How Does Limulus Amebocyte Lysate Help You Live a Better Life?

Why Primitive Horseshoe Crabs are so Crucial and Handy Strategies to Help us Conserve them.

In this article, we’ll see how these horseshoe crabs have been used by traditional and modern cultures and learn a little bit about their biology and ecology. We’ll also see how horseshoe crab blood is used to make injections and other medical procedures safer for us. Read it on Medium.

This Lichen Might Help You Fight Cancer!

Lichens Produce Anticancer compounds. How long before we see them used to treat cancer?

“Late in life I have come on fern.

Now lichens are due to have their turn.”


Have you ever noticed the yellow lichens that grow on trees and rocks?

They’re quite a brilliant yellow and I see them in so many different places.  The other day I was out for a walk around a local pond and saw some growing on the trees.

If you’ve been following my blog, you know I’m a big fan of lichens.  I see lichens everywhere! On fence posts, rocks, trees, sidewalks, and especially when I’m hiking.  If I see a really nice patch, I photograph them and often I forget to take the time to identify them.

But these yellow ones just called out to me to be identified!

So I took a close-up picture and when I got back home, I took out my favourite lichen book and there it was, Xanthoria parietina. There are lots of common names for it including Maritime Sunburst Lichen, Common Orange lichen, Yellow Scale, Stonebreaker, Stoneflower, and Shore lichen.

Photo taken by Rich Sobel

The species was first described by Carl Linnaeus in 1753, as Lichen parietinus. Aptly enough, the species name, parietina, means “on walls” so we can guess where he first collected it almost 5 centuries ago!

The book’s description provided some great anatomical details and taxonomic info but that’s about it.  And it tells me I can find it on bark, wood and stone, common in coastal areas.

Origin of the word Lichen: There are 2 possibilities. It may derive from the Greek LEIKO ‐ to lick or lick up. This refers to how some species appear to “lap their tongues” all over the host. The second possibility is from Dioscorides.  He thought they resembled the skin of afflicted people (“leprous, warts or eruption”). The French scientist Tournefort officially named them in 1700 AD.

How disappointing! There’s got to be more information about a lichen this beautiful!

Ok, I Google it and sure enough, this is one very interesting lichen!

First I found out a bit more about its ecology and distribution.

The species is found growing over both inland and maritime rocks between elevations of 5 to 283 m. It is known from Australia, Pacific Islands, Antarctica, Africa, Europe, South America, North and Central America, and Asia.

Then I came across a whole lot more information that discussed how traditional cultures have used it and other lichens as food and medicines over the millenia.

Next, I searched for scientific articles about it and found out it produces some very intriguing compounds. They include anthraquinones, xanthones, dibenzofurans, depsides and depsidones.

Ok, those names mean nothing to most of us!  What’s so intriguing about those compounds?

Simple. Those classes of compounds are being tested for treating various infectious diseases and cancer.

Even more interesting is the fact that many of these compounds are only made by lichens. And to top it off, X. parietina is one of the primary lichens being investigated for producing them!

As a matter of fact, X. parietina is so ubiquitous and important that it was chosen by the Joint Genome Institute as the first lichen to sequence!

Xanthoria parietina was chosen as a model organism to represent lichen-forming fungi because it has a wide distribution (being found in temperate and circumpolar regions worldwide), …and is one of the most commonly studied lichenized fungi….Genome analysis is anticipated to provide insights into the genetic basis of biological phenomena such as mutualistic symbiosis, adaptation to harsh environments, secondary metabolism, fungal sexuality, and control of growth rate in the lichenized habit.”

This is a lichen worth telling a story worth about!

In this article, you’ll learn a little bit about Xanthoria parietina and a few other lichens and how they are used as food and medicines in traditional cultures. That piqued the curiosity of modern researchers. They began to explore the medicinal properties of lichens, including X. parietina, and how they might be used to produce more effective drugs for treating cancer.

How Did Traditional Cultures Use Lichens?

Lichens as Food

Humans have been using lichens for a long time! There are over 15,000 different species of lichens and in some regions, they are quite abundant.  So it’s not surprising that we have found ways to make use of them. We’ve used them to make perfumes, alcohol and dyes. 

And just like deer and other animals, humans eat lichens.  

Documented use of lichens in Europe started in the 15th and 16th centuries.  Many of the ways they were employed were based on the early Greek “Doctrine of Signatures”.  This doctrine suggested that “plants bearing parts that resembled human body-parts, animals, or other objects were thought to have useful relevance to those parts, animals or objects.”

Crops in Europe during the mid 18th century were badly affected by frosts and droughts that caused a famine. Because of their easy availability, cheapness and nutritive value people ate lichens to help keep themselves from starving.

Lichens as Medicines

In addition to their use as food, many traditional cultures have also used them as medicines to treat diseases and for their therapeutic values. 

Some of the ways they are commonly used is as dressing for wounds, as a disinfectant, or to stop bleeding.  They have also been applied directly to skin infections and sores to promote healing or reduce the pain.  

For example, in Nepal the local inhabitants of different regions have a long tradition of using lichens among the lichenophilic communities residing in the eastern mountainous parts of Nepal. Although the different regions of Nepal have different names for lichens, the most common is Jhyauu, which means “brittle stuff”.

Nepalese use the lichen Heterodermia diademata (one of the many lichens also called shield lichens) against cuts and to heal wounds. Peoples in the Western region of Nepal use it to treat moles.

Heterodermia diademata shield lichen (left) and Usnea beard lichen (right)

Different regions of the world employ different lichen genera in their traditional medicines, with another genus, Usnea (also known as Old Man’s Beard or Beard Lichen), being the most widely used.

Other traditional societies in the temperate and arctic regions commonly used lichens for treating wounds, skin disorders, respiratory and digestive issues. They were also employed to treat obstetric and gynecological problems, and for urinary and sexually transmitted infections.

Less commonly, they have also been used to treat eye and foot problems and are found in smoking mixtures.

Remember X. parietina, the lichen that got me started down this path?

Because of its color (remember the Doctrine of Signatures?) X. parietina has been used against jaundice in traditional medicine since antiquity.

In Andalucia, Spain, it is commonly called Rompepiedrea (Stonebreaker) or Flor de piedra (Stoneflower) and is used as a painkiller.

The Andalucians prepare a decoction of the surface-contacting part of X. parietina with wine and use that to treat menstrual complaints. A decoction in water of the aerial parts of the plant is taken to treat kidney disorders and relieve toothaches and several other pains.

It is also one of the ingredients of a cough syrup they make. They combine it with carob and fig fruits, flowers and leaves of oregano, the pericarp of almonds, olive tree leaves and abundant sugar or honey.

Note: a decoction is what you get when you boil plant materials like stems, roots, bark or leaves and then discard the materials. A very crude extract.

It has also been used in Europe during the 18th and 19th centuries to treat jaundice, stop bleeding, replace quinine to treat malaria and for treating hepatitis.

So X. parietina was and continues to be used for a variety of traditional treatments and remedies.

Using Lichens to Treat Cancer

I mentioned above that all these traditional uses sparked interest in some modern researchers to investigate their medicinal properties more thoroughly.  

What they initially found was that many of the lichens had antibiotic, antitumour, antifungal, and antiviral activity. They also inhibited some important enzymes and plant growth.  

Recent developments in analytical techniques have allowed the identification of over 1000 lichen substances that included the anthraquinones, xanthones, dibenzofurans, depsides and depsidones I mentioned above.

Maybe the pharmaceutical or agricultural industries could put these to use?   

An article published earlier this year by Zuzana Solárová and colleagues reviewed the most recent papers dealing with anticancer activities of lichen substances. They were particularly interested in their potential clinical use for cancer management.

The previous work used some of the compounds mentioned above to treat human cancer cell lines.  When the cells were exposed to the lichen substances they were either killed or they stopped growing and failed to produce new cells.

And that brings us back to X. parietina and how they did these kinds of tests. 

Basically, they collect the lichens in the field, then bring them back to the lab and extract the compounds from them. 

When they did this with X. parietina, its extract inhibited the proliferation of MCF-7 and MDA-MB-231, two of the most commonly used breast cancer cell lines in breast cancer research laboratories. 

It also stopped the cells from growing by inhibiting their cell cycle.  And it caused increased expression of 2 proteins that are associated with increased cell death.  It also decreased the levels of another protein, one that protects against cell death!

Growing just the fungal part

Ok, we need a quick refresher on some basic lichen biology to understand what happens next.

Lichens are not a single organism.  Most often they are a combination of an algae and a fungus that mutually “agree” to team up and form a single organism. 

Because the algal partner uses photosynthesis to generate energy for the lichen, it is often referred to in the lichen literature as the photobiont.

The fungal partner is called the mycobiont. “myco” comes from the Greek: μύκης (mukēs), meaning “fungus”. A “-biont” is a discrete living organism. 

It turns out that you can isolate either the photo- or myco- bionts and grow them independent of each other. 

One of the neat things about being able to grow just the algae or the fungus, is then you can vary the temperature, supply them with different kinds of nutrients, grow them in liquid culture or on solid media like agar.  

When you do that, they respond by making different compounds and at different amounts.  At first we didn’t know a lot about the biological activities of substances made by the separated bionts.

And our favourite lichen, X. parietina

In a study conducted in Beata Guzow-Krzemińska’s laboratory, they looked at the anticancer activity of three common lichens, Caloplaca pusilla, Protoparmeliopsis muralis and X. parietina.  

The Guzow-Krzemińska team isolated and grew just the fungal component (mycobiont) of these lichens on G-LBM media (See the image below). Then they ground them up and extracted them as I described above.

The three lichen mycobionts were incubated for 2 months on G-LBM media. Taken from the paper cited above.

When they grew the X. parietina fungus under two different culture nutrient conditions, they decreased the viability of HeLa cells or MCF-7 cancer cells. HeLa cells are derived from a cervical cancer patient and are one of the most famous cell lines used for cancer research.

Note: viability is the measure of the number of live cells vs dead cells in a cell culture.  Wikipedia defines it as “the ability of a thing (a living organism, an artificial system, an idea, etc.) to maintain itself or recover its potentialities.“

When X. parietina mycobiont was grown on PDA and G-LBM it decreased the viability of MCF-7 and HeLa cell lines.

The C. pusilla mycobiont showed the highest potency in decreasing MCF-7, PC-3 (a cell line derived from prostate cancer) and HeLa cancer cells viability. It also showed greater amounts of cell death in HeLa, PC-3 and MCF-7 cell lines as they were treated with increasing concentrations of the C. pusilla extract.

Why was this work so important?

Back to basic lichen biology.

If you want to use lichens for treating a disease as prevalent as cancer, you’re going to need quite a bit of it. Again and again.

Have you ever watched a lichen grow?  Don’t! 

Ummm, they grow quite slowly. Like, if you took a picture of one this year and then came back and took it again the next year and the year after, you might not notice much difference in the size or shape of it.  

That means that if you wanted to use any of these lichen compounds in significant amounts, you’d have to harvest a lot of lichens! And once they’re harvested, it would take years for them to grow back.  

The beauty of being able to grow the lichen mycobiont in the lab is that you can experiment to find ways to speed up its growth by varying things like sugar and other chemical concentrations.  So you can grow a lot pretty fast. Over and over and over again.  

If you can do that, there’s no need to harvest them from the wild. 

I like that! Very eco-friendly. 👏

You can also do breeding and mutation studies to select for strains that grow even better than the wild types and produce more of the chemicals you are interested in. 

And that is what big pharmacological companies look for.  Something they can easily manufacture in large batches to get lots of the chemical compound they want to use for making a drug or additive they can sell.

But before they invest the millions of dollars and years of time required, they want a little reassurance that what they are going to produce is going to work on people. And to know that, they have to do clinical trials. 

While the lichens have produced some interesting anticancer candidates, I don’t know of any clinical studies that have been performed to see if they actually reduce or eliminate tumours in people. 

That is the critical next step.

So let’s keep our eyes and ears open and if you hear of any clinical trials using lichen anticancer compounds, please let me know and I’ll do the same for you!

I hope you enjoyed the path this article took you down.  We started with wanting to know a bit more about a pretty lichen and look where we ended up! 

Possibly having new compounds in our arsenal to fight cancer.  

That’s one of the things I love about science.  You never know where the questions you ask and the answers you get will take you! 

Until next time,


For Additional Reading: The main sources I used to gather the information.

  1. Lichens Used in Traditional Medicine, Stuart D. Crawford, from his chapter in the book, “Lichen Secondary Metabolites” pp 27-80, Dec 2014, and personal communication.
  2. Anticancer Potential of Lichens’ Secondary Metabolites, Zuzana Solárová,1 Alena Liskova, Marek Samec, Peter Kubatka, Dietrich Büsselberg, and Peter Solár, Biomolecules. 2020 Jan; 10(1): 87
  3. Antibacterial and anticancer activities of acetone extracts from in vitro cultured lichen-forming fungi, Agnieszka Felczykowska, Alicja Pastuszak-Skrzypczak, Anna Pawlik, Krystyna Bogucka, Anna Herman-Antosiewicz, and Beata Guzow-Krzemińska, BMC Complement Altern Med. 2017; 17: 300.
  4. Indigenous knowledge and use of lichens by the lichenophilic communities of the Nepal Himalaya, Shiva Devkota, Ram Prasad Chaudhary, Silke Werth, and Christoph Scheidegger, J Ethnobiol Ethnomed. 2017; 13: 15. Published online 2017 Feb 21.
  5. Biopharmaceutical potential of lichens, Vasudeo P. Zambare & Lew P. Christopher, Pharmaceutical Biology, 50:6, 778-798, 2012
  6. Medicinal Lichens, by Robert Rogers
  7. Antiproliferative, Antibacterial and Antifungal Activity of the Lichen Xanthoriaparietina and Its Secondary Metabolite Parietin, Basile A., Rigano D., Loppi S., Di Santi A., Nebbioso A., Sorbo S., Conte B., Paoli L., De Ruberto F., Molinari A., et al.. IJMS; 16:7861–7875, 2015
  8. Three Lichens Used in Popular Medicine in Eastern Andalucia (Spain), Gonzalez-Tejero, M. R., M. J. Martinez-Lirola, M. Casares-Porcel, and J. Molero-Mesa, Economic Botany 49(1) 96-98. 1995.
  9. Have lichenized fungi delivered promising anticancer small molecules? Alessio Cimmino, Pier Luigi Nimis, Marco Masi, Laura De Gara, Willem A. L. van Otterlo, Robert Kiss, Antonio Evidente, Florence Lefranc, Phytochem Rev. 2019, 18:1–36.

Have You Gone Viral?

All the basic information you need to know about viruses that infect people.

What do you actually know about viruses?

Most people just know that viruses infect them and make them sick. So in these trying times with COVID-19, maybe it’s a good idea for us to all learn some basic viral biology.

There’s so much information out there about COVID-19 that I’m not going to say much about it. This article tells you about the main categories of viruses, how they reproduce, how they infect cells, their physical characteristics, and much more.

Let’s get started.

What are viruses?

Viruses are infectious particles.  We call them particles because they are not the same as cells and here’s why.

They lack any of the normal internal subcellular “machinery” that all other living organisms’ cells have. This includes the structures needed to make proteins or the proteins that are needed for independent metabolism and to make new copies of their nucleic acid genome.

Because of this, they fall into the category of what we call obligate intracellular parasites.  They can only reproduce inside a host cell.

Are they alive?

The perennial viral question.  It depends how you define life so some folks say yes and some say no.  As we stated above, they need to be inside a host cell to reproduce. No host cell available, no more viruses made.

But they do contain all the instructional material necessary to make new copies of themselves once inside a host.  So is that a form of life? You get to decide for yourself.

How big are viruses?

This is a very important question to answer.  Do you want to protect yourself from getting a viral infection? Then you need to either destroy or deactivate the viral particles or hide behind a barrier that the virus can’t penetrate.

To construct a viral barrier you need to make sure that the pore size is small enough to keep them from getting through it.  And know what CAN pass through it.

Viruses range in size from 20 nanometres (nm) up to about 250 nm. But what does that actually mean?  How can I “picture” that? Do you remember the microscope you used in high school Biology? Well, the smallest thing we can see with it is about 500 nm.

The width of a human hair is 80,000 to 100,00 nm wide.

The largest virus is around 250 nm. It would take about 300-400 of them stacked up on top of each other to equal the width of a single human hair!

And a few million of the 20 nm large viruses will fit on the head of a pin!

Now think for a moment about those face masks everyone is wearing these days to guard against COVID-19.  Do you think they can filter out something that small? Or even slow them down? Nope, they can’t. You can wear it if it makes you feel better to do so but it doesn’t serve any real purpose.

From Wikipedia “Surgical masks are not designed to protect the wearer from inhaling airborne bacteria or virus particles…” 

So let’s talk a bit about what makes a virus.

Viral structure

The general structure of most viruses is quite simple.  Their genome is a piece of DNA or RNA packaged inside a capsule made of proteins.  This structure is called the capsid.

Then, depending on what kind of virus it is, the capsid may be enclosed in a membranous structure called an envelope.

When there is an envelope, it usually contains additional molecules that protrude from the envelope.  Viruses like SARS or COVID-19 are called coronaviruses because the protruding molecules make them look like a sun with coronal flares.

The figure below is an electron microscope picture of typical SARS virus particles. You can see the protein molecules that stick out from the envelope quite nicely.

Typical coronavirus particles

CDC/Dr. Fred Murphy - This media comes from the Centers for Disease Control and Prevention’s Public Health Image Library (PHIL), with identification number #4814.

Kinds of Virus

Viruses were originally classified into 2 types, DNA viruses and RNA viruses. As we learned more, we discovered it wasn’t quite that simple!

By looking at their genomes and the proteins included in the capsid, modern viral taxonomy has distinguished 7 different classes of viruses.

This figure shows the 7 classes of viruses.  Here’s what the abbreviations mean if you’re curious but I’m not going to get into any detail about them in this article. Too technical!  ds is double-stranded, ss is single-stranded, (+) is the plus strand, (-) is the minus strand, RT is reverse transcriptase.

Viral structure

What do viruses look like? What are they made of?

In Biology, we call the appearance of an entity its morphology.  As an example, human morphology includes a trunk (abdomen and chest) supported on 2 legs which also has 2 arms that extend from it on either side.  And then there is a short tube at the top of the trunk that has another structure that has several openings and has 2 eyes, a nose and a mouth and 2 ears etc.  You get the idea. It can get very detailed! I barely started here.

This figure shows just how different the morphology for some of the 7 different types is.

The figure was taken from this article.

How do viruses infect their hosts and reproduce?

Again, I don’t want to get too technical here.  This is not a course to teach you everything about viruses but is a quick overview of what viruses are and how they do what they do.

Because different kinds of viruses infect all the other kinds of creatures on this planet, there is no one method of infection that they all use.  And even looking just at the ones that infect humans, there are a few different ways they do this.

One of the most common ways viruses infect humans is by essentially “merging” with the cells to enter them.  How did they come to be able to do that?

This is sort of a chicken and egg question because we don’t exactly know how viruses evolved this method.  What we do know is the ones that use this method have a membranous coating that they picked up from the last cell they invaded.

To best get the idea, let’s start with the virus already having entered the cell.  Enzymes inside the cell digest the envelope (if there is one) and the capsid, which releases the viral genomic nucleic acids (DNA or RNA). The genome contains the “instructions” to make the proteins that make more viral genomes. The viral genome is then “read” by the cell’s “machinery” that it uses to read its own genome and makes the proteins encoded in the viral genome.

These viral proteins now co-opt other parts of the subcellular “production line” and use them to manufacture more viral genomes, viral capsid proteins and envelope glycoproteins.

The capsid proteins then assemble and form new capsids around a strand of the new viral genome, one or two genomes per capsid.  At the same time, the cell transports the new viral envelope glycoproteins to its cellular membrane. The new genome-containing capsids are transported to the cell membrane where they bud out from the cell.  They surround themselves with the host cell membrane which also contains viral envelope proteins.

Here’s a nice figure to summarize all that information.

The figure was taken from this site

It turns out that these viral glycoproteins in the envelope actually bind to receptor molecules embedded in that particular type of cell’s membrane.  Let’s use our lung cells as an example. All the lung’s cells have that receptor molecule in and on their membranes.

The new viral particles’ envelopes bind to the same receptors present on other nearby cells and the cycle repeats over and over.  In some cases, the original host cell is killed but in others, it is not. Even if it is not killed, it is making new viral particles so it can’t perform the function it was originally designed for nearly as well, if at all. That plus the inflammatory response from the immune system is what causes the sickness or disease the creature suffers from. Especially when a high percentage of that particular cell type is infected.

Why are viruses specific to a particular host?

Let’s stay with the virus that infected our lungs. Its envelope only contains glycoproteins recognized by receptors on other lung cells.  It is not recognized by the liver, brain, kidney or any other tissue lacking the receptor. This is why viruses are so specific.  For example, the hepatitis virus only infects liver tissue cells and HIV only infects a specific kind of immune cell called a T cell. HIV kills this class of T cells which are a critical component of our immune system. The whole immune system is disabled without these T cells.

Some viruses can actually remain latent in the cell.  Herpes virus is one example. It actually makes copies of itself inside the cell nucleus. Then it buds from the nucleus with an envelope made from the nuclear membrane, not the cell’s outer membrane.  Some copies do not actually bud out of the nucleus but remain inside it as minichromosomes.

These minichromosomes stay inside the nucleus until some kind of stress signal activates them to open up and start producing more virus particles.  These particles then cause blisters such as cold sores or genital sores. And that’s why herpes infection is life-long. Some particles always remain behind just “waiting” to become active again!

What are other viral hosts?

Viruses are found in every other life form.  All the other creatures in the plant and animal kingdoms, and they also infect other microorganisms including bacteria and archaea, single-celled organisms that are not bacteria.

Viruses that infect bacteria are called bacteriophages. “The term comes from “bacteria” and the Greek φαγεῖν (phagein), meaning “to devour”. They are often referred to simply as phages.

Many early molecular biology studies used phage particles and their bacterial hosts as model systems to begin to understand basic molecular genetic and genomic biology.

 What else do I need to know?

I’ve covered all the basic biology of viruses you need to feel a bit more knowledgeable about them.

You know how small they are and the different parts that make a virus particle. You also know the different classes of viruses, how they infect humans, how they reproduce and the different organisms they use as hosts.

Any more information would start to get us into serious viral biology.

Note: I have specifically avoided talking about the COVID-19 coronavirus. Because there is so much information out there, I would just be repeating everything everyone else has already written about.

I hope you found this interesting and worth spending a few minutes of your time to read.

Until next time,


Hey! If you enjoyed this article then please subscribe to my newsletter to hear about my latest articles and grab my free ebook here.

Carl Zimmer’s Newsletter About the Covid-19 Virus

Do you know who Carl Zimmer is? If you are a regular reader of this blog, then you probably do know. And if you don’t know who he is, then read on.

Carl is one of the premier biological science columnists at the New York Times. He has his own website and blog, and he publishes a weekly newsletter, Friday’s Elk, that I avidly subscribe to. And you should too!

This past Friday’s Elk was about the Covid-19 virus and is one of the best-unbiased sources of information about this outbreak that I have read, yet.

I asked Carl for his permission to share it with you, my readers, and he graciously granted that. Here is what Carl has to say.

“Things have certainly changed since the last Friday’s Elk. The world has experienced over 100,000 infections of Covid-19, caused by a virus, SARS-CoV-2, that we didn’t even know about till a few weeks ago.

At first, we Americans complacently looked at the news as just another overseas disaster. As of this afternoon, there are 370 confirmed cases in the United States (one just a thirty-minute drive from where I live in Connecticut). Because our testing program is a mess, it’s certain there are many more–and transmission will bring more in weeks to come.

Anyone who says that no one could imagine this happening is ignorant or lying. Virologists have been tracing the origin of new human diseases from animal hosts for decades. The new virus, SARS-CoV-2, belongs to a lineage of bat viruses that has already produced two worrisome human diseases, SARS and MERS, in the past two decades. We know a fair amount now how viruses circulate in other species, how they spill over into ours, and then how they spread–either a little or a lot. You didn’t have to read virology journals to know about this. We science writers have been writing this story over and over again.

When I started out in journalism, my senior colleagues were writing about emerging diseases like Ebola and Four Corners Disease and HIV. Laurie Garrett published the far-sighted book The Coming Plague in 1994. Other books followed. I later wrote a short primer, A Planet of Viruses, in which I emphasized that viruses have always been with us, indeed even making up a sizable part of our genome. But even as we triumphed over smallpox and rinderpest, we were coming to appreciate just how many viruses we might run up against as we continued to devastate the natural world. David Quammen’s 2012 Spillover documented this threat in vivid detail.

So here we are, facing a new virus with which we have no experience whatsoever–both scientifically and immunologically. Scientists are working hard to estimate the key variables about this virus–such as how quickly it spreads from person to person and how likely an infection is to turn fatal. Those are not fixed values like the mass of an electron or the speed of light. Viruses spread more slowly when public health systems put up barriers between their hosts. Viruses can be deadlier when people can’t get decent medical care.

Roughly speaking, Covid-19 is much less deadly than SARS, but much more deadly than seasonal flu. While SARS had trouble spreading outside of hospitals, Covid-19 is spreading readily on cruise ships, within families at home, and among the elderly in long-term care facilities. While everyone seems vulnerable to infection, children typically only develop mild symptoms, while older people are at greater risk for serious illness or death.

For most people who get the virus, it will be a mild infection. But according to one rough estimate from Marc Lipsitch at Harvard, 20 to 60 percent of all adults may get infected. That could translate into a terrible toll, not just in terms of deaths but in terms of patients who need ventilators to stay alive. If thousands of cases hit American hospitals at once, it’s not clear how well the healthy system will hold up.

We don’t know if the virus will keep spreading into the spring and summer, or if it will fade as other winter respiratory viruses do. If it ebbs, chances are it will come back in the fall, perhaps in a roaring second wave. Vaccines won’t be ready till next year at the earliest. It’s possible that an effective antiviral may emerge in the coming months, which might help the desperately ill.

But for now, the best weapons against this virus are the classic ones. Social distancing, including school closures, may help to slow the coming wave so that fewer people need help at any moment. And washing hands keeps the virus from using them as a springboard to get into your mucous membranes–and ultimately your lungs. 

So let us give thanks to Ignaz Semmelweis! Washing hands may seem tediously obvious as a way to stop diseases, but it wasn’t until the mid-1800s that Semmelweis noticed that doctors themselves could spread fevers from patient to patient. If you find yourself looking for books to read during self-imposed quarantine, let me recommend The Doctor’s Plague by Sherwin Nuland, a short, potent account of Semmelweis’s struggle to make hand-washing our best weapon against enemies we can’t see and struggle to understand.

Check in on the CDC Covid-19 page for updated information on the disease and what to do about it.

If you still find yourself hankering for something to read–perhaps something not about viruses–I have a feature in the Atlantic this week about one of the strangest stories of the nuclear age. We released a vast pulse of radiocarbon into the atmosphere in the 1950s, which has infiltrated the biosphere ever since, including our own brains and bones. I’ve written a biography of the “bomb spike,” and what it has told us about our world.

Usually at the end of these emails, I list my upcoming talks. I’m going to skip them this time around because I’m honestly not sure how much traveling I’m going to do for the next few months. I’d rather not help spread SARS-CoV-2 any further than it’s going to get without me. I’ll update as the situation clarifies.

Stay well!

My award-winning book, She Has Her Mother’s Laugh, is now out in paperback. You can order it now from fine book mongers, including AmazonBarnes and NobleBAMHudson Booksellers, and IndieBound.

You can find information and ordering links for my books here. You can also follow me on TwitterFacebookGoodreads, and LinkedIn. If someone forwarded this email to you, you can subscribe to it here.

Best wishes, Carl

Friday’s Elk by Carl ZimmerYale University English Department P.O. Box 208302 New Haven, CT 06520-8302 USA

What is the Intimate Connection Between Delicious Spot Prawns and Diseased Starfish?

Is the loss of starfish affecting the supply and price of our delicious spot prawns?

In this article, you’ll learn how the populations of both starfish and spot prawns also depend on 2 other species, sea urchins and kelp. And how the decline in the starfish population due to a wasting disease is affecting the supply of our spot prawns…More

January 22, 2020

How Keeping Brain Cells Alive May Help You Fully Recover from Stroke

New work shows that there are tiny little packages that can deliver powerful healing to brain cells.

Do you know anyone who has suffered from stroke?

A stroke can be devastating because of the dramatic physical and emotional effects that can result from you or your loved ones experiencing one.

Stroke is usually associated with elderly men. But women get strokes, too.

Scientists at the University of Georgia have just published an article showing that delivering little fluid filled packages called exosomes into the brains of pigs can lead to their complete recovery from a stroke….More

We’re Just Big Slime Buckets – Part 3

Image by OpenClipart-Vectors from Pixabay

Why, when, where and how our slime is created and what happens when things go wrong.

In this article, Part 3, I look at our upper respiratory system to illustrate how and where mucus is made and by which cells, what its constituents are and how it works to protects us from infections and keeps our bodies operating like well oiled machines.

You’ll also learn about mucin genes and see how turning them on and off ensures that we maintain the amount of mucus we need for everyday usage. You’ll also see what happens when an infection is detected…More

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