Let’s get one thing straight. In terms of capacity to kill you SARS-CoV-2-19 is an extraordinarily weak virus.
The fatality rates being thrown around are all over the place, 8% for Italy, 3.4% from WHO, 2% from the early days for China. But there is a good reason to believe all of these are nonsensical. They’re accurate for what they represent, which is the ratio between recorded instances of infection and fatalities where infection was present, but they are absolutely not the fatality rate of either the SARS-CoV-2-19 infection or even of the COVID-19 disease.
Data from Italy suggests the median age of fatalities is 79.5 years, where Italian life expectancy is 82.5 years. Of the 2500+ victims, only 17 were under 50. Also, 99 percent of all fatalities had pre-existing conditions. True enough, Italian health authorities were rather liberal in their inclusion of “pre-existing conditions” counting even often rather benign conditions like high blood pressure. But there is something else you have to consider:
48.5 percent of those died had 3 or more illnesses and 25.6 percent had at least two
The thing about statistics of natural phenomena is that there’s a sea of difference between something occurring 95% of the time and 99% of the time. For example, at a normal distribution to go from covering 95% of the population to 99.7% you need to go from 2 standard deviations to 3. If 90 percent of fatalities had at least one pre-existing condition I’d think nothing of it, but tell me it’s 99 percent (!) and you’ve got my attention.
So then, how is it that a viral disease that according to empirical data collected by Italian health authorities has the capacity to kill only the most enfeebled of us is stacking up a kill rate of 2, 3.4 or 8 percent? Simple: It isn’t.
In fact, this data indicates that SARS-CoV-2-19 is very similar to other coronaviruses in that it represents next to no risk to a healthy individual, but can stack up a body count when it encounters a population that is particularly frail:
…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 U.S. 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.
In fact, the actual infection death rate is almost certainly below 1%, possibly as low as 0.05% (a death rate of 1 in 2000):
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 U.S. 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 U.S. population vary from 0.05% to 1%.
Keep in mind that a virus is driven only to multiply and to spread. To accomplish that it has to sneak past your immune system, or disable it, or fight it, but it doesn’t gain anything from killing the host. To the contrary, it needs the host to replicate itself further and, as it does not have cells of its own, to even fully exist. Evolutionary successful viruses, which the coronaviruses are, do not cause massive damage to the host — albeit the damage they do cause may be enough to push someone who is already frail over the edge.
Ah, but supposedly SARS-CoV-2 is a new specimen from the coronavirus family that has mutated in a way that for it this is no longer holds true. That is possible in principle, but as we’ve seen above that isn’t where data is pointing to.
Of course, even if it is no more lethal than some of the other coronaviruses that we make zero fuss about SARS-CoV-2 could still be a uniquely dangerous threat if it was far more contagious. I wonder if that is true either. Sure the figures on its spread that media is serving daily look impressive when they’re served in a vacuum and when that is everything anyone talks about and looks at. But what is the context? How would those numbers look like served side-by-side with numbers on your run-of-the-mill influenza pandemic that we’re hit with each winter?
And who is to say this spread started only just now? Seeing just how mild and non-lethal the SARS-CoV-2 is, is it possible it was already present but we just didn’t notice it, and what we’re following right now isn’t so much its spread, but rather its discovery, detection, and mapping?
After all, it’s not as if coronaviruses had not been killing high numbers of frail people all along:
In the U.S., 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.