Chapter 3 — Why is this different from anything that we had in the last 100 years?

Short answer: Because the Spanish flu was 102 years ago.

Long answer: To answer this, we need to understand how a virus spreads.

Chapter Summary:

3.1 — What is Covid-19?

3.2 — What are the symptoms this coronavirus causes?

3.3 — We need to know how many people were diagnosed over time.

3.4 — The median duration between onset of infection and its diagnosis.

3.5 — The number of cases, on average, an infected person will cause during their infectious period.

3.6 — The relationship between viral concentration and disease severity.

3.7 — How the virus will mutate in the future

3.1 — What is Covid-19 — the illness that started in Wuhan in Dec 2019?

Currently, scientists still do not know COVID-19’s origin, though suspect it is zoonotic, meaning it likely started in an animal before spreading to humans.

It is caused by a member of the coronavirus family that has never been encountered before.

“Covid-19 is sometimes compared to seasonal influenza, and while seasonal influenza is responsible for 18,000 deaths this year alone, this is with vaccines, antiviral and having a portion of the population that's immune from severe disease because of previous exposure to the virus. We have none of these things at our disposal to battle COVID-19" — Johns Hopking Experts Brief Capitol Hill on Coronavirus — 5th March 2020

The name Covid-19 was announced on 11 February by the World Health Organization (WHO).

“We had to find a name that did not refer to a geographical location, an animal, an individual or group of people, and which is also pronounceable and related to the disease. Having a name matters to prevent the use of other names that can be inaccurate or stigmatising.” — Tedros Adhanom Ghebreyesu— director general WHO

If you have direct personal contact with an infected person, the probability of infection is between 1% and 5%. [source]

How fast does it spread?

31 January — 2 Chinese persons detected with the virus in Italy

6th of February — 1 Chinese citizen infected with coronavirus in Italy.

All three recovered until the 22nd of February. Everything looked ok.

But on the 21st of February, they discover 16 cases in Lombardia.

On the second day, 60 new cases. First dead on the same day.

On the 8th of March in Italy, 366 deaths, 133 just today.

The total number of cases in Italy as of 8th March: 7,375.

Some numbers from Vlad Coroama

“The weekly growth of infections outside China is 272%, this means that at this time next week there will be 3.7 times more infections than today.

In Europe the rate is 548%, so a weekly growth of 6.5 times bigger.

In China, the rate is down to 2% growth per week.”

https://www.statnews.com/2020/03/09/people-shed-high-levels-of-coronavirus-study-finds-but-most-are-likely-not-infectious-after-recovery-begins

Financial Times published on the 12th of march this article where they outline that the spread is similar among all countries, just the timing is different

“Case numbers since outbreaks began in several countries have tracked a ~33% daily rise. This is as true for UK, France, Germany as Italy; the latter is simply further down the path.” [source]

3.2 — What are the symptoms this coronavirus Covid-19 causes?

“The virus can cause pneumonia. Those who have fallen ill are reported to suffer coughs, fever and breathing difficulties. In severe cases, there can be organ failure.

As this is viral pneumonia, antibiotics are of no use. The antiviral drugs we have against the flu will not work. Recovery depends on the strength of the immune system. Many of those who have died were already in poor health.” [source]

After the SARS outbreak in 2002–2003, the World Health Organization reported that the disease typically attacked the lungs in three phases:

viral replication, immune hyper-reactivity pulmonary destruction.

“During the third phase, lung damage continues to build — which can result in respiratory failure. Even if death doesn’t occur, some patients survive with permanent lung damage.

According to the WHO, SARS punched holes in the lungs, giving them “a honeycomb-like appearance” — and these lesions are present in those afflicted by a novel coronavirus, too.” [source]

The below virus shoes how the Coronavirus actually kills the human host, and discuss three published papers that can reduce the mortality from 40% down to 16%.

And we need to acknowledge that a lot we don`t know, like Laurence Ion, was stating today 11th march on Facebook:

3.3— We need to know how many people were diagnosed over time.

During an epidemic, typically the number of diagnosed infections over time is known, because:

As more people fell sick, they will go to the hospital. The hospitals will report to the Centers for Disease Control and Prevention (CDC) of their country The CDC will provide the data to the WHO.

3.4— The median duration between onset of infection and its diagnosis.

For the 2009 H1N1 pandemic the median duration between onset of infection and its diagnosis was 5 days (range: 1–20).

2009 H1N1 Pandemic Timeline

⚫️April 15 — First human infection with new influenza A H1N1 virus detected in California.

⚫️June 25 — CDC estimated at least 1 million cases of 2009 H1N1 influenza had occurred in the United States.

In 2009, during the H1N1 pandemic, in the span of 71 days the US had gone from 0 to 1 million cases in the United States.

The time from when a person is exposed and infected with common flu to when symptoms begin is about 2 days but can range from about 1 to 4 days. Also, a lot of people are already vaccinated against the common cold, so this reduces the total number of cases every year.

The 1918 Spanish Flu had an incubation period between 2 and 7 days.

The “incubation period” means the time between catching the virus and beginning to have symptoms of the disease. Most estimates of the incubation period for COVID-19 range from 1–14 days, most commonly around five days. These estimates will be updated as more data become available.(WHO)

⚠️With COVID-19, we are talking about a new virus and we do not have immunity against it, that will spread much faster because infected people can carry the disease for one to two weeks before having any symptoms, also there are cases where the patients are asymptomatic, meaning that they will transmit to others, but will probably never know that they had carried the COVID-19 virus and infected other persons.

| Disease | between | and | period |

|----------------------|---------|---------------|--------|

| 1918 Spanish Flu | 2 | 7 | days |

| Influenza | 1 | 3 | days |

| Common cold | 1 | 4 | days |

| SARS | 1 | 10 | days |

| 2009 H1N1 pandemic | 1 | 20 | days |

| Coronavirus COVID-19 | 2 | 14 (up to 24) | days |

“A study involving 28 COVID-19 patients in Japan has shown that the virus’s serial interval — the time between successive cases — is close to or shorter than its median incubation period, suggesting pre-symptomatic transmission may play a key role in the outbreak and case isolation alone might not be as effective as hoped.

Serial interval estimated at 4.0 to 4.6 days

In the Japanese study, published in the International Journal of Infectious Diseases, investigators calculated that the time from symptom onset in a primary COVID-19 patient to symptom onset in secondary patients, or the serial interval, was 4.0 to 4.6 days.”

“When the serial interval is shorter than the incubation period, the pre-symptomatic transmission is likely to have taken place and may even occur more frequently than symptomatic transmission,” the authors wrote.

Six people infected in the assembly. Four deputies and two agents of the National Assembly tested positive for Covid-19, says the ARS. “Health surveys are under way and management measures have been taken by the Assembly services to limit the possible spread of the virus. AThey add, “The COVID-19 serial interval is also shorter than the serial interval of severe acute respiratory syndrome (SARS), indicating that calculations made using the SARS serial interval may introduce bias.”

Because of the shorter serial interval, “contact tracing methods must compete against the rapid replacement of case generations, and the number of contacts may soon exceed what available healthcare and public health workers are able to handle,” they wrote.

Of the 28 infector-infectee pairs, 12 pairs were parts of family clusters. [source]

3.5— The number of cases, on average, an infected person will cause during their infectious period.

How much will a disease spread?

The reproduction number, R0 for short, describes how many additional cases of a disease each infected person will cause during their infectious period. The numbers are a range because they depend on a variety of factors that vary from situation to situation.

It’s affected by the properties of the pathogen, such as how infectious it is, the environment, including things like demographics, socioeconomic and climatic factors.

What makes R0 useful in public health?

Demographer Alfred Lotka proposed the reproduction number in the 1920s, as a measure of the rate of reproduction in a given population.

In the 1950s, epidemiologist George MacDonald suggested using it to describe the transmission potential of malaria. He proposed that, if R0 is less than 1, the disease will die out in a population, because on average an infectious person will transmit to fewer than one other susceptible person. On the other hand, if R0 is greater than 1, the disease will spread. [source]



| --------------------------- | -------------------------- |

| Influenza | |

| (1918 pandemic) | 2 to 3 |

| H1N1 Influenza, 2009 | 1.46 to 1.48 |

| Seasonal Influenza | 2 to 3 |

| MERS, 2012 | around 1 |

| SARS, 2003 | <1 to 2.75 |

| Coronavirus COVID-19 | 1.4 to 4.08 | | **DISEASE** | **REPRODUCTION NUMBER R0** || --------------------------- | -------------------------- || Seasonal Influenza | 2 to 3 || MERS, 2012 | around 1 || SARS, 2003 | <1 to 2.75 |

The H1N1 Influenza, 2009 had a reproduction number R0 of 1.46 to 1.48

⚠️The reproduction number R0 for Wuhan Coronavirus 2019-nCoV is between 1.4 to 4.08

“Containment is becoming less likely, because of the contagiousness of the virus, the possibility that people can spread it before they have symptoms and the increasing number of outbreaks around the world. “ 29 February 2020 — NYTimes

What Worked in 1918–1919?

I will post in full the article written by Alex Tabarrok, as I consider this to be one of the most effective ways to contain the spread of the virus :

Alex Tabarrok March 7, 2020 at 4:25 pm

The influenza pandemic of 1918 was the most contagious calamity in human history. Approximately 40 million individuals died worldwide, including 550 000 individuals in the United States…[C]an lessons from the 1918–1919 pandemic be applied to contemporary pandemic planning efforts to maximize public health benefit while minimizing the disruptive social consequences of the pandemic as well as those accompanying public health response measures?

That’s the question Markel et al. analyzed in 2007 by gathering historical data on outcomes and what 43 US cities, covering about 20% of the US population, did to combat influenza in 1918–1919.

Nonpharmaceutical interventions were considered either activated (“on”) or deactivated (“off”), according to data culled from the historical record and daily newspaper accounts. Specifically, these nonpharmaceutical interventions were legally enforced and affected large segments of the city’s population. [1] Isolation of ill persons and quarantine of those suspected of having contact with ill persons refers only to mandatory orders as opposed to voluntary quarantines being discussed in our present era. [2] School closure was considered activated when the city officials closed public schools (grade school through high school); in most, but not all cases, private and parochial schools followed suit. [3] Public gathering bans typically meant the closure of saloons, public entertainment venues, sporting events, and indoor gatherings were banned or moved outdoors; outdoor gatherings were not always canceled during this period (eg, Liberty bond parades); there were no recorded bans on shopping in grocery and drug stores.

The authors define “public health response time” as the number of days from the day the excess death rate was double baseline to the day that at least one of their three key public health measures was implemented. Cities that responded very early have a negative public health response time. The basic result is shown in the figure below.

The longer the public health response time the greater the total excess deaths (the arrow is my least squares eyeball).

Moreover, although it’s difficult to control for other factors, cities that combined school closures, isolation and quarantining, and public gathering bans tended to do better. Some cities let up on their public health interventions and these cities seem to correlate well with bi-modal distributions in excess death rates, i.e. the death rate increased. Denver was an example where the public gathering ban was dropped and the school ban was lifted temporarily and the excess death rate rose after having fallen.

The authors conclude:

…the US urban experience with nonpharmaceutical interventions during the 1918–1919 pandemic constitutes one of the largest data sets of its kind ever assembled in the modern, post germ theory era. …Although these urban communities had neither effective vaccines nor antivirals, cities that were able to organize and execute a suite of classic public health interventions before the pandemic swept fully through the city appeared to have an associated mitigated epidemic experience. Our study suggests that nonpharmaceutical interventions can play a critical role in mitigating the consequences of future severe influenza pandemics (category 4 and 5) and should be considered for inclusion in contemporary planning efforts as companion measures to developing effective vaccines and medications for prophylaxis and treatment. The history of US epidemics also cautions that the public’s acceptance of these health measures is enhanced when guided by ethical and humane principles.

3.6 — The relationship between viral concentration and disease severity.

“A 29-year-old doctor in Wuhan has become the latest victim of the coronavirus as China reported infections in prisons in three provinces, as well as clusters in Beijing.

Peng, who had been featured in state media previously for delaying his wedding to continue working, was admitted to hospital on 25 January. His condition dramatically worsened by 30 January, when he was sent to the Jinyintan hospital in Wuhan for emergency treatment. He died on Thursday at 9.50pm, according to a statement from his hospital.”

Another Chinese doctor who tried to issue the first warning about the deadly coronavirus outbreak has died, the hospital treating him has said.

Li Wenliang contracted the virus while working at Wuhan Central Hospital.

He had sent out a warning to fellow medics on 30 December but police told him to stop “making false comments”.[source]

We don`t know yet what is the difference between persons that are just infected and develop the disease but remain in isolation and the doctors that spend more than half of their time in a hospital full of patients.

Do they have a higher chance of dying?

There is a correlation between how much are you exposed to the virus and your chances of dying? At the moment the answer is: “we don`t know”

Hopefully, in the following months, we will have an answer to this and other questions.

3.7 — How the virus will mutate in the future

Even if this is not confirmed in another lab, scientists from China say that the Coronavirus already mutated and we are now dealing with 2 forms of the virus.

“Coronavirus has mutated into two strains, one which appears to be far more aggressive, scientists have said, in a discovery which could hinder attempts to develop a vaccine.

Researchers at Peking University’s School of Life Sciences and the Institut Pasteur of Shanghai, discovered the virus has evolved into two major lineages — dubbed ‘L’ and ‘S’ types.

The older ‘S-type’ appears to be milder and less infectious, while the ‘L-type’ which emerged later, spreads quickly and currently accounts for around 70 per cent of cases.” [source]