COVID-19 R and more (13/05 update)

28/05 - Apologies for the font size ... it happened when I switched to the new blogger format!

In the earlier post on Life in the Time of Corona, I remarked that some calculations (back of envelope stuff) were probably simplistic and since then I have been trying to catch up a little with my understanding of the R number. I have edited the section in my earlier blog post but thought it might be useful to put the bare bones of R here, as well. As before, I shall update this as more information becomes available. I'm also expanding this post to cover some other biological aspects of COVID-19.

R0 and R (my own understanding)


The R number is a shorthand method of estimating viral contagion. In order to spread, the virus must reproduce itself in the host and then be transmitted to another host. If it cannot transmit itself to more than one new host the contagion cannot take hold. Where a population is completely susceptible (as in a novel disease, such as COVID-19) the basic reproduction number is given by R0. For contagion to happen R0 must be greater than 1. The higher the R0, the more contagious the virus is (measles R0  is often cited as being between 12 and 18). Once there is some immunity in a population R0 becomes R, the effective reproduction number, which is less than R0. Separately, by lessening the susceptibility of the population (e.g. by social distancing) R can be manipulated and further reduced. The combination of the two processes can lessen R to less than 1 and the contagion be halted. This is 'herd immunity'.

Initially, R0 for COVID-19 was put at 2-3, which with 60% immunity reduces R to between 0.8 and 1.2. However, as knowledge about COVID-19 increases, so it seems does its R0 value. One estimate is that R0 is nearer 5.7 which requires 82% immunity to reduce the R figure to ~1 [The calculation is R = R0 x, where x is the % susceptibility].

Potential Deaths in the UK

Even while R0 was regarded as 2-3, it was the 500,000 deaths that made Johnson suddenly drop 'herd immunity'. Now, if a 1% mortality rate of 60% of the population results in 500,000 deaths, for 82% this would rise to over 680,000.

Mortality Rate

Above I used Neil Ferguson's figure for mortality rate. This figure will need updating but WHO as of 3/03 were estimating a rate of 3.4% globally. Comparing mortality rates is hugely difficult as most are co-morbidities with other health issues, such as compromised immune systems. Also, while most mortality may be indirect there are concerns that there may be direct effects as well (see Cause of Death, below). The finding that BAME deaths are disproportionately higher than in the general populace puts a spotlight on the inequalities in society.

Immunity

There is still little information on immunity - its quality and longevitiy.

Cause of Death

Early on in the pandemic, it was considered that the major effect of COVID-19 was to create a 'cytokine storm' in the patient's immune system, leading to sepsis and organ failure. This is now being questioned as the virus seems to have direct effects in some cases. Additionally, the possibility of evolution of the virus (SARS-CoV-2) itself could be a concern.

SARS-CoV-2 Evolution

There is clear evidence from genetic marker studies that the virus has a zoonotic origin, with indication that bats may provide a reservoir of the progenitor which this study (with Rhinolophus affinis as the bat species) indicates may have involved pangolin as an intermediate.


Random Notes

1. How does a virus transmit from bats to pangolins?  ... faecal matter; and are the pangolins diseased? ... yes (in this article)

2. The pangolins coronavirus (Pangolin‐CoVs) was found in sick pangolins in October 2019 at the Guangdong Wildlife Rescue Center (+800 km from Wuhan). Could the 'wet market' at Wuhan be a mistaken epicentre for the disease?

3. Also could the pathogenicity of the virus have increased through mutation within a human host? The question is raised here as one of two scenarios.