which I asked if I could put up in full, including his name. (I don’t like paraphrasing other people’s words, especially when they’re as good as the analysis below). Jeff said that was fine, and so here is his take, indented. I have to say that I agree with it, and have a few comments of my own at the bottom.

Around 30 minutes ago I happened across a dreadful video on the New Yorker‘s website, which drove my temptation to meet head with keyboard through the roof. This piece of ‘journalism’ was entitled: “Fighting COVID-19 with Ancestral Wisdom in the Amazon”. And yes, It’s as bad as it sounds: unscientific, irresponsible nonsense. Complete tosh.

The message which the piece attempts to convey is that COVID-19 can be dealt with by ‘lived experience’, ancient ‘ways of knowing’, and a few bits of boiled tree bark. Then, if you hadn’t had enough already, Just before the end, a caption pops up saying: “With a new stock of plants, the Siekopai are prepared to address future outbreaks of the virus according to their traditions.” Urrrhhgg.

You’ll notice that they are canny enough to maintain a degree of plausible deniability by making no definite claims. To me this demonstrates the very worst of journalism:

  • Conveying mistruths to support an ideology
  • Lacking the courage to commit to claims by asserting them as supportable facts

That’s bottom of the barrel journalism at the best of times, but now it’s irresponsible, reckless even. It presents a clear message that indigenous knowledge and ancient wisdom are perfectly acceptable ways of dealing with the pandemic. At no point is it mentioned that these ‘remedies’ are not backed by evidence, clinical or otherwise.

As you know, many western societies have huge anti-vax movements which often distrust and denounce mainstream medicine. Unfortunately, this video just adds fuel to the anti-vaxers fire. By failing to mention that these plant ‘remedies’ have zero efficacy, they are providing implicit support to the anti-science, anti-vax groups. Worse still, they are acting like digital snake oil salesmen, imbuing members of the public with false confidence that that they can avoid or fight off this virus with a couple of well chosen tree bark specimens. It’s dangerous, irresponsible nonsense.

Click below to see the video:

My own comments are few. First, it looks like the “remedy” includes cinchona bark, the source of quinine, as a palliative (the remedy seems directed at symptomatic relief rather than a cure).

Second, even “lived experience”, while useful, is no substitute for double-blind clinical trials. Granted, the Siekipai can’t do that, but they sure as hell should take the vaccination when it gets to them.  And, like Jeff, I think it’s totally irresponsible of The New Yorker to present this video without any kind of caveat. After all, when Trump skirts the truth, they don’t hesitate to correct him.  I guess “lived experience of indigenous people” is a different matter—it’s not as if they’re recommending drinking bleach or anything.

My doctor’s new post about the Pfizer vaccine: your questions answered (and you can ask the doc if you have others)

December 14, 2020 • 10:15 am

My GP, Dr. Alex Lickerman, has once again put up a coronavirus post on his practice’s website, and allowed me to reference it here. It’s timely because it’s all about the new Pfizer vaccine. (A ICU nurse in New York may have been the first to get the shot.) How effective is it, and how do we know that? Is it safe? What about kids under 16, who weren’t part of the clinical trials? And pregnant women, who also weren’t tested? Since this is a mRNA rather than a killed-virus vaccine, should we have extra concerns about safety? What adverse reactions have been reported? If you were already infected, does the vaccination also reduce your risk of getting reinfected?  When will “normal” people who aren’t healthcare workers or nursing-home patients be able to get their jabs?

Alex has kindly agreed, as he has before, to answer readers’ questions about the new vaccine, so put your questions in the comments section below and he’ll address them as he has time. Alex has read all the relevant scientific literature, as well as the data from the vaccine trials, so ask away! But do read his 4-page summary beforehand, as it has a lot of information.

I’m not going to put up his whole post; you can go to his site to see it,  which you can do by clicking on the screenshot below:

I’ll just post Alex’s recommendations, followed by his list of “unanswered questions” (indented). The short message: GET THE SHOT AS SOON AS YOU CAN!

CONCLUSIONS

  1. The vaccine is highly effective in preventing symptomatic COVID-19 infection.
  2. The vaccine is safe. Adverse reactions, both local and systemic, are mostly minor. Though the study hasn’t yet gone on long enough to prove there are no serious long-term adverse affects, such adverse affects, if they exist, are likely to be rare and non-life-threatening based on other Phase I and II studies of other RNA vaccines.
  3. We recommend everyone who is eligible to receive the vaccine should receive it when it becomes available to them.
  4. It very well may take all of 2021 to get everyone who’s willing to be vaccinated to receive the shots, which means it likely won’t be until early 2022 that life returns to pre-pandemic normal. In the meantime, continue to wear a mask when indoors with anyone you don’t live with, wash your hands frequently, and refrain from dining indoors at restaurants.

UNANSWERED QUESTIONS

  1. While suggested by the study, still left unproven is whether BNT162b2 [Pfizer’s name for the vaccine] prevents severe COVID-19 infection, whether it prevents COVID-19 infection after just one dose, and whether it prevents COVID-19 infection in subjects who’ve already had COVID-19.
  2. The study didn’t look to see if the vaccine prevents asymptomatic infection. Nor did it assess whether subjects who developed COVID-19 despite vaccination are less likely to transmit the virus. Thus, it’s not yet clear how effective the vaccine will be in containing the spread of the infection.
  3. The study hasn’t gone on long enough to tell if subjects who were vaccinated yet still contracted COVID-19 have a lower risk of long-term effects of COVID-19.
  4. We don’t yet know if the vaccine reduces the risk of dying from COVID-19.
  5. There was insufficient data to draw conclusions about safety and efficacy of the vaccine in children younger than 16, pregnant or lactating women, and patients who are immunocompromised.
  6. We don’t yet know how long immunity lasts and whether or not booster shots will be necessary.

Pfizer vaccine deemed safe and effective by the FDA, and a question for readers

December 8, 2020 • 8:45 am

Ripped from the headlines of CNN!  Click on the screenshot to read:

Many of us know that the FDA is meeting Thursday to decide whether to approve the Pfizer vaccine for general use. If the approval occurs, vials of vaccine will be making their way across the U.S., ready for immediate transfer into the arms of Americans.

Now, judging by the headline above, it looks almost certain that the FDA will indeed approve the vaccine in two days, and the first ranks of Americans will start getting vaccinated. Who gets it first appears to vary from state to state, but, rightly, healthcare workers and nursing-home patients (and their carers) will almost always be the first in line—and that’s what the FDA recommended as well.  After all, if the vaccine is safe and effective, why wouldn’t it be approved?

The good news gets even better: it appears that some immunity is conferred even after the first dose, which appears by itself to be 50% effective (two are required for the 95% effectiveness). Flu vaccine—the single shot we should all have gotten already this year, is only between 40% and 60% effective. “Effectiveness” is the reduction of risk that you get when you are vaccinated.

From CNN:

An advisory committee to the US Food and Drug Administration on Tuesday released a briefing document detailing data on Pfizer and BioNTech’s Covid-19 vaccine candidate, which will be considered this week for emergency use authorization in the United States.

The document confirms that the vaccine’s efficacy against Covid-19 was 95%, occurring at least seven days after the second dose – an efficacy that had been previously reported by Pfizer. The proposed dosing regimen for the vaccine is to administer two 30-microgram doses 21 days apart.

However, the document also notes that the vaccine, called BNT162b2, appears to provide “some protection” against Covid-19 following just one dose.

The document describes the efficacy of Pfizer’s vaccine in the time between the first and second dose as 52.4%, but the document notes that “the efficacy observed after Dose 1 and before Dose 2, from a post-hoc analysis, cannot support a conclusion on the efficacy of a single dose of the vaccine, because the time of observation is limited by the fact that most of the participants received a second dose after three weeks.”

In other words, “the trial did not have a single-dose arm to make an adequate comparison.”

The document goes on to detail the safety profile of the vaccine as “favorable” and notes that the most common adverse reactions to the vaccine have been reactions at the injection site, fatigue, headache, muscle pain, chills, joint pain and fever.

Severe adverse reactions occurred in less than 4.6% of participants, were more frequent after the second dose and were generally less frequent in older adults as compared to younger participants, according to the document. The document adds that swollen lymph nodes also may be related to vaccination.

That’s good enough for me, and I’ll be taking the shots as soon as my doc recommends it—which I presume will be as soon as I’m permitted to get them.

A STAT-Harris Poll published last month, however, showed that the proportion of Americans willing to get vaccinated depends on the vaccine’s efficacy, but only weakly.  Below are those data in graphic form.  What’s disturbing is that if the vaccine were 50% effective, only 60% of Americans would be likely to get the shots. And even with over 90% effectiveness, which is the case with all the vaccines about to hit the market, the willingness rises to only about 63%—a pathetically low figure. I’ve heard that the acquisition of herd immunity in the U.S. to coronavirus requires that 70% of Americans have immunity; even counting those who were infected, the figures on willingness to get vaccinated doesn’t give us that level of immunity. However, it will protect those smart people who get the shots.

So here’s the question: assuming you can get the shots because you don’t have a condition that bars them, are you going to get vaccinated? (I’m assuming that the Pfizer vaccine, or one with similar effectiveness, is the one on offer.) If not, why not?

New article: coronavirus lingers on surfaces longer than we thought

October 14, 2020 • 9:45 am

While most cases of Covid-19 are surely contracted via interperson contact (hugging, respiratory droplets, talking next to someone, handshakes, and so on), this new article from Virology Journal, produced by five Australian researchers, suggests that the virus can linger on various surfaces substantially longer than we suspected, and those infection-bearing surfaces (called “fomites”) can carry a viral load large enough to cause infection. Remember when you thought that paper and cardboard could be “disinfected” by leaving it untouched for 24 hours, so that the virus would all die? That doesn’t seem to be the case, at least according to this paper.

Click below to read the screenshot; the pdf is here , and the reference is at the bottom.

The results can be conveyed briefly. The researchers inoculated live virus onto six types of surfaces that might be encountered by people on a daily basis: Stainless steel (cookware, etc.), polymer currency (used in Australia), paper currency (no longer used in Australia but used in many other places), a glass surface (cellphones, touchscreens, etc.), vinyl, and cotton fabric.  The materials were incubated at three temperatures (20, 30, and 40 Celsius, corresponding respectively to 68, 86, and 104 degrees Fahrenheit, respectively), and incubation was in the dark, as UV light kills the virus more quickly (hint, put your envelopes and packages in the light when disinfecting them).  The relative humidity was 50%, though higher humidity also decreases viral survival.

The virus titer is said by the researchers to “represent a plausible amount of virus that may be deposited on a surface”. Samples were taken over 28 days, and the amount of living (i.e., infectious) virus measured by standard methods.

The attrition of the virus due to death over time was measured in three ways: the D value (time at which only 10% of the original sample remained), the half life (time at which half the original sample remained), and Z values (the increase in temperature required to reduce the D value by 90%, in other words to kill 99% of the inoculate).

The table below tells you everything you need to know: the D values and half lives (latter in parentheses) for all six materials at three temperatures, as well as the Z values:

Now what we don’t know about these values, and what is really important, is how much virus has to remain on the surface before it loses its ability to infect you (remember, probability of getting infected is proportional to the amount of virus you pick up and transfer to your nose, mouth, or eyes). This isn’t discussed in the paper, but I’d say a reasonable precaution is the D value: 90% loss of titer.  Perhaps readers in the know can tell us after they’ve read the paper.

But even if you use the half life, at 20°C, two days is a minimum for any surface save cotton (1.7 days). Paper loses half its virus load in three days, and glass in two. But remember, this is in the dark, and half-lives will be shorter in sunlight. Half-lives and Z values decrease dramatically at higher temperatures, though I think 20°C is what we should pay attention to because it’s close to room temperature.  If 10% of the original titer is not enough to infect you, you’ll have to wait 10 days for paper and 6 days for glass. Surprisingly, cotton cloth was the material that retained viable virus for the shortest amount of time.

The Z values show that an increase in temperature of about 15°C is enough to kill 99% of the virus existing at a given temperature.

The researchers also found that except for cotton, viable virus was still found on all surfaces after 28 days.

What’s the lesson for us? Well I can’t say (nor do I wish to purvey public-health advice!), because the crucial information—the amount of virus normally deposited on a surface, and how much of that must remain to give you an appreciable chance of getting infected if you pick it up—is missing. What the authors conclude is this:

The data presented in this study demonstrates that infectious SARS-CoV-2 can be recovered from non-porous surfaces for at least 28 days at ambient temperature and humidity (20 °C and 50% RH). Increasing the temperature while maintaining humidity drastically reduced the survivability of the virus to as little as 24 h at 40 °C. The persistence of SARS-CoV-2 demonstrated in this study is pertinent to the public health and transport sectors. This data should be considered in strategies designed to mitigate the risk of fomite transmission during the current pandemic response.

I guess we’ll have to leave it to the “considerers”, i.e., medical researchers and public health experts, to translate these results into recommended behaviors. But I think it’s smart to disinfect paper for two days instead of one after getting it, and use as little currency as possible (currency is like a circulating Petri dish, carrying E. coli as well as coronavirus. Use your credit card instead, and wipe it off with ethanol or wash it with soap and water after you use it. Put it in the machine, and don’t hand it to anyone unless you have to. Oh, and don’t let anybody use your cellphone.

___________________

Riddell, S., Goldie, S., Hill, A. et al. The effect of temperature on persistence of SARS-CoV-2 on common surfaces. Virol J 17, 145 (2020). https://doi.org/10.1186/s12985-020-01418-7

Covid 19 may hijack pain receptors, reducing pain and increasing the spread of the virus: a possible result of natural selection

October 8, 2020 • 9:00 am

The paper below, which has just been published (click on screenshot to go to page, then click the “download” button to the left to get the pdf), has a unique twist that may say something about evolution in pathogens, but the evolutionary angle hasn’t been mentioned. It’s a complex and technical paper, using rat models (i.e., tissue and analyses), to study whether the Covid-19 virus has the ability to reduce pain.

There’s also a publicity piece from the University of Arizona that explains the results in simpler language, and a two-minute video below that dumb things down a bit, but gives the gist.

From the publicity piece:

SARS-CoV-2, the virus that causes COVID-19, can relieve pain, according to a new study by University of Arizona Health Sciences researchers.

The finding may explain why nearly half of all people who get COVID-19 experience few or no symptoms, even though they are able to spread the disease, according to the study’s corresponding author Rajesh Khanna, PhD, a professor in the UArizona College of Medicine – Tucson’s Department of Pharmacology.

Rajesh Khanna, PhD. (Photo: Kris Hanning/University of Arizona Health Sciences)“It made a lot of sense to me that perhaps the reason for the unrelenting spread of COVID-19 is that in the early stages, you’re walking around all fine as if nothing is wrong because your pain has been suppressed,” said Dr. Khanna. “You have the virus, but you don’t feel bad because your pain is gone. If we can prove that this pain relief is what is causing COVID-19 to spread further, that’s of enormous value.”

The paper, “SARS-CoV-2 Spike protein co-opts VEGF-A/Neuropilin-1 receptor signaling to induce analgesia,” was published today in PAIN, the journal of the International Association for the Study of Pain.

. . .The U.S. Centers for Disease Control and Prevention released updated data Sept. 10 estimating that 50% of COVID-19 transmission occurs prior to the onset of symptoms and 40% of COVID-19 infections are asymptomatic.

“This research raises the possibility that pain, as an early symptom of COVID-19, may be reduced by the SARS-CoV-2 spike protein as it silences the body’s pain signaling pathways,” said UArizona Health Sciences Senior Vice President Michael D. Dake, MD. “University of Arizona Health Sciences researchers at the Comprehensive Pain and Addiction Center are leveraging this unique finding to explore a novel class of therapeutics for pain as we continue to seek new ways to address the opioid epidemic.”

In other words, the virus’s famous spike protein nullifies the effect of another protein, VEGF—one of the several proteins that normally causes pain. And that’s all ye need to know unless you work on this system.

But here’s where the evolution comes in. Remember, pain is an adaptation whose evolution was doubtlessly prompted by its ability to tell us that there’s something wrong, like “Hey, your hand is in the fire.” People who don’t feel pain, like those with Hansen’s disease (leprosy) and some rare neurological conditions, often incur severe damage to their bodies because they’re unaware of injuries. The reason Hansen’s sufferers lose their fingers and other bits is not because the bacteria eat away at those bits; rather, it’s because the bacteria numb feelings of pain, and so you start damaging your body without being aware of it. So pain is a good thing to have, even though it feels bad.

But if a virus that normally causes pain because it injures your innards can somehow block that pain, it might spread faster. This would be true for viruses like COVID-19, which is spread by human-to-human contact, and depends on its transmission for people going about and infecting others. If you take to bed because you’re in pain, the virus won’t spread as well.

And what that means is that mutant variants of the virus that reduce pain will spread faster than forms that cause pain. This differential would create natural selection for the mutants that reduce pain, and the virus “species” would evolve painlessness as one “symptom”.

As far as I can see, nobody in either the paper or the puff pieces have mentioned this possibility. Now we don’t know if this speculation is true, or if it’s just fortuitous that the spike protein blocks pain receptors. Further, while this might be an evolved property of the virus, it could also be an inherent property of the spike protein, evolved for other reasons, that simply allowed the virus to spread quickly.

I’m merely suggesting this as one possibility in a field called “Darwinian medicine,” which analyzes symptoms of diseases from an evolutionary viewpoint. Other suggestions from this area involve things like malaria. When you have a malaria outbreak, the malaise and fever put you flat on your back. And that facilitates the spread of the malaria pathogen (a protozoan), because that protozoan is transmitted by mosquitoes. When you’re prostrate in bed and sick, you’re not as liable to slap a biting mosquito as when you’re walking around, and so those protozoans that knock you flat will more readily find a mosquito vector. (This is all speculation, of course.)

Another suggestion involves the virus for the common cold. It doesn’t debilitate you, but rather makes you a bit grotty but still able to walk around—and transmit the virus to other people. If a common cold were to knock you out like malaria, the virus wouldn’t spread so well.

And so many of the symptoms that are caused by pathogens may well have evolved in those pathogens to facilitate their own transmission. This must certainly be true in some cases, but of course proving it is very hard to do. You couldn’t do experiments in humans, though I suppose you could in model animals like rats, but I wouldn’t be keen on hurting animals to test evolutionary hypotheses. (I even anesthetized all my fruit flies before killing them.) It is curious, though, that I haven’t seen this new and striking result mentioned as a possible example of natural selection in the virus.

Here’s the video, though you might not learn much if you’ve read what’s above.

h/t: Charles

Click to access 2020.07.17.209288.full.pdf