Kurzgesagt – In a Nutshell

Sources Corona

Please note: we will put a comment under each of our sources that marks the date and time of retrieval. For the latest up-to-date sources on the development of the pandemic please refer to the WHO or the responsible website of your respective government.

#WHO advice for public:


( Last updated March 18, 2020)

#WHO Q&A on coronavirus:


( Last updated March 9, 2020)

#Coronavirus Resource Center, 2020


( Last updated March 18, 2020)

We would like to thank the following experts for their support:

  • Dr James Gurney

Doctor of Microbiology

  • Dr Max Roser (OWID)

Founder of Our World in Data

  • Dr Daniel Cornforth

Doctor of Evolutionary Biology

  • Professor Joshua Weitz

Director of the Interdisciplinary PhD in Quantitative Biosciences, Georgia Tech

For this video we got a lot of help from our friends from Our World in Data. In the past weeks they were working extremely hard to break down the complexity of this topic and to filter out the facts, what we know for sure and what we can not really tell at the moment. Their website on the Coronavirus is updated frequently and is based on official statements by the World Health Organization (WHO).

If you want to learn more about the global scale of the pandemic and what we actually know about it, check out Our World in Data.


( Last updated March 17, 2020)

Another note:

A lot of the sources are dealing with another coronavirus: SARS.

It is very likely that in general the mechanisms for infection and the impacts in the body are largely the same. We have tried to use papers that directly use SARS-CoV-2, but unfortunately the scientific community has not had sufficient time to fully study the novel virus.


– In December 2019 the Chinese authorities notified the world that a virus was spreading through their communities. In the following months it spread to other countries, with cases doubling within days.

China informed the WHO (World Health Organization) on December 31th 2019:

#Coronavirus disease (COVID-19) outbreak, 2020


Quote: ”On 31 December 2019, WHO was informed of a cluster of cases of pneumonia of unknown cause detected in Wuhan City, Hubei Province of China.”

(Last updated March 9, 2020)

On January 22th, there were 580 cases, two days later the number of confirmed cases had jumped to 1,317:

#Coronavirus Cases, total cases, worldometer, 2020


(Last updated March 19, 2020)

#Total confirmed cases of COVID-19, 2020


(Last updated March 17, 2020)

COVID-19 is the disease that the virus SARS-CoV-2 causes. It is also commonly referred to as Coronavirus.

SARS-CoV-2/COVID-19 is not the first Coronavirus. There are four main sub-groups and all together seven identified types of Coronavirus that can infect humans:

#Coronaviruses, 2020


(Last updated February 15, 2020)

One of them is referred to as SARS and it seems to show similar mechanisms as COVID-19.

This paper shows that SARS and COVID-19 are more closely related than SARS and MERS. Given how similar the diseases SARS and MERS were, it is not unreasonable to assume COVID-19 and SARS would be very similar. Especially the pathogenesis (how the disease is actually caused) seems to be closely related.

#Emerging coronaviruses: Genome structure, replication, and pathogenesis, 2020


Quote: “Most of the nsps of nsp1‐16 have been reported for their specific roles in the replication of CoVs. However, the functions of some of the nsps are unknown or not well understood. The known functions of the 16 nsps are summarized in Table 1.”

(Published January 21, 2020)

For example, this study shows that some of the non-structural proteins (nsp), which are present in SARS-patients are also present in SARS-CoV-2. Nsps form in a cell after it has been taken over by a virus and typically are what causes the symptoms of viruses. Nsp1 (responsible for IFN signalling reduction), nsp3 (blocks innate immune response and promotes cytokine expression), nsp16 (reduces innate immune expression) are for example present in both.

These virulence factors are evidence that a similar path to infection is occurring in COVID-19. The virus is down regulating the innate response and interfering with signalling.

This paper is a review article and presents some first hand data for COVID-19:

#The epidemiology and pathogenesis of coronavirus disease (COVID-19) outbreak, 2020


Quote: “Patients infected with COVID-19 showed higher leukocyte numbers, abnormal respiratory findings, and increased levels of plasma pro-inflammatory cytokines”

“The laboratory studies showed leucopenia with leukocyte counts of 2.91 × 10^9 cells/L of which 70.0% were neutrophils.”

(Published February 26, 2020)

This study also outlines some important findings which we know differ between SARS and COVID-19:

#The epidemiology and pathogenesis of coronavirus disease (COVID-19) outbreak, 2020


Quote: “Significantly high blood levels of cytokines and chemokines were noted in patients with COVID-19 infection that included IL1-β, IL1RA, IL7, IL8, IL9, IL10, basic FGF2, GCSF, GMCSF, IFNγ, IP10,MCP1, MIP1α, MIP1β, PDGFB, TNFα, and VEGFA. Some of the severe cases that were admitted to the intensive care unit showed high levels of pro-inflammatory cytokines including IL2, IL7, IL10, GCSF, IP10,MCP1, MIP1α, and TNFα that are reasoned to promote disease severity”

(Published February 26, 2020)

In SARS IL8 is noted as an important factor in disease progression. IL 8 is another cytokine that is important in the recruitment of neutrophiles, which in these disease will just cause more damage to the lungs.

# Severe Acute Respiratory Syndrome (SARS) Coronavirus-Induced Lung Epithelial Cytokines Exacerbate SARS Pathogenesis by Modulating Intrinsic Functions of Monocyte-Derived Macrophages and Dendritic Cells


(Published November 5, 2008)

The previous paper did not show IL8 being linked to ICU patients but it was still higher in all COVID-19 patients than in healthy people.

So while there are many similarities between SARS and COVID-19, the limited data we have so far suggests that IL8 might be more ‘important’ for disease in SARS than COVID-19. But the difference is likely to be highly detailed and obscure. It might take several years until we can describe the biochemical differences between these viruses in detail. Given that peer reviewed papers are making the same comparisons as we do we feel confident that this is both the best and limit of our current understanding of SARs-CoV-2 aka COVID-19.

If you are wondering how the name SARS-CoV-2 aka COVID-19 turned into the much catchier term Coronavirus – this name comes from the crown spikes. But the name is highly generic, calling this virus Corona is like simply calling all cat breeds from Tigers to Persians “kittens.” Coronaviruses are a family of viruses that can go from causing a very mild cold to diseases like SARS.

#Coronaviruses, 2020


Quote: “Coronaviruses are named for the crown-like spikes on their surface.”

(Last updated February 15, 2020)

xkcd has an idea how they really came up with the name (probably):


– A virus is really just a hull around genetic material and a few proteins.

#Viruses: Structure, Function, and Uses, 2000


Quote: “Most viruses have either RNA or DNA as their genetic material. The nucleic acid may be single- or double-stranded. The entire infectious virus particle, called a virion, consists of the nucleic acid and an outer shell of protein.”

(Published 2000)

– Corona may spread via surfaces, but it is still uncertain how long it can survive on them. Its main way of spreading seems to be droplet infection when people cough or if you touch someone who is ill and then your face, say, rubbing your eyes or nose.

It is pretty certain that the Coronavirus also spreads via surfaces. Once again, we assume this, because SARS is transmitted like this:

#Stability of SARS coronavirus in human specimens and environment and its sensitivity to heating and UV irradiation., 2003


Quote: “The results showed that SARS coronavirus in the testing condition could survive in serum, 1:20 diluted sputum and feces for at least 96 h, whereas it could remain alive in urine for at least 72 h with a low level of infectivity. The survival abilities on the surfaces of eight different materials and in water were quite comparable, revealing reduction of infectivity after 72 to 96 h exposure.”

(Published 2003)

When the video was produced there were no peer-reviewed studies asking how long the virus could survive on surfaces. This is why we were cautious with this claim in the video and based our knowledge on SARS. However, this paper, which was released as recently as March 17 2020 after the video basically finished, says that COVID-19 might survive better on cardboard than SARS, but the effect isn't very well replicated. The study is great evidence that the virus is capable of surviving much the same as SARS (up to 72 h) on most surfaces, which is what the video alludes to.

#Aerosol and Surface Stability of SARS-CoV-2 as Compared with SARS-CoV-1, 2020


Quote: “We found that the stability of SARS-CoV-2 was similar to that of SARS-CoV-1 under the experimental circumstances tested. This indicates that differences in the epidemiologic characteristics of these viruses probably arise from other factors, including high viral loads in the upper respiratory tract and the potential for persons infected with SARS-CoV-2 to shed and transmit the virus while asymptomatic.3,4 Our results indicate that aerosol and fomite transmission of SARS-CoV-2 is plausible, since the virus can remain viable and infectious in aerosols for hours and on surfaces up to days (depending on the inoculum shed). These findings echo those with SARS-CoV-1, in which these forms of transmission were associated with nosocomial spread and super-spreading events,5 and they provide information for pandemic mitigation efforts.”

(Published March 17, 2020)

Following the same logic, several health agencies have also warned about this detail of COVID-19:

#How it spreads, 2020


Quote: “Spread from contact with contaminated surfaces or objects. It may be possible that a person can get COVID-19 by touching a surface or object that has the virus on it and then touching their own mouth, nose, or possibly their eyes, but this is not thought to be the main way the virus spreads.”

(Published March 4, 2020)

#Infection prevention and control for COVID-19 in healthcare settings, 2020


Quote: “Due to the possible persistence of the virus on surfaces (including bodies) for several days[28], the contact with a deceased body without using PPE should be avoided.”

(Published March, 2020)

– Corona seems to spread via droplet infection when people cough or if you touch someone who is ill and then your face, say, rubbing your eyes or nose.

What we know for sure is that COVID-19 spreads via droplets:

#How COVID-19 Spreads, 2020


Quote: “The virus is thought to spread mainly from person-to-person.

  • Between people who are in close contact with one another (within about 6 feet).
  • Through respiratory droplets produced when an infected person coughs or sneezes.

These droplets can land in the mouths or noses of people who are nearby or possibly be inhaled into the lungs.“

(Last updated March 4, 2020)

– The lungs are lined with billions of epithelial cells.

#Strategies for Whole Lung Tissue Engineering, 2015


Quote: “This translates to 80 billion endothelial cells (largely microvascular), 60 billion interstitial cells, and 35 billion epithelial cells in the alveolar region alone. For successful lung tissue engineering, each category of cells will have to be provided for.”

(Published March 28, 2015)

– The cell, ignorant of what is happening, executes the new instructions, which are pretty simple: copy and reassemble. It fills up with more and more copies of the original virus until it reaches a critical point and receives one final order: Self destruct.

The copy-and-reassemble mechanism is how viruses generally replicate. They take advantage of the host cell and multiply within it:

#Virus Replication – An Introduction, 2003


Quote: “The essential steps of virus replication are similar for all virus classes: first, a virus particle (virion) must attach to the outer surface of the host cell. Next, it penetrates the cell membrane and enters the cytoplasmic environment. Some or all of the outer surface layers of the virus (envelope and capsid) are removed, so that the viral genome (DNA or RNA) becomes accessible to the cellular organelles and enzymes which will initiate the replication process. […] The newly synthesized viral nucleic acid and proteins are then assembled (maturation) into new viral particles which may leave the cells either by simple cell lysis [break down of the cells membrane, It’s basically dead] or by a budding process at the membranes of the outer cell surface or in the endoplasmic reticulum.”

(Published February 1, 2003)

Not all viruses kill the host cell, but COVID-19 is one of the viruses that does:

#Coronavirus Resource Center, 2020


Quote: “Once a virus enters a living cell (the host cell) and takes over a cell's inner workings, the cell cannot carry out its normal life-sustaining tasks. The host cell becomes a virus manufacturing plant, making viral parts that then reassemble into whole viruses and go on to infect other cells. Eventually, the host cell dies.”

(Last updated March 18, 2020)

– The number of infected cells grows exponentially. After about 10 days millions of body cells are infected and billions of viruses swarm the lungs.

# Pathology and Pathogenesis of Severe Acute Respiratory Syndrome, The American Journal of Pathology, 2007


Quote: “Histopathologically, the lungs in SARS characteristically show DAD [diffuse alveolar damage]. During the first phase of the disease (7 to 10 days), SARS lungs display the following features of acute exudative DAD”

(Published April, 2007)

– Cells have neither ears nor eyes, they communicate mostly via tiny information proteins called cytokines.

#Cell-Cell Communication Via Extracellular Membrane Vesicles and Its Role in the Immune Response, 2013


Quote: “Cell-cell communication is mediated by a complex network that includes soluble factors such as cytokines, chemokines, and metabolites exported from cells, as well as membrane-bound receptors and their ligands. “

(Published August 31, 2013)

– Two kinds of cells in particular wreak havoc: First, neutrophiles, which are great at killing stuff, including ourselves! First, neutrophiles, which are great at killing stuff, including ourselves! As they arrive in their thousands, they start pumping out enzymes that destroy as many friends as enemies.

In general neutrophiles can be of great help for our immune system: They are especially known for killing bacteria and fungi:

#How neutrophils kill microbes, 2005


Quote: “Neutrophils provide the first line of defense of the innate immune system by phagocytosing, killing, and digesting bacteria and fungi.”

(Published 2015)

But unfortunately, they also harm the host tissues:

# The balancing act of neutrophils, 2014


Quote: “releasing an arsenal of enzymes, antimicrobial peptides, and other molecules into the surrounding tissue. These include proteases that degrade virulence factors and toxins, lysozyme that degrades the bacterial cell wall, and antimicrobials like bactericidal/permeability-increasing protein (BPI), cathelicidins, and defensins that can kill bacteria directly. […] Once released, these molecules have powerful antimicrobial capacities, but they also harm the host tissue by collateral damage. ”

(Published 2014)

We talk about neutrophiles in the script for a good reason, they are recruited in large quantities. For reference, a normal white blood cell count would have around 1×10^10 white blood cells (upto which 70% could be neutrophils). So, the blood of COVID-19 patients has a low level of white blood cells – this is probably because they are all in the lungs. Given all the recruitment molecules, the cytokines, found in the lungs of COVID-19 patients, it is clear that a driving cause of damage in the disease is by the mis-recruitment of the neutrophiles to the lung.

#The epidemiology and pathogenesis of coronavirus disease (COVID-19) outbreak, 2020


Quote: “The laboratory studies showed leucopenia with leukocyte counts of 2.91 × 10^9 cells/L of which 70.0% were neutrophils.”

(Published February 26, 2020)

– Killer T-Cells usually order infected cells to commit controlled suicide. Confused as they are, they start ordering healthy cells to kill themselves too.

# T-cell mediated cytotoxicity, Immunobiology: The Immune System in Health and Disease, 2001


Quote: “Cytotoxic T cells kill their targets by programming them to undergo apoptosis”

(Published 2001)

A new study gives us more information about which types of T-cells are responsible for fighting COVID-19 in our immune system: It is CD8+ and CD4+ T-cells.

#Breadth of concomitant immune responses prior to patient recovery: a case report of non-severe COVID-19, 2020


Quote: “Bottom right histograms and line graphs, staining of granzyme A (GZMA (A)), granzyme B (GZMB (B)), granzyme K (GZMK (K)), granzyme M (GZMM (M)) and perforin (Prf) in parent CD8+ and CD4+ T cells and activated CD38+HLA-DR+ CD8+ and CD4+ T cells.”

(Published March 16, 2020)

If you want to know more about CD8 cells and how their antiviral response, this is an excellent article:

#Regulation of Antiviral CD8 T-Cell Responses, 2013


(Published 2013)

– This might get so bad that it can cause permanent irreversible damage that leads to lifelong disabilities.

#Report of the WHO-China Joint Mission on Coronavirus Disease 2019 (COVID-19), 2020


Quote: “Lung tissue also displayed cellular and fibromyxoid exudation,desquamation of pneumocytes and pulmonary oedema.”

(Published February 24, 2020)

#Long-term bone and lung consequences associated with hospital-acquired severe acute respiratory syndrome: a 15-year follow-up from a prospective cohort study, 2020


Quote: “Ong et al. evaluated the pulmonary function and health utility of 94 patients 1 year after being rehabilitated from SARS.17 The outcomes showed that 63% of the patients maintained normal lung function, with slightly reduced FEV1/FVC values in 5% of patients and moderately a reduced FVC value in one case. Of these patients, 18% and 3% had mildly and moderately impaired diffusion function, respectively.”

(Published February 14, 2020)

– The majority of people infected by Corona will get through it with relatively mild symptoms.

#Report of the WHO-China Joint Mission on Coronavirus Disease 2019 (COVID-19), 2020


Quote: “An increasing number of patients have recovered;as of 20 February,18264(24%) reported cases have recovered. Encouragingly, a report on 20 February from the Guangdong CDC suggests that of 125 severe cases identified in Guangdong, 33 (26.4%) have recovered and been released from hospital, and 58 (46.4%) had improved and were reclassified as having mild/moderate disease(i.e. + milder pneumonia).

(Published February 24, 2020)

As you can see in the figure provided by the WHO, a majority of infected people shows only mild symptoms and a vast majority recovers:

This paper, published on March 17th describes the immune system response in a relatively mild case of COVID-19

#Breadth of concomitant immune responses prior to patient recovery: a case report of non-severe COVID-19, 2020


(Published March 17, 2020)

A mixture of the adaptive immune response in the form of CD4+ and CD8+ t cells, antibodies (IgM and then IgG) removed the virus.

81% of infected people only show mild symptoms:


(Last updated March 17, 2020)

– But many cases become severe or even critical. We don’t know the percentage because not all cases have been identified, but it is safe to say that is a lot more than with the flu.

It is very hard to give a definite number of fatal cases, since not all cases have been reported. But based on the cases that are confirmed we can say that the death rate is around 3.48% globally, while higher in China than in the rest of the world:


Quote: “ Case fatality rate globally = 3.48% [based on 109,578 confirmed cases and 3809 deaths]

Case fatality rate in China: 3.86% [based on 80,904 confirmed cases and 3123 deaths]

Case fatality rate for the rest of the world: 2.39% [based on 28,674 confirmed and 686 deaths]“

(Last updated March 17, 2020)

The death rate for the flu is somewhere around 0.1%:

This graph from Our World in Data compares the death rate of COVID-19 to the death rate of the seasonal flu:


(Last updated March 17, 2020)

This is a recent study on COVID-19 (releases March 16, 2020). The researchers observed a patient with mild symptoms, provide valuable biochemical details of those symptoms and determine cd8+ and cd4+ as the T-cells responsible for fighting COVID-19 in our body.

#Breadth of concomitant immune responses prior to patient recovery: a case report of non-severe COVID-19, 2020


Quote: “Thus, the emergence and rapid increase in activated CD38+HLA-DR+ T cells, especially CD8+ T cells, at days 7–9 preceded the resolution of symptoms.“

(Published March 16, 2020)

– In more severe cases, millions of epithelial cells have died and with them the lungs’ protective lining is gone. That means that the alveoli, tiny air sacs via which breathing occurs, can be infected by bacteria that aren’t usually a big problem. Patients get pneumonia, respiration becomes hard or even fails and patients need ventilators to survive.


Quote: “SARS viral particles and genomic sequence were detected in a large number of circulating lymphocytes, monocytes, and lymphoid tissues, as well as in the epithelial cells of the respiratory tract, the mucosa of the intestine, the epithelium of the renal distal tubules, the neurons of the brain, and macrophages in different organs. SARS virus seemed to be capable of infecting multiple cell types in several organs; immune cells and pulmonary epithelium were identified as the main sites of injury. A comprehensive theory of pathogenesis is proposed for SARS with immune and lung damage as key features.”

“Multinuclear giant syncytial cells found in the alveoli contained a large amount of SARS viral sequences.”

# Role of Lung Epithel Cells in Defense against Klebsiella pneumoniae Pneumonia


Quote: “CPS allows the bacteria to evade both mechanisms, leading to pneumonia and dissemination of the infection.”

(Published March, 2002)

#Report of the WHO-China Joint Mission on Coronavirus Disease 2019 (COVID-19), 2020


Quote: “Symptoms of COVID-19 are non-specific and the disease presentation can range from no symptoms (asymptomatic) to severe pneumonia and death.”

(Published March 24, 2020)

– While the exact death rate is hard to pin down during an ongoing pandemic, we know for sure that it is much more contagious and spreads faster than the flu.

The contagiousness of a disease is measured with the so called reproduction number, which is the number of secondary infections generated from one infected individual. The reproduction number for the flu was estimated to be between 1.4 and 1.6.

#Modeling influenza epidemics and pandemics: insights into the future of swine flu (H1N1), 2009


Quote: “We discuss how the feasibility of controlling an epidemic critically depends on the value of the Basic Reproduction Number (R0). The R0 for novel influenza A (H1N1) has recently been estimated to be between 1.4 and 1.6”

(Published June 22, 2009)

While this study estimated the reproductive number for COVID-19 to be somewhere between 2.47 and 2.86:

#Nowcasting and forecasting the potential domestic and international spread of the 2019-nCoV outbreak originating in Wuhan, China: a modelling study, 2020


Quote: “In our baseline scenario, we estimated that the basic reproductive number for 2019-nCoV was 2·68 (95% CrI 2·47–2·86) and that 75 815 individuals (95% CrI 37 304–130 330) have been infected in Wuhan as of Jan 25, 2020.”

(Published January 31, 2020)

and the official WHO-study estimated it to be between 2 and 2.5:

#Report of the WHO-China Joint Mission on Coronavirus Disease 2019 (COVID-19), 2020


Quote: “The reproductive number –the number of secondary infections generated from one infected individual –is understood to be between 2 and 2.5 for COVID-19 virus, higher than for influenza.”

(Published February 24, 2020)

But the same WHO-study also gives us another interesting bit of information. The time for the flu to develop into being infectious might be shorter. So, a person who ‘catches’ flu might be able to spread it in 3 days, a person with COVID-19 may not spread the virus until day 5. Hence the WHO also notes:

#Report of the WHO-China Joint Mission on Coronavirus Disease 2019 (COVID-19), 2020


Quote: “This means that influenza can spread faster than COVID-19. “

(Published February 24, 2020)

The number of infected people per person is lower in flu, but can happen quicker. Still, COVID-19 seems to be more contagious in the sense that one infected person causes more infections.

– A FAST pandemic will be horrible and cost many lives. The worst case scenario for a FAST pandemic begins with a very rapid speed of infection, because there are no counter measures in place to slow it down.

Our World in Data illustrates the “worst case” scenario and the “best-case” scenario: The yellow line shows the number of cases in the worst case, the purple one shows the development if measures are taken to slow down the rate of infection:


– A pandemic is slowed down by the right responses, especially in the early period, so that everyone who gets sick can get treatment and there is no crunch time with overwhelmed hospitals.

There are a couple of historical examples for pandemics that slowed down quickly. The Spanish flu pandemic in the beginning of the 20th century for example was responded to in very different ways. Communities that acted quickly were far less affected than communities that didn’t:

#Rapid Response was Crucial to Containing the 1918 Flu Pandemic, 2007


Quote: “Cities where public health officials imposed multiple social containment measures within a few days after the first local cases were recorded cut peak weekly death rates by up to half compared with cities that waited just a few weeks to respond. […] Officials in St. Louis introduced a broad series of public health measures to contain the flu within two days of the first reported cases. Philadelphia, New Orleans and Boston all used similar interventions, but they took longer to implement them, and as a result, peak mortality rates were higher.”

(Published 2007)

This chart illustrates the different developments of the pandemic in St. Louis and Philadelphia. While Philadelphia went through with a big parade and saw a huge spike in infections and death rate afterwards, St. Louis reacted with closing schools, playgrounds and many other public facilities, limiting public transport and banning meetings of more than 20 people.

#Public health interventions and epidemic intensity during the 1918 influenza pandemix, PNAS, 2007


Quote: “ We obtained data on the timing of 19 classes of NPI in 17 U.S. cities during the 1918 pandemic and tested the hypothesis that early implementation of multiple interventions was associated with reduced disease transmission. Consistent with this hypothesis, cities in which multiple interventions were implemented at an early phase of the epidemic had peak death rates ≈50% lower than those that did not and had less-steep epidemic curves. “

(Published 2007)

#Lessons Learned from the 1918–1919 Influenza Pandemic in Minneapolis and St. Paul, Minnesota, 2007


Quote: “In reviewing this history, some lessons stand out. Recent analyses of nonpharmaceutical interventions during 1918 indicate cities in which multiple interventions were implemented early in the pandemic fared better.45 Of primary importance is developing a plan ahead of time that incorporates all levels of government health infrastructure and describes clear lines of responsibilities and roles. Plans for surge capacity and community containment must be discussed with stakeholders and consensus must be achieved.”

(Published 2007)

– Since we do not have a vaccine for Corona we have to socially engineer our behaviour to act like a social vaccine. This simply means two things: Not getting infected and Not infecting others.

Both, not getting infected and not infecting others, can be achieved via social distancing – which basically means staying at a distance from other people, working from home, cancelling meetings or gatherings and staying home as much as possible.

#Preventing COVID-19 Spread in Communities, 2020


Quote: “Currently a vaccine or drug is not available for COVID-19. Community-based interventions such as school dismissals, event cancellations, social distancing, and creating employee plans to work remotely can help slow the spread of COVID-19. Individuals can practice everyday prevention measures like frequent hand washing, staying home when sick, and covering coughs and sneezes. “

(Last updated March 18, 2020)

Harry Stevens, a graphic designer from the Washington Post, created a computer simulation that illustrates how social distancing can help to slow down the spread on his twitter account:

credit: Washington Post

This is an interactive simulation; go check it out for yourself here:


– The corona virus is encased in what is basically a layer of fat. Soap breaks that fat apart and leaves it unable to infect you.

#Guidance, COVID-19: infection prevention and control guidance, 2020


Quote: “As coronaviruses have a lipid envelope, a wide range of disinfectants are effective. PPE and good infection prevention and control precautions are effective at minimising risk but can never eliminate it.”

(Last updated March 13, 2020)

Thorough washing is crucial here – this is how you should do it:

#Clean hands protect against infection, 2020


(Last updated 2020)

If you have a hard time remembering how to do it, you can use this hand-wash-instruction-generator:


– The next thing is Social distancing. Which is not a nice experience but a nice thing to do. This means no hugging, no handshakes. If you can stay at home, stay at home to protect those who need to be out for society to function.

The WHO advises people to be more distant in their everyday lives:

#Advice for public, 2020


Quote: “When someone coughs or sneezes they spray small liquid droplets from their nose or mouth which may contain virus. If you are too close, you can breathe in the droplets, including the COVID-19 virus if the person coughing has the disease.”

(Last updated March 18, 2020)

Other advices include:

  • Avoid touching eyes, nose and mouth
  • Cough and sneeze in your elbows
  • If you have fever, cough and difficulty breathing, seek medical care early

– Quarantines are not great to experience and certainly not popular. But they buy us and especially the researchers working on medication and vaccination crucial time – so if you are put under quarantine, you should understand why and respect it.

You are most probably not in the risk group of suffering from severe symptoms or even from dying from the Coronavirus. But it is important to understand that you – even if you are not at risk – might be a risk factor for others, like people with critical medical preconditions. In the current situation you should not think of yourself but of others. Not only can this save lives, but on the scale of whole societies, it will also diminish the spread of the virus and help to keep infections low.

As the example of the Spanish flu in 1918 shows, quarantines and the cancellation of public events in an early stage can be a very effective tool against pandemics.

#Rapid Response was Crucial to Containing the 1918 Flu Pandemic, 2007


Quote: “Schools, theaters, churches and dance halls in cities across the country were closed. Kansas City banned weddings and funerals if more than 20 people were to be in attendance. New York mandated staggered shifts at factories to reduce rush hour commuter traffic. Seattle’s mayor ordered his constituents to wear face masks. The first study found a clear correlation between the number of interventions applied and the resulting peak death rate seen. Perhaps more importantly, both studies showed that while interventions effectively mitigated the transmission of influenza virus in 1918, a critical factor in how much death rates were reduced was how soon the measures were put in place.”

(Published 2007)

Pandemics have been occurring throughout human history. With our modern technology we have a great advantage compared to other historical examples, in terms of spreading prevention methods and communicating global strategies.

Basically to sum this all up: