Kreative contra Corona — 150 Plakaten eingereicht.

Auch das geht vorbei, Karo Grafik (links) und Zuhause bleiben, Virus und Kurve flach machen, Cosimo Wunderlin

7. Mai 2020 — Wie geht man mit der Krise verantwortungsvoll um? Design heisst, für Probleme eine Lösung zu finden. Grafiker und Grafikerinnen der Region Basel sind aufgerufen worden, Plakate im B4-Format zur Bewältigung von Corona zu gestalten. Die Resultate werden ohne Jurierung ab Mitte Mai während zwei Wochen ein Aushang stattfinden.

Stay at home, Siorin und Wir halten Abstand, Takelwerk

Next up: Stop climate change before it stops us, Karo Grafik und Social Distancing, Philipp Jeker

No! Rona, Miriam Sterki und Wir schauen zueinander, Martin Wülser

Das Rappaz-Museum wird in Zusammenarbeit mit der Plakatsammlung der Schule für Gestaltung Basel zudem eine Ausstellung zu Kreative contra Corona durchführen. Die Vernissage ist zurzeit auf den 4. Juni angesetzt – natürlich unter Einhaltung aller Corona-Schutzkonzepte.

Vernissage: 4. Juni 2020, Rappaz-Museum, Klingental 11, 4058 Basel, www.rappazmuseum.ch

Die Aktion Kreative contra Corona wurde initiiert von der BZ Zeitung in Zusammenarbeit mit Pro Innerstadt Basel, Basel Live und jjsscc – unter Mithilfe der Merian-Iselin-Klinik, Clear Channel, Druckerei Creaplot, KreaB, Rappaz-Museum, die Basler Stadtreinigung und die Plakatsammlung der Schule für Gestaltung Basel.

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.

Warum wir alle Masken tragen sollten
von Andreas Kunz

Die Influenza-Pandemie hat sich zwischen Januar 1918 und Dezember 1920 verbreitet. Insgesamt sollen etwa 500 Millionen Menschen infiziert worden sein — etwa ein Viertel der damaligen Weltbevölkerung.

6. April 2020 — Im Coop hustet der Jungspund auf das eingeschweisste Kotelett, das die Grossmutter später in den Einkaufskorb legt. In der Migros bedienen Kassiererinnen Hunderte Kunden täglich weiterhin ohne Mundschutz. Im ÖV sind die Maskenträger zwar zahlreicher geworden, aber noch immer werden sie von vielen als paranoide Wichtigtuer taxiert. Oder als angeblich gefährliche asiatische Touristen.

Im Gegensatz zu Ländern wie China, Japan oder Südkorea besitzt die Schweiz keine Kultur des Maskentragens. Im Gegenteil: Sich das Gesicht zu verdecken und öffentlich unerkannt zu bleiben, gilt als Affront, als etwas, das sich höchstens strenggläubige Musliminnen oder jugendliche Schlägertrupps leisten. Kein Wunder, waren Schutzmasken hierzulande seit Ausbruch der Corona-Epidemie nur selten zu sehen. Und kein Zufall, gibt es sie bis heute fast nirgends zu kaufen.

Der Bund hat das Maskenthema massiv unterschätzt. Nicht nur bei der Pandemievorsorge, bei der gerade mal 180’000 der besonders schützenden Modelle gelagert wurden. Auch seit Ausbruch der Krise zieht BAG-Mann Daniel Koch die Nützlichkeit demonstrativ in Zweifel. Masken böten “keinen wirklichen Schutz vor Viren”, behauptet er unablässig — ganz so, als würden sich Millionen seuchengeplagter Asiaten seit Jahren irren.

In Wahrheit bieten Schutzmasken die beste Chance auf einen möglichst schnellen Ausweg aus dem Shutdown. Das haben Virologen ausserhalb der Schweiz längst erkannt. Auch wenn Gesunde trotz Maske weiterhin infiziert werden können, verringert sich dadurch das Risiko einer Tröpfcheninfektion. Wir fassen uns damit auch nicht ins Gesicht. Und wenn Infizierte einen Mundschutz tragen, können wir sogar den Sicherheitsabstand durchbrechen. Dies sei besonders wichtig, weil rund 80 Prozent von ihnen keine oder nur leichte Symptome zeigen, sagt der deutsche Professor für Virologie Alexander Kekulé und bringt es auf den Punkt: “Wenn alle eine Maske tragen, tragen auch die Kranken eine.”

Für Kekulé und andere Fachleute können gewisse Branchen den Betrieb wieder aufnehmen und Schulen oder auch Gartencenter geöffnet werden, wenn die Menschen Schutzmasken tragen sowie die anderen Hygieneregeln wie Händewaschen und Desinfizieren befolgen. Doch die Schweizer Behörden verwedeln und verdrängen das Thema auch zwei Wochen nach Ausruf des Shutdowns.

Inserat aus Illustrated Current News, 18. Oktober 1918

Zwar sei man emsig daran, “so viele Masken wie möglich” aus dem Ausland aufzukaufen, heisst es beim BAG. Doch der weltweite Bedarf sei derart gross, dass nicht nur die Preise explodierten, sondern auch bereits versprochene Bestellungen nicht einträfen. Findige Schweizer Unternehmen haben deshalb begonnen, selber Masken herzustellen. Aber die Produktion reicht bei weitem nicht. Und eine grosse nationale Anstrengung, das Problem baldmöglichst zu beheben, ist bislang kaum festzustellen.

Der Bund muss nicht gerade eine Maskenschlacht ausrufen analog der Anbauschlacht im Zweiten Weltkrieg. Aber er sollte noch viel mehr Firmen zur Produktion bewegen und das Tragen von Schutzmasken in die Infokampagne aufnehmen. Vor allem aber ist es an der Zeit, dass das BAG nicht mehr weiter Unwahrheiten über die Wirksamkeit verbreitet. Dass Spitäler oder Altersheime Vorrang haben müssen bei der Verteilung der derzeitigen Restbestände, verstehen alle. Dass Masken aber nicht essenziell beim Ausweg aus dem Shutdown sein sollen, versteht kein Mensch.

Im Westen ist man noch nicht gewohnt, im öffentlichen Raum Masken zu tragen. Das wird sich sehr schnell ändern.

Diese Krise wird das Land und seine Einwohner verändern; früher oder später werden wir uns auch an maskierte Mitmenschen gewöhnen. Noch zeigen wir vornehme Zurückhaltung, diese Art bürgerlichen Tabubruch zu begehen: das Gesicht — unser persönlichstes Merkmal überhaupt — voreinander zu verbergen. Wir sollten uns ein Vorbild an den Asiaten nehmen: Sie tragen ihre Masken als Zeichen der Höflichkeit und Solidarität.

Dieser Artikel wurde ursprünglich am 28. März 2020 in mehreren Schweizer Zeitungen veröffentlicht.

> Schweizer Journalist Andi Kunz auf Twitter


20. März 2020 — Downloaden, ausdrucken, aufhängen und elektronisch teilen:

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

Coronavirus: Symptome, Statistiken und tägliche Tracking.

Olafur Eliasson, The Weather Project, Turbinenhalle in der Tate Modern, London, 2003.

15. März 2020 — In der Tat, it’s the end of the world as we know it. Wir haben einige Informationen über die Symptome und den Zyklus des Coronavirus gesammelt. Alle Quellen finden Sie weiter unten.

Typische Symptome von Covid-19
Covid-19 verursacht typischerweise grippeähnliche Symptome wie Fieber und Husten. Bei einigen Patienten — insbesondere bei älteren Menschen und bei Patienten mit anderen chronischen Erkrankungen — können sich diese Symptome zu einer Lungenentzündung mit Engegefühl in der Brust, Schmerzen in der Brust und Atemnot entwickeln. Es scheint mit Fieber zu beginnen, gefolgt von einem trockenen Husten.

Nach einer Woche kann es zu weiterer Atemnot kommen, wobei etwa 20% der Patienten eine Krankenhausbehandlung benötigen. Insbesondere scheint die Covid-19-Infektion selten eine laufende Nase, Niesen oder Halsschmerzen zu verursachen (diese Symptome wurden nur bei etwa 5% der Patienten beobachtet). Halsschmerzen, Niesen und verstopfte Nase sind meist Anzeichen einer Erkältung.

80% der Fälle sind mild
Basierend auf allen 72.314 Fällen* von Covid-19 in China zum 11. Februar 2020:
— 80,9% der Infektionen sind mild (mit grippeähnlichen Symptomen) und können sich zu Hause erholen
— 13,8% sind schwer und entwickeln schwere Krankheiten wie Lungenentzündung und Atemnot
— 4,7% als kritisch und können Folgendes umfassen: Atemversagen, septischer Schock und Multiorganversagen
— 2% der gemeldeten Fälle sind tödlich
— Das Todesrisiko steigt, je älter Sie sind
— Relativ wenige Fälle wurden bei Kindern beobachtet

* Aus einem Forschungsbericht über bestätigte, vermutete und asymptomatische Fälle, der am 17. Februar 2020 vom chinesischen CCDC veröffentlicht und im Chinese Journal of Epidemiology veröffentlicht wurde.

Bereits bestehende Krankheiten, die das Risiko für Patienten erhöhen:
— Herzkreislauferkrankung
— Diabetes
— Chronische Atemwegserkrankung
— Bluthochdruck

Es muss angemerkt werden, dass einige ansonsten gesunde Menschen nach einer Infektion mit dem Virus eine schwere Form der Lungenentzündung entwickelt haben. Der Grund dafür ist unbekannt und wird noch untersucht.

Tägliche Verfolgung der Symptome

Erste 1–3 Tage 
— Die Symptome ähneln denen der Erkältung
— Halsentzündung
— Keine Grippe, nicht müde, immer noch normal essen

Tag 4
— Halsentzündung
— Erste Anzeichen von Krankheit
— Körpertemperatur steigt von 36.5° (variiert von Person zu Person)
— Der Appetitverlust beginnt, es ist schwer zu essen
— Leichte Kopfschmerzen
— Milder Durchfall

Tag 5
— Halsschmerzen, Husten
— Leicht heisser Körper, Temperatur steigt auf 36.5–36.7°
— Müde, schwindelig, Schmerzen in den Gelenken
— Dieses Stadium ist schwer als Erkältung oder Grippe zu diagnostizieren

Tag 6
— Leichtes Fieber beginnt, ca. 37°
— Kruppenhusten oder trockener Husten
— Halsschmerzen beim Essen, Sprechen oder Schlucken
— Müdigkeit, Übelkeit
— Das Atmen ist schwierig
— Möglicher Durchfall, Erbrechen

Tag 7
— Das Fieber hat sich erhöht, 37.4–37.8°
— Viel Husten
— Körperschmerzen, der Kopf fühlt sich schwer an
— Häufiges Erstickungsgefühl
— Mehr Durchfall
— Erbrechen

Tag 8 
— Fieber ist 38°+
— Schwer zu atmen, Kurzatmigkeit
— Weiterer Husten
— Kopfschmerzen, Gelenkschmerzen, Rückenschmerzen 

Tag 9 (in diesem Stadium sollten Blutuntersuchungen und Lungenröntgenaufnahmen durchgeführt werden
— Die Symptome verschlechtern sich
— Hohes Fieber
— Nicht husten, aber die Symptome verschlimmern sich
— Atembeschwerden

Die Symptome variieren je nach Widerstand und Immunität des Patienten. Es dauert 10 bis 14 Tage, bis sich bei einer gesunden Person Symptome entwickeln, bei einer Person mit gesundheitlichen Problemen nur 4 bis 5 Tage.

> healthxcenter.com

Beispiele für eine mögliche Entwicklung von Symptomen (aus tatsächlichen Fällen)

Ein Mann in den Vierzigern in Japan:
— Tag 1: Körperliche Beschwerden und Muskelschmerzen
— Später mit Lungenentzündung diagnostiziert

Ein Mann in den 60ern in Japan:
— Tag 1: Erste Symptome von leichtem Fieber und Halsschmerzen

Ein Mann in den Vierzigern in Japan:
— Tag 1: Schüttelfrost, Schwitzen und Unwohlsein
— Tag 4: Fieber, Muskelschmerzen und Husten

Eine Frau in den 70ern in Japan:
— Tag 1: 38° Fieber für einige Minuten
— Tag 2+3: Sie ist auf einer Bustour gegangen
— Tag 5: ins Krankenhaus eingeliefert
— Tag 6: Symptome einer Lungenentzündung

Eine Frau in den Vierzigern in Japan:
— Tag 1: Niedriges Fieber
— Tag 2: 38° Fieber
— Tag 6: Ist zu Hause behandelt worden

Ein Mann in den 60ern in Japan:
— Tag 1: Erkältungssymptome
— Tag 6: Fieber von 39°C (102.2°F)
— Tag 8: Lungenentzündung

Ein weiterer Patient in China mit Typ-2-Diabetes und Bluthochdruck in der Vorgeschichte:
— 22. Januar: Fieber und Husten
— 5. Februar: ist gestorben

Erster Tod auf den Philippinen (44 Jahre alte Chinesen, andere vorbestehende Gesundheitszustände):
— 25. Januar: Fieber, Husten und Halsschmerzen (ins Krankenhaus geliefert)
— Entwickelte eine schwere Lungenentzündung
— 2. Februar: ist gestorben

Wie lange dauern die Symptome?

Unter Verwendung der verfügbaren vorläufigen Daten wurde in dem am 28. Februar 2020 von der WHO veröffentlichten Bericht der Gemeinsamen Mission WHO-China, der auf 55’924 im Labor bestätigten Fällen basiert, die folgende mittlere Zeit vom Auftreten der Symptome bis zur klinischen Genesung beobachtet:

— Leichte Fälle: ca. 2 Wochen
— Schwere oder kritische Erkrankung: 3–6 Wochen
— Zeit vom Beginn bis zur Entwicklung einer schweren Krankheit (einschliesslich Hypoxie, Sauerstoffmangel an einem bestimmten Körperteil): 1 Woche

Bei verstorbenen Patienten liegt die Zeit vom Auftreten der Symptome bis zum Ergebnis zwischen 2 und 8 Wochen.

> 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).

> Palli Thordarson on Twitter
> Coronavirus Tech Handbook (in Deutsch)
> SARS-CoV-2 and the lessons we have to learn from it

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!

> Listen to Shadowplay

K’Werk-Programm 2020: Neon is the New Orange.

17. Februar 2020 — Die K’Werk Bildschule entstand im Jahr 2005 mit dem Ziel, im bildnerischen und gestalterischen Bereich ein den Musikschulen vergleichbares Bildungsangebot zu schaffen. Es richtet sich an Kinder und Jugendliche zwischen 5 und 16 Jahren, die ihre kreativen Fähigkeiten in einer experimentierfreudigen und konzentrierten Atmosphäre entdecken und entwickeln möchten.

Die K’Werk Bildschule ist Teil der Schule für Gestaltung Basel und damit ein öffentliches Bildungsangebot des Kantons Basel-Stadt.

K’Werk Programm 1. Halbhahr 2020, 48 Seiten, 2-farbig mit einem 4-farbigen Bildteil. Erhältlich bei K’Werk Bildschule: www.kwerk.ch oder direkt bei uns.

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.