by Morley Evans
My friend Dr Hardy has invited me to post his thoughts on the coronavirus pandemic. It is an honour to be so invited.
Coronavirus 2020
As a medical scientist, it comes as no surprise that many people have asked my opinion on the recent coronavirus pandemic. Therefore, I’ve decided to share what I have learned and try to include some of the most recent data available.
Probably the questions I’m most frequently asked are, firstly, why do health authorities and governments seem to take coronavirus more seriously than influenza which sickens, makes seriously ill and kills more people annually? After all, we don’t cancel travel, demand self-isolating and close schools and businesses from November through March every year.
And, secondly, how long might it go on for, how will it end and could it become a regular annual event like the flu?
Why do we fear the coronavirus more than the influenza virus?
If we exclude the most serious pandemics of 1918, 1957, 1968 and 2009, then typically the flu kills as many as 650,000 people every year whereas, at least to date, COVID-19 has been responsible for ‘only’ 150,000. I stress to date because we still don’t know what the final figure will be. However, we can compare the fatality rates which are the number of people who die divided by the number of people affected, most of whom will recover after a mild illness. For influenza, it is typically considerably less than 1%. For coronavirus, we still don’t have sufficient data to arrive at a definite figure. However, because of the typical lag time of 8 -10 days from diagnosis to death, epidemiologists are suggesting our best estimate of the fatality rate might be the number of deaths to date divided by the number of confirmed cases 9 days ago which comes to about 10%. That is ten times higher than that for the flu.
Another reason is that “the devil you know is better than the devil you don’t”.
We’ve had a long history of observing annual bouts of influenza and accumulating enormous amounts of data. In the Northern hemisphere at least, I’d put money on the flu season starting in late fall and concluding in early spring. I can think of three reasons for this. In winter we spend more time indoors when closer contact with others facilitates transmission of respiratory infections. The virus lives longer indoors because the air is less humid than outside and the longer the virus is ‘alive’ in the air, the easier it is for people to inhale it and become infected. In comparison, the coronavirus is completely new to us and even our experts are quite literally learning as the pandemic evolves. And, finally, herd immunity is more readily achieved for the flu than it is for COVID-19. Herd immunity describes the state when enough people in a community are immune that the virus has nowhere left to go and simply dies out. To achieve herd immunity, the percentage of those who need to be immune increases as the disease becomes more infectious. As an example, measles is extremely infectious and requires 90-95%, polio and influenza rather less so at 80-85%. One optimistic early estimate has suggested that 50% of us will need to acquire immunity to coronavirus before we can rely on significant protection from herd immunity. There are two good reasons why this is not going to happen soon. Herd immunity comes from two sources: immunity acquired after recovery from infection and immunity acquired from vaccination. Once again it’s too early to know what level of immunity and for how long it will last in people who have been infected and recovered but early signs are not encouraging. In Italy and South Korea, people confirmed to have a coronavirus infection both clinically and by testing positive and who then tested negative after recovering are now testing positive again. Either coronavirus can lay dormant and come back after a few weeks (rather like herpes zoster that causes chickenpox in children and can return decades later to cause shingles in adults) or more likely immunity after an infection is temporary at best. I prefer the latter explanation if only because several previous studies have found that immunity acquired from coronavirus infections is generally shorter-lived than that from other viral infections. Time will tell.
Of course, as yet there is no vaccine for COVID-19 although scientists all over the world are working hard to develop one as soon as possible. Fortunately, we’re not starting from scratch since a tremendous amount of work on coronavirus vaccines has been carried out over the past few years in the expectation that we would almost certainly see another novel virus following our experiences with SARS (2002) and MERS (2012). The CDC has suggested that we might have a usable vaccine by September of this year sufficient to treat medical staff and first responders with enough for the rest of us by next spring. Before, then, of course, it will have to go through the usual three stages of clinical trials to confirm both safety and efficacy. My concern is that, as happens with the flu vaccine every year, the anti-vax brigade will take to social media in an attempt to convince people not to take it. Believe it or not, it’s started already. One recent internet gem* is claiming that the coronavirus vaccine will actually contain microchips so that ‘they’ will be able to track all of our movements and exert some form of mind control! I wish I was joking.
When is it all going to end?
I wish I knew so that I could go ahead and rebook the vacation I’ve just had to cancel! There’s really no timeframe yet but I can give you an idea of a few factors, some preferable to others, that might bring it to a close. The first is that it miraculously mutates into a less lethal form and, while still around, becomes no more harmful than the common cold. I doubt anyone seriously believes this with the possible exception of King Donald. In fairness, however, there is a tendency for novel viruses to mutate in such a way that they do gradually become less lethal. Their function in life, if they actually were ‘alive’, would be to go forth and multiply (Genesis 9:7) and to kill their host would be to commit suicide, a distinct evolutionary disadvantage. It’s possible, of course, that, like the influenza virus, warmer weather and increasing humidity is not to its liking. It could simply fade away during the summer months but this would not stop its return, once again like the flu, in the fall and winter when we could be back to square one. There’s no doubt that travel bans, social distancing, contact tracing and staying indoors will reduce the spread of the virus but that’s not something we can do forever. The concern is that once we relax these restrictions and the virus is still out there then it will begin to re-infect people and return as a second wave possibly more deadly than the first if our experience of the Spanish flu (1919) is anything to go by. Developing herd immunity is by far our best bet but, as I’ve previously said, a prior infection may not be sufficient and, even if it were, we’re a long way off from achieving even a 50% infected, recovered and now immune population. We know this thanks to some new data from Iceland* with a tiny population of only 364 thousand but who have recently tested a random selection of 36 thousand people selected from the phone book representing almost 10% of its inhabitants. Of these, only 1700 tested positive which is less than half of one per cent of the population, a long way short of the very conservative estimate (50%) needed to achieve herd immunity.
Finally, I’d like to share with you the concept of Rzero, usually written as R0. This is the average number of new cases resulting from infection by each infected individual before they are no longer infectious. Two factors determine the size of R0: it increases with the ‘infectiousness’ of the virus and also with the number of susceptible (non-immune) people the affected individual comes into contact with. We can’t influence the former but we can reduce the latter which explains why staying at home and social distancing are so effective. Let me give you an example. Imagine R0 is exactly 1.0. This means that each infected person infects just one other before they are no longer infectious. If we start with 100 infected people and allow five cycles of infection, there will still be 100 infected, but different, individuals. R0 values greater than 1.0 will see disease numbers increase exponentially while values below 1.0 will see them decline. Preliminary data from the United Kingdom at the beginning of the coronavirus pandemic suggest an R0 value of about 2.5. Starting out with the same one hundred infected individuals, after the same five cycles, the number of infectious cases will have risen to almost ten thousand. After several weeks of social distancing, contact tracing, stay-at-home rules, closing schools, workplaces, sports and entertainment venues etc, R0 had fallen to about 0.6. Under these conditions, the original one hundred cases had fallen to only eight. Clearly, the preventive measures we have been taking are very effective but likely only as long as they are maintained.
Like it or not, permanently emerging from this crisis will almost certainly depend on the development of a safe and effective vaccine as soon as possible and when it finally arrives I’ll be first in line to receive it. Until then stay safe and I wish you all well. Please feel free to share this with others.
Dr Michael Hardy April 17th 2020
* Thanks to Aisling Young for bringing the Iceland data to my attention and to Gianna Manca for the coronavirus vaccine-microchip ‘conspiracy theory’.
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