Two bobs on COVID from Dr Alan...
At the risk of boring you all senseless, I am going to add my two bobs worth into the corona virus mix, for what it’s worth, as we are all – even the experts, dare I say – speaking from positions of tenuous worth...yet here it goes.
From my reading of the various reports produced by my learned colleagues, I gather we are currently facing COVID19 type A, B, and C strains, with substrains of each type in all of the regions in which it has emerged. It is not too hard to imagine how this could be. When you understand that a human host infected with a strain of a corona virus can generate trillions of viral particles, one can imagine that the generation of this number of particles is likely to produce some variants of the genome and structural components, so called mutants. Most of these mutations are likely to lead to virus particles that are non-viable, but among those potential millions of mutants, there is the potential to generate viable variants. Those mutants less pathogenic for the host may thrive, given that it is not in the best interests of a virus to harm its host, as this may sicken the host and limit viral spread. The most efficient and effective viral parasites are those you are unaware you are carrying, and hence you freely interact with your peers, providing the opportunity for contact with new hosts to the passenger you unwittingly carry.
The more lethal the virus to its host, the less likely it will spread widely, given the reduction of potential hosts from attrition, and the lower likelihood of a sick host moving freely among their peers and transmitting the virus.
COVID-19 has now been renamed by the authorities who give viruses their official titles (The International Committee on Taxonomy of Viruses) as SARS CoV 2, given that it is a member of the same family of viruses that gave us SARS and MERS (Severe Adult Respiratory Syndrome and Middle Eastern Respiratory Syndrome), and that has come from a long taxonomy of corona viruses dating back, I gather, to at least 8000 BCE in the fossil record1. There are at least four coronaviruses we have known about for many years that contribute to the common cold syndrome, which produce mostly mild coryzal symptoms, spread readily, and are clearly well adapted to their human hosts.
The three more lethal strains of coronavirus that have arisen recently (MERS CoV, SARS CoV 1, and SARS CoV 2) are clearly less well adapted to their host, and have greater lethality. It is interesting that the SARS CoV 2 is less lethal to humans than SARS CoV 1, its predecessor. This makes sense when we understand the evolution of viruses in the human host; towards a more peaceful coexistence, for the benefit of the virus’ persistence in the host population, and for the ongoing survival of the host. Let’s face it, a 100% lethal virus is likely to wipe out its host population, and expire with us.
Another fascinating aspect of the SARS CoV 2 organism is the suggestion that children in particular may be relatively resistant to colonisation with the virus, or certainly do not seem to express the virus in the same manner as adults, and, indeed, may not spread the virus as readily as first thought. This thinking underpins the push to have children back in schools in the near future, although I stress this is, at present, a clinical impression, and has not been convincingly demonstrated by clinical studies.
There is an observation in the UK that children exposed to SARS CoV 2 may have a low risk of developing vasculitic complications, the so-called Kawasaki syndrome being probably the best known. This is a condition where the human response to the virus generates inflammatory changes in the small blood vessels of the body leading to tissue injury from hypoxia. Remember, the blood vessels act like Australia Post, delivering nutrients and oxygen to your tissues, much as Australia Post delivers your online shopping. If your blood vessels stop working, so do your body parts as they run out of fuel. While one may not expire if your parcel fails to arrive, expiring body parts may well lead to expiry of the whole without intensive clinical management.
Gratefully, this appears to be a very rare complication with only a dozen or so cases described in the UK and Europe. What is the risk? We don’t know, as we do not have studies to tell us how far the virus has spread among the world’s children as yet. As a very rough guess, it would seem to be of the order of one case per hundred thousand children infected, or so. Best guess at this point.
Our own government is undertaking a study of sorts with the drive to test people widely over the next two weeks, symptomatic or not, and the widespread screening of health staff, with a view to trying to gain an understanding of how far the virus has penetrated our population. Then we may have some idea, however limited, of the relative risk of contracting the virus that each of us faces.
So, where are we going with this virus? Why has the overseas experience been so variable, and why have we been relatively spared? Good question. The straight answer: I don’t know. I suspect the virus does spread widely with likely very mild symptoms or perhaps even no symptoms in some hosts, and only announces its presence when a cluster of vulnerable people are exposed, with predictable significant morbidity (illness) and mortality (death). As such, in those populations with very high death rates, such as the USA, the UK, and Europe, my suspicion is that the virus penetrated those populations much more widely than was previously thought, and hence the death toll seemed to ‘take off’ as exposure finally infiltrated the more vulnerable fractions of the population. As a more geographically isolated population, more diffused and less travelled, I suspect, than our northern colleagues, we have experienced a lesser penetration by this virion. And yet, we are not spared by any means, as the slow but steady rise of case numbers and deaths attest.
Will a vaccine save us? Hmmm…
An excellent article in The Medical Republic (27 April 2020) authored by Ms. Penny Durham2, and contributed to by some of Australia’s leading virologists and vaccine researchers, painted a realistic picture of the challenges they face in engineering a vaccine to address SARS CoV 2. Similar to the influenza virus (a highly variable virus), the most common vaccine target particles (the surface proteins) seem to be the most variable, and hence one engineering a vaccine to ‘fit’ the target protein will likely find that it has mutated during development, and that the vaccine needs to be re-engineered to fit the latest iteration. Virologists must be eternally patient, having struggled through the process to identify a target molecule, engineered an effective vaccine to address the target molecule, trialled it to demonstrate efficacy (effectiveness), only to find the virus has mutated in the host population in the meantime and that the vaccine no longer works on the latest version of the virus…and then, back to square one!
If a vaccine is achievable, and this is still an ‘if’, we may find ourselves in the same position that we are with the influenza virus, needing to redevelop the vaccine periodically to address changes in the viral coat proteins, with the possibility of only short-term vaccine efficacy (effectiveness), and the need for periodic revaccination.
If viral evolution with SARS CoV 2 mirrors that of its many viral predecessors, it is likely that the virus will attenuate over time, towards a more harmonious existence with its host. Though, how long that might take, and how many of us may succumb in the meantime, remains a frightening rumination.
As a member of the target group with the highest mortality so far (males, aged 50 to 70), I am electing to face this in the same manner I face the everyday threat of riding my motorcycle to work. Should my time come, then let it be so, but for now I have far too much to live for to waste any of the time I have left on the contemplation of my end. Deal with that when it happens...or not, as the case may be.
‘til we meet again…
Dr Alan Underwood.