Local graffiti wars — What’s going on?

The reoccuring incident of beautiful murals being vandalized.

20 October 2020 — For an innocent bystander, it appears that some graffiti artists may be jealous when others have the opportunity to create public art. In 1971, Marvin Gaye had something important to say, a message which is still rings home today:

Mother, mother
There’s too many of you crying
Brother, brother, brother
There’s far too many of you dying
You know we’ve got to find a way
To bring some lovin’ here today, yeah

Father, father
We don't need to escalate
You see, war is not the answer
For only love can conquer hate
You know we’ve got to find a way
To bring some lovin’ here today

Picket lines and picket signs
Don’t punish me with brutality
Talk to me
So you can see
Oh, what’s going on
What’s going
What’s going on
What’s going on

Right on, baby
Right on
Right on

Mother, mother
Everybody thinks we’re wrong
Oh, but who are they to judge us
Simply because our hair is long
Oh, you know we’ve got to find a way
To bring some understanding here today

Picket lines and picket signs
Don’t punish me with brutality
Come on talk to me
So you can see
What’s going on
What’s going on
Tell me what’s going on
I’ll tell you ya, what’s going on
Right on, baby
Right on, baby
Right on, baby

Originally inspired by a police brutality incident, What’s Going On by American singer Marvin Gaye was released in 1971 on the Motown subsidiary Tamla.

Let’s keep our egos under control, please. If anyone knows what is going on here, please enlighten us and send an email. In the meantime, in the upcoming months we will be featuring some other nice graffiti — sometimes just typographic — spotted around Basel’s Klybeck and St. Johann districts:

Did the Spraycan [sic] Samurai take some calligraphy classes at the Basel School of Design?

George Floyd RIP.

Habit formation is the process by which a behavior, through regular repetition, becomes automatic or habitual.

True luxury means having Mondays off and cooking risotto.

Say their names — Black Lives Matter.

New mural including an image of Breonna Taylor, a cityscape and three swimmers, near the Dreirosen Bridge in Kleinbasel.

29 August 2020 — As of today in the USA, 27,839 people have been killed and 24,358 have been injured this year due to gun violence.

> US Gun Violence Archive.
> 2020 US Shootings.

Black Lives Matter.

> Black Lives Matter.

Creatives against Corona — 150 posters submitted in local PR campaign.

This too shall pass, Karo Graphic Design (left) and Stay home and finally flatten the virus and the curve, Cosimo Wunderlin

7 May 2020 — How should one deal with this crisis on a responsible level? Design means finding a solution to problems. Graphic designers from around Basel have been called upon to create posters in B4 format to cope with the coronavirus. The posters will be hung in the region for two weeks starting in mid-May.

Stay at home, Siorin and We are keeping a distance, Takelwerk

Next up: Stop climate change before it stops us, Karo Graphic Design and Social Distancing, Philipp Jeker

No! Rona, Miriam Sterki and We look after each other, Martin Wuelser

In cooperation with the Poster Collection of the Basel School of Design, the Rappaz Museum will be making an exhibition of the posters. The opening reception is scheduled for June 4th — in compliance with all government regulations.

Opening reception: 4 June 2020, Rappaz Museum, Klingental 11, 4058 Basel, www.rappazmuseum.ch

The campaign Kreative contra Corona was initiated by the BZ Zeitung in cooperation with Pro Innerstadt Basel, Basel Live and jjsscc – with the help of the Merian-Iselin-Klinik, Clear Channel, Druckerei Creaplot, KreaB, Rappaz Museum, the Basel City Cleaning Department and the poster collection the Basel School of Design.

A fiasco in the making? As the coronavirus pandemic takes hold, we are making decisions without reliable data
by John P. A. Ioannidis

A nurse holds swabs and a test tube to test people for Covid-19 at a drive-through station set up in the parking lot of the Beaumont Hospital in Royal Oak, Michigan. (Photo: Paul Sancya, AP)

12 April 2020 — At a time when everyone needs better information, from disease modelers and governments to people quarantined or just social distancing, we lack reliable evidence on how many people have been infected with SARS-CoV-2 or who continue to become infected. Better information is needed to guide decisions and actions of monumental significance and to monitor their impact.

Draconian countermeasures have been adopted in many countries. If the pandemic dissipates — either on its own or because of these measures — short-term extreme social distancing and lockdowns may be bearable. How long, though, should measures like these be continued if the pandemic churns across the globe unabated? How can policymakers tell if they are doing more good than harm?

The data collected so far on how many people are infected and how the epidemic is evolving are utterly unreliable. Given the limited testing to date, some deaths and probably the vast majority of infections due to SARS-CoV-2 are being missed. We don’t know if we are failing to capture infections by a factor of three or 300. Three months after the outbreak emerged, most countries, including the US, lack the ability to test a large number of people and no countries have reliable data on the prevalence of the virus in a representative random sample of the general population.

This evidence fiasco creates tremendous uncertainty about the risk of dying from Covid-19. Reported case fatality rates, like the official 3.4% rate from the World Health Organization, cause horror — and are meaningless. Patients who have been tested for SARS-CoV-2 are disproportionately those with severe symptoms and bad outcomes. As most health systems have limited testing capacity, selection bias may even worsen in the near future.

The one situation where an entire, closed population was tested was the Diamond Princess cruise ship and its quarantine passengers. The case fatality rate there was 1.0%, but this was a largely elderly population, in which the death rate from Covid-19 is much higher.

Projecting the Diamond Princess mortality rate onto the age structure of the US population, the death rate among people infected with Covid-19 would be 0.125%. But since this estimate is based on extremely thin data — there were just seven deaths among the 700 infected passengers and crew — the real death rate could stretch from five times lower (0.025%) to five times higher (0.625%). It is also possible that some of the passengers who were infected might die later, and that tourists may have different frequencies of chronic diseases — a risk factor for worse outcomes with SARS-CoV-2 infection — than the general population. Adding these extra sources of uncertainty, reasonable estimates for the case fatality ratio in the general US population vary from 0.05% to 1%.

That huge range markedly affects how severe the pandemic is and what should be done. A population-wide case fatality rate of 0.05% is lower than seasonal influenza. If that is the true rate, locking down the world with potentially tremendous social and financial consequences may be totally irrational. It’s like an elephant being attacked by a house cat. Frustrated and trying to avoid the cat, the elephant accidentally jumps off a cliff and dies.

Could the Covid-19 case fatality rate be that low? No, some say, pointing to the high rate in elderly people. However, even some so-called mild or common-cold-type coronaviruses that have been known for decades can have case fatality rates as high as 8% when they infect elderly people in nursing homes. In fact, such “mild” coronaviruses infect tens of millions of people every year, and account for 3% to 11% of those hospitalized in the US with lower respiratory infections each winter.

These “mild” coronaviruses may be implicated in several thousands of deaths every year worldwide, though the vast majority of them are not documented with precise testing. Instead, they are lost as noise among 60 million deaths from various causes every year.

Although successful surveillance systems have long existed for influenza, the disease is confirmed by a laboratory in a tiny minority of cases. In the US, for example, so far this season 1,073,976 specimens have been tested and 222,552 (20.7%) have tested positive for influenza. In the same period, the estimated number of influenza-like illnesses is between 36,000,000 and 51,000,000, with an estimated 22,000 to 55,000 flu deaths.

Note the uncertainty about influenza-like illness deaths: a 2.5-fold range, corresponding to tens of thousands of deaths. Every year, some of these deaths are due to influenza and some to other viruses, like common-cold coronaviruses.

In an autopsy series that tested for respiratory viruses in specimens from 57 elderly persons who died during the 2016 to 2017 influenza season, influenza viruses were detected in 18% of the specimens, while any kind of respiratory virus was found in 47%. In some people who die from viral respiratory pathogens, more than one virus is found upon autopsy and bacteria are often superimposed. A positive test for coronavirus does not mean necessarily that this virus is always primarily responsible for a patient’s demise.

If we assume that case fatality rate among individuals infected by SARS-CoV-2 is 0.3% in the general population — a mid-range guess from my Diamond Princess analysis — and that 1% of the US population gets infected (about 3.3 million people), this would translate to about 10,000 deaths. This sounds like a huge number, but it is buried within the noise of the estimate of deaths from “influenza-like illness.” If we had not known about a new virus out there, and had not checked individuals with PCR tests, the number of total deaths due to “influenza-like illness” would not seem unusual this year. At most, we might have casually noted that flu this season seems to be a bit worse than average. The media coverage would have been less than for an NBA game between the two most indifferent teams.

Some worry that the 68 deaths from Covid-19 in the US as of March 16 will increase exponentially to 680, 6,800, 68,000, 680,000 … along with similar catastrophic patterns around the globe. Is that a realistic scenario, or bad science fiction? How can we tell at what point such a curve might stop?

The most valuable piece of information for answering those questions would be to know the current prevalence of the infection in a random sample of a population and to repeat this exercise at regular time intervals to estimate the incidence of new infections. Sadly, that’s information we don’t have.

In the absence of data, prepare-for-the-worst reasoning leads to extreme measures of social distancing and lockdowns. Unfortunately, we do not know if these measures work. School closures, for example, may reduce transmission rates. But they may also backfire if children socialize anyhow, if school closure leads children to spend more time with susceptible elderly family members, if children at home disrupt their parents ability to work, and more. School closures may also diminish the chances of developing herd immunity in an age group that is spared serious disease.

This has been the perspective behind the different stance of the United Kingdom keeping schools open, at least until as I write this. In the absence of data on the real course of the epidemic, we don’t know whether this perspective was brilliant or catastrophic.

Flattening the curve to avoid overwhelming the health system is conceptually sound — in theory. A visual that has become viral in media and social media shows how flattening the curve reduces the volume of the epidemic that is above the threshold of what the health system can handle at any moment.

Yet if the health system does become overwhelmed, the majority of the extra deaths may not be due to coronavirus but to other common diseases and conditions such as heart attacks, strokes, trauma, bleeding, and the like that are not adequately treated. If the level of the epidemic does overwhelm the health system and extreme measures have only modest effectiveness, then flattening the curve may make things worse: Instead of being overwhelmed during a short, acute phase, the health system will remain overwhelmed for a more protracted period. That’s another reason we need data about the exact level of the epidemic activity.

One of the bottom lines is that we don’t know how long social distancing measures and lockdowns can be maintained without major consequences to the economy, society, and mental health. Unpredictable evolutions may ensue, including financial crisis, unrest, civil strife, war, and a meltdown of the social fabric. At a minimum, we need unbiased prevalence and incidence data for the evolving infectious load to guide decision-making.

In the most pessimistic scenario, which I do not espouse, if the new coronavirus infects 60% of the global population and 1% of the infected people die, that will translate into more than 40 million deaths globally, matching the 1918 influenza pandemic.

The vast majority of this hecatomb would be people with limited life expectancies. That’s in contrast to 1918, when many young people died.

One can only hope that, much like in 1918, life will continue. Conversely, with lockdowns of months, if not years, life largely stops, short-term and long-term consequences are entirely unknown, and billions, not just millions, of lives may be eventually at stake.

If we decide to jump off the cliff, we need some data to inform us about the rationale of such an action and the chances of landing somewhere safe.

John P. A. Ioannidis is professor of medicine and professor of epidemiology and population health, as well as professor by courtesy of biomedical data science at Stanford University School of Medicine, professor by courtesy of statistics at Stanford University School of Humanities and Sciences, and co-director of the Meta-Research Innovation Center at Stanford at Stanford University.

> This article originally appeared on 17 March 2020 in STAT.

Why we should all be wearing protective face masks
by Andreas Kunz

The so-called ‘Spanish flu’ pandemic lasted from January 1918 to December 1920, infecting 500 million people — about a quarter of the world’s population at the time.

6 April 2020 — In Coop, a Swiss grocery store, a youngster coughs on a shrink-wrapped pork chop, which a grandmother then later puts in her shopping basket. At the Migros grocery store, cashiers continue to serve hundreds of customers every day without wearing protective facial masks. Although mask wearers have become more numerous on public transportion, they are still regarded by many as being paranoid busybodies. Or maybe they are supposedly dangerous Asian tourists.

In contrast to countries such as China, Japan or South Korea, Switzerland is not a mask-wearing society. On the contrary: hiding your face and remaining undetected in public is regarded here as an affront, something that only strictly religious Muslim women or youthful thugs tend to do. In Germany, it is no wonder that protective face masks are rarely seen since the outbreak of the corona virus. And it is no coincidence, because all of the shops that carry them are sold out.

The Swiss government has massively underestimated the importance of wearing masks, as well as their level of preparedness for a pandemic, with only 180,000 of the special protective models being stored. Since the outbreak of the crisis, Daniel Koch of the Federal Office of Public Health (BAG) has demonstratively questioned the usefulness of wearing masks. They “do not offer any real protection against viruses,” he claims incessantly — as if millions of disease-stricken Asians have been wrong for years.

In fact, protective masks offer the best chance of getting out of this lockdown as quickly as possible. Virologists outside Switzerland have long recognized this. Although it is possible that healthy people can catch the virus while wearing a mask, this greatly reduces the risk of droplet spread. And we tend not to touch our face as often when wearing one. If infected people wear a face mask, we can even minimize the safety distance. This is particularly important because around 80 percent of those infected show no or only slight symptoms, says the German professor of virology Alexander Kekulé and sums it up in one sentence: “If everyone wears masks, that means the sick would also be wearing masks.”

For Kekulé and other professionals, certain industries could resume operations and schools or garden centers could be opened if people wear protective masks and follow other rules of hygiene, such as washing and/or disinfecting your hands. But the Swiss authorities have continued to brush off the topic, even two weeks after the lockdown was first announced.

Advertisement from the Illustrated Current News, 18 October 1918.

The Federal Office of Public Health stated that it is busy trying to buy “as many masks as possible” from abroad. But the global demand is so great that not only did prices explode, but orders that were already promised have not arrived. Some Swiss companies have been smart enough to make their own masks, but the amount is far from the amount needed. And a major national effort to solve this problem as soon as possible has hardly been reached.

The federal government does not have to declare a crisis on mask production, similar to the Swiss cultivation program to grow food during WWII. But they should persuade many more companies to make their own protective masks and include the idea of wearing masks in their official campaign to fight the virus. Above all, it is time that the Federal Office of Public Health stops spreading falsehoods about the effectiveness of wearing masks. Everyone understands that hospitals and retirement homes must have priority in the distribution of the current remaining stocks. But no one should be led to believe that masks are not essential in getting us out of this lockdown.

Not wearing masks will quickly become a thing of the past here in the west.

This crisis will change the country and its people. Sooner or later we will get used to wearing masks. We still show noble reluctance to commit to this kind of bourgeois taboo breach: to hide the face — our most personal characteristic — from each other. We should follow the example of the Asians: They wear facial masks as a sign of courtesy and solidarity.

This article was originally published in German on 28 March 2020, in several Swiss newspapers.

> Swiss journalist Andi Kunz on Twitter

New poster:

20 March 2020 — Download, print out, hang up and share electronically:

> Poster, English
> Plakat, Deutsch
> Affico, italiano
> Affiche, français

Coronavirus: Symptoms, statistics and daily tracking.

Olafur Eliasson, The Weather Project, Turbine Hall at the Tate Modern, London, 2003.

15 March 2020 — Indeed, it’s the end of the world as we know it. We collected a bit of information about the symptoms and the cycle of the coronavirus. All source links are provided below.

Typical symptoms of Covid-19
Covid-19 typically causes flu-like symptoms including a fever and cough. In some patients — particularly the elderly and those with other chronic health conditions — these symptoms can develop into pneumonia, with chest tightness, chest pain and shortness of breath. It appears to start with a fever, followed by a dry cough.

After a week, it can lead to further shortness of breath, with about 20% of patients requiring hospital treatment. Notably, the Covid-19 infection rarely seems to cause a runny nose, sneezing, or sore throat (these symptoms have been observed in only about 5% of patients). Sore throat, sneezing, and stuffy nose are most often signs of a cold.

80% of the cases are mild
Based on all 72,314 cases* of Covid-19 in China as of 11 February 2020:
— 80.9% of infections are mild (with flu-like symptoms) and can recover at home
— 13.8% are severe, developing severe diseases including pneumonia and shortness of breath
— 4.7% as critical and can include: respiratory failure, septic shock, and multi-organ failure
— 2% of reported cases are fatal
— The risk of death increases the older that you are
— Relatively few cases haven been seen among children

* Taken from research a paper about confirmed, suspected and asymptomatic cases which was released on 17 February 2020 by the Chinese CCDC and published in the Chinese Journal of Epidemiology.

Pre-existing illnesses that put patients at a higher risk:
— Cardiovascular disease
— Diabetes
— Chronic respiratory disease
— Hypertension

It must be noted, some otherwise healthy people have developed a severe form of pneumonia after being infected by the virus. The reason for this is unknown and is still being investigated.

Daily tracking of symptoms

First 1–3 days 
— Symptoms are similar to those of the common cold
— Sore throat
— No flu, not tired, still eating normally

Day 4
— Sore throat
— First signs of becoming sick
— Body temperature increasing from 36.5° (varies from person to person)
— Loss of appetite begins, difficult to eat
— Mild headache
— Mild diarrhea

Day 5
— Sore throat, coughing
— Slightly hot body, temperature rises to 36.5–36.7°
— Feeling tired and dizzy, pain in the joints
— This stage is difficult to diagnose as either a cold or flu

Day 6
— Mild fever begins, about 37°
— Croup cough or dry cough
— Sore throat when eating, talking or swallowing
— Fatigue, nausea
— Breathing is difficult
— Possible diarrhea, vomiting

Day 7
— The fever is higher from 37.4–37.8°
— Much coughing
— Body aches and pains, the head feels heavy
— Frequent feeling of suffocation
— More diarrhea
— Vomiting

Day 8 
— Fever is 38°+
— Hard to breathe, shortness of breath
— Continued coughing
— Headache, joint pain, back pain 

Day 9 (in this stage, blood tests and lung xrays should be made
— Symptoms worsen
— High fever
— Not coughing but symptoms worsen
— Breathing difficulties

Symptoms vary depending on the individual’s resistance and immunity. It takes 10–14 days for symptoms to develop in a healthy person, only 4–5 days for a person with health issues.

> healthxcenter.com

Examples of possible development of symptoms (from actual cases)

A man in his 40s in Japan:
— Day 1: Bodily discomfort and muscle pain
— Later diagnosed with pneumonia

A man in his 60s in Japan:
— Day 1: Initial symptoms of low-grade fever and sore throat

A man in his 40s in Japan:
— Day 1: Chills, sweating and malaise
— Day 4: Fever, muscle pain and cough

A woman in her 70s, in Japan:
— Day 1: 38° fever for a few minutes
— Day 2+3: Went on a bus tour
— Day 5: Visited a medical institution
— Day 6: Showed symptoms of pneumonia

A woman in her 40s, in Japan:
— Day 1: Low-level fever
— Day 2: 38° fever
— Day 6: Being treated at home

A man in his 60s, in Japan:
— Day 1: Cold symptoms
— Day 6: Fever of 39°C (102.2°F)
— Day 8: Pneumonia

Another patient, in China with a history of type 2 diabetes and hypertension:
— 22 January: Fever and cough
— 5 February: Died

First death in the Philippines (44 year old Chinese other pre-existing health conditions):
— 25 January: Fever, cough, and sore throat (hospitalized)
— Developed severe pneumonia
— 2 February: Died

How long do symptoms last?

Using available preliminary data, the Report of the WHO-China Joint Mission published on 28 February 2020 by WHO, which is based on 55,924 laboratory confirmed cases, observed the following median time from symptoms onset to clinical recovery:

— Mild cases: approximately 2 weeks
— Severe or critical disease: 3–6 weeks
— Time from onset to the development of severe disease (including hypoxia, a lack of oxygen to a specific part of the body): 1 week

Among patients who have died, the time from symptom onset to outcome ranges from 2–8 weeks.

> healthxcenter.com

Combating the coronavirus: Why soap works so well.
by Palli Thordarson

Coronaviruses are a group of viruses that have a halo, or crown-like (corona) appearance when viewed under an electron microscope. Photo: Dr. Fred Murphy (Centers for Disease Control and Prevention)

9 March 2020 — A two-part Twitter thread about soap, viruses and supramolecular chemistry.
(Ed. By the way, SARS-CoV-2 is the virus, COVID-19 is the disease.)

Part 1

Why does soap work so well on the SARS-CoV-2, the coronavirus and indeed most viruses? Because it is a self-assembled nanoparticle in which the weakest link is the lipid (fatty) bilayer. A two part thread about soap, viruses and supramolecular chemistry.‬

The soap dissolves the fat membrane and the virus falls apart like a house of cards and dies, or rather, we should say it becomes inactive as viruses aren’t really alive. Viruses can be active outside the body for hours, even days.

Disinfectants, or liquids, wipes, gels and creams containing alcohol (and soap) have a similar effects but are not really quite as good as normal soap. Apart from the alcohol and soap, the antibacterial agents in these products don’t affect the virus structure much at all.

Consequently, many antibacterial products are basically just an expensive version of soap in terms of how they act on viruses. Soap is the best but alcohol wipes are good when soap is not practical or handy (e.g. office receptions).

But why exactly is soap so good? To explain that, I will take you through a bit of a journey through supramolecular ‪chemistry‬, nanoscience and virology. I try to explain this in generic terms as much as possible, which means leaving some specialist chemistry terms out.

I point out to that while I am expert in supramolecular chemistry and the assembly of nanoparticles, I am not a virologist. The image with the first tweet is from an excellent post here which is dense with good virology info:

The weakest link of the coronavirus is it's fatty bilayer (lipid).
E = small envelope protein
S = spike glycoprotein
M = membrane
Illustration: David M. Knipe and Peter M. Howley (ed.), Fields Virology, 6th Edition. Wolters Kluwer, 2013.

I have always been fascinated by viruses as I see them as one of them most spectacular examples of how supramolecular chemistry and nanoscience can converge. Most viruses consist of three key building blocks: RNA, proteins and lipids.

The RNA is the viral genetic material — it is very similar to DNA. The proteins have several roles including breaking into the target cell, assist with virus replication and basically to be a key building block (like a brick in a house) in the whole virus structure.

The lipids then form a coat around the virus, both for protection and to assist with its spread and cellular invasion. The RNA, proteins and lipids self-assemble to form the virus. Critically, there are no strong covalent bonds holding these units together.

Instead the viral self-assembly is based on weak non-covalent interactions between the proteins, RNA and lipids. Together these act together like a velcro so it is very hard to break up the self-assembled viral particle. Still, we can do it (e.g. with soap!).

Most viruses, including the coronavirus, are between 50–200 nanometers — so they are truly nanoparticles. Nanoparticles have complex interactions with surfaces they are on. Same with viruses. Skin, steel, timber, fabric, paint and porcelain are very different surfaces.

When a virus invades a cell, the RNA hijacks the cellular machinery like a computer virus (!) and forces the cell to start to makes a lot of fresh copies of its own RNA and the various proteins that make up the virus.

These new RNA and protein molecules, self-assemble with lipids (usually readily present in the cell) to form new copies of the virus. That is, the virus does not photocopy itself, it makes copies of the building blocks which then self-assemble into new viruses!

All those new viruses eventually overwhelm the cell and it dies/explodes releasing viruses which then go on to infect more cells. In the lungs, some of these viruses end up in the airways and the mucous membranes surrounding these.

When you cough, or especially when you sneeze, tiny droplets from the airways can fly up to 10 meters (30 ft)! The larger ones are thought to be main coronavirus carriers and they can go at least 2 m (7 ft). Thus — cover your coughs and sneezes to people!

These tiny droplets end on surfaces and often dry out quickly. But the viruses are still active! What happens next is all about supramolecular chemistry and how self-assembled nanoparticles (like the viruses) interact with their environment!

Now it is time to introduce a powerful supramolecular chemistry concept that effectively says: similar molecules appear to interact more strongly with each other than dissimilar ones. Wood, fabric and not to mention skin interact fairly strongly with viruses.

Contrast this with steel, porcelain and at least some plastics, e.g. teflon. The surface structure also matter – the flatter the surface the less the virus will stick to the surface. Rougher surfaces can actually pull the virus apart.

So why are surfaces different? The virus is held together by a combination of hydrogen bonds (like those in water) and what we call hydrophilic or fat-like interactions. The surface of fibres or wood for instance can form a lot of hydrogen bonds with the virus.

In contrast steel, porcelain or teflon do not form a lot of hydrogen bond with the virus. So the virus is not strongly bound to these surfaces. The virus is quite stable on these surface whereas it doesn’t stay active for as long on say fabric or wood.

For how long does the virus stay active? It depends. The SARS-CoV-2 coronavirus is thought to stay active on favourable surfaces for hours, possibly a day. Moisture (dissolves), sun light (UV light) and heat (molecular motions) all make the virus less stable.

The skin is an ideal surface for a virus! It is organic and the proteins and fatty acids in the dead cells on the surface interact with the virus through both hydrogen bonds and the fat-like hydrophilic interactions.

So when you touch say a steel surface with a virus particle on it, it will stick to your skin and hence get transferred onto your hands. But you are not (yet) infected. If you touch your face though, the virus can get transferred from your hands and on to your face.

And now the virus is dangerously close to the airways and the mucus type membranes in and around your mouth and eyes. So the virus can get in… and voila! You are infected (that is, unless your immune system kills the virus).

If the virus is on your hands you can pass it on by shaking someone’s else hand. Kisses, well, that’s pretty obvious… It comes without saying that if someone sneezes right in your face you are kind of stuffed. Part 2 about soap coming next (25 post limit reached)!

Part 2

About soap, supramolecular chemistry and viruses. So how often do you touch your face? It turns out most people touch the face once every 2–5 minutes! Yeah, so you at high risk once the virus gets on your hands unless you can wash the active virus off.

So let’s try washing it off with plain water. It might just work. But water only competes with the strong glue-like interactions between the skin and virus via hydrogen bonds. They virus is quite sticky and may not budge. Water isn’t enough.

Soapy water is totally different. Soap contains fat-like substances knowns as amphiphiles, some structurally very similar to the lipids in the virus membrane. The soap molecules compete with the lipids in the virus membrane.

The soap molecules also compete with a lot other non-covalent bonds that help the proteins, RNA and the lipids to stick together. The soap is effectively dissolving the glue that holds the virus together. Add to that all the water.

The soap also outcompetes the interactions between the virus and the skin surface. Soon the viruses get detached and fall a part like a house of cards due to the combined action of the soap and water. The virus is gone!

The skin is quite rough and wrinkly which is why you do need a fair amount of rubbing and soaking to ensure the soap reaches very crook and nanny on the skin surface that could be hiding active viruses.

Alcohol based products, which pretty includes all disinfectants and antibacterial products contain a high-percentage alcohol solution, typically 60–80% ethanol, sometimes with a bit of isopropanol as well and then water plus a bit of a soap.

Ethanol and other alcohols do not only readily form hydrogen bonds with the virus material but as a solvent, are more lipophilic than water. Hence alcohol do also dissolve the lipid membrane and disrupt other supramolecular interactions in the virus.

However, you need a fairly high concentration (maybe +60%) of the alcohol to get a rapid dissolution of the virus. Vodka or whiskey (usually 40% ethanol), will not dissolve the virus as quickly. Overall alcohol is not quite as good as soap at this task.

Nearly all antibacterial products contain alcohol and some soap and this does help killing viruses. But some also include active bacterial killing agents, like triclosan. Those, however, do basically nothing to the virus!

To sum up, viruses are almost like little grease-nanoparticles. They can stay active for many hours on surfaces and then get picked up by touch. They then get to our face and infect us because most of us touch the face quite frequently.

Water is not very effective alone in washing the virus off our hands. Alcohol based product work better. But nothing beats soap – the virus detaches from the skin and falls apart very readily in soapy water.

Here you have it – supramolecular chemistry and nanoscience tell us not only a lot about how the virus self-assembled into a functional active menace, but also how we can beat viruses with something as simple as soap.

Thank you for reading my first thread. Apologies for any mistakes in the above. I might have some virology details wrong here as I am not a virologist unlike ‪@MackayIM‬ who I am a big fan of! But I hope this inspires you not only to use soap but to read up on chemistry!

Palli Thordarson (@PalliThordarson), B.Sc. (Iceland) 1996, Ph.D. (Sydney) 2001, CChem, FRACI, FRSC
Professor, School of Chemistry UNSW, Sydney, New South Wales

Research Group website: http://thordarsongroup.org

Biographical Details
B.Sc. Chemistry from the University of Iceland (1996), Researcher, Science Institute, the University of Iceland (1996–1997). Ph.D, The University of Sydney (1997–2001). Postdoctoral Fellow, the University of Nijmegen, The Netherlands (2001), Marie Curie Postdoctoral Fellow, the University of Nijmegen, The Netherlands (2001–2003). The University of Sydney SESQUI Postdoctoral Research Fellow (2003–2005). Australian Research Council, Australian Research Fellow, The University of Sydney (2006–2007) and UNSW (2007–2010). Appointed Senior Lecturer, UNSW (2007); Australian Research Council Future Fellow (2012–2016), Associate Professor (2013). Professor (2017).
Marie Curie Fellowship (2001), Sesqui Fellowship (2003), NSW Young Tall Poppy Science Prize (2008), The International Society of Porphyrins and Phthalocaynines/Journal of Porphyrins and Phthalocyanines) Young Investigator Award (2010), Le Fèvre Memorial Prize by the Australian Academy of Science (2012). Fellow of the Royal Australian Chemical Institute (2017), Fellow of the Royal Socieity of Chemistry UK (2017).

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News update: Studio concert postponed.

2 March 2020 — Today’s studio concert by Shadowplay has been postponed to help prevent the spread of Covid-19. We will keep you posted when the concert has been re-scheduled. Stay healthy!

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K’Werk 2020 Program: Neon is the New Orange.

17 February 2020 — The K’Werk Bildschule (German for image school) was founded in 2005, offering classes and workshops in the visual arts, a concept similar to that of what music schools have been providing for decades. Children and adolescents between the age of 5 and 16 can discover and develop their creative skills in a fun and concentrated atmosphere.

The K’Werk Bildschule is part of the Basel School of Design and is a public educational program in the canton of Basel-Stadt.

K’Werk 2020 program, published twice yearly, 48 pages, 2-color printing with a 4-color photo section. The new program booklet is available at K’Werk Bildschule: www.kwerk.ch or from us directly.

New book release: Mixing, Punks and Background Noise.

2 January 2020 — This little paperback is an explosive collision of two of our favorite subjects: Real Punk Ginger Beer and music. Mixing, Punks and Background Noise is packed with 35 mixed drink recipes and 31 black and white photographs of 15 bands and 49 musicians from around the globe.

Learn to mix common cocktails such as Moscow Mule and Dark and Stormy and the lesser known Matcha Ginger Beer, Ginger Beer Caipirinha and Vintage Punk. All of the recipes use our own Real Punk Ginger Beer as a mixer. And for the especially ambitioned, we have included 2 recipes for making your own DIY infused aromatic bitters.

The musicians are not only esteemed stars, but also local artists who we highly admire. The concert photos include the following performers: Steve Albini & Shellac, Asbest, Bernie the Attorney, Jehnny Beth & Savages, Big Muff, Nick Cave, Dead Moon, Denner Clan, Michael Gira & Swans, Gustav Gurke & Peter Paprika, Debbie Harry, Rowland S. Howard, L’Arbre bizarre, Lombego Surfers, John Maher of Buzzcocks, Dominic Aitchison and Stuart Braithwaite of Mogwai, Chris Pravdica, Joey Ramone, Henry Rollins, Siouxsie Sioux, Mark E. Smith, Thurston Moore, Todd Trainer, Totem Nevada, Treelove, The Tutu Three, Warpaint, Norman Westberg, Bob Weston and Jack White.

Many thanks to Andy Chislehurst (John Maher), David Corio (Nick Cave, Rowland S. Howard, Mark E. Smith), Ed Perlstein (Joey Ramone) and Derek Ridgers (Siouxsie Sioux) for graciously allowing us to use their vintage photographs! All other photographs are by Susan Knapp.

Mixing, Punks and Background Noise — Real Punk Ginger Beer and the Art of Mixology: 167 x 215 mm, 64 pages, 31 black and white photographs, softcover, in English, limited edition of 250 copies. CHF 10, EUR 9 plus shipping. Real Punk Ginger Beer can be ordered directly from us at Karo Publishing.