Providing communities with accurate, timely and logical information about coronavirus is essential to avoid complacency and panic, writes Professor John Dwyer.
THE GLOBAL epidemic of infections with a unique member of the family of so-called “corona” viruses, COVID-19, is responsible for much illness and death, threatening recession, disrupting supply lines and changing everyday living patterns for millions.
Harm reduction at this time requires us all to understand the characteristics of the responsible virus, the factors associated with its dissemination into our communities and the actions we must take to protect ourselves and others.
COVID-19: The villain of the piece
Life and living are inextricably linked to replication. We humans reproduce billions of new cells every day to keep us living. Our cells contain all the genetic information and machinery required to reproduce themselves. Viruses cannot do this. These tiny, almost living entities, contain the genetic information they need to reproduce but not the machinery (factory) to set up the production line. To reproduce therefore they have to invade a cell that contains the necessary machinery and instruct it to reproduce them. Viruses are parasites. The mechanism used to invade an unwilling host cell is all-important to this discussion about the current epidemic.
A simple analogy would see us thinking of a virus in terms of the common “memory sticks” we use to store information we can introduce into a computer. The characteristics of the memory stick, relevant here, are its ability to store a message in code and the precise three-dimensional shape of the projection that can slip exactly into the accepting portal on the computer. Once tightly fitted, the computer can read the message on the stick and respond.
Electron microscope pictures show that the coronavirus has tightly coiled proteins on its surface from which it gains its name. Those “crowns” are equivalent to the “male” projections on the memory stick. If they could find a cell with the three-dimensional “female” equivalent, they could bind to the cell’s surface as a key in a lock. In nature, such binding usually signals to the cell that it should swallow the bound structure!
The surface of the cells in our lips, nasal passages, mouth and respiratory tract and lungs have just such a structure — an angiotensin-converting enzyme (ACE) receptor. The virus enters and takes over the reproductive machinery issuing instructions in its RNA genetic code creating many new viral particles.
The invaded cells lining our nasal passage and airways are much irritated by this invasion, and as our nose "weeps" and we cough or spit, we spray newly-created viruses into the air whence they fall onto surrounding surfaces. Once there, the viral structure is maintained for between nine and 12 hours. If we touch the virus it can stick to our skin. If we then touch our mouth, nose, lips and so on, the virus can bind to the ACE receptors and we are infected.
These viruses are very good at doing just that, which is why they are so contagious. The logic of recommending frequent thorough hand washing and the avoidance of unnecessary hand contacts between individuals is obvious.
Importantly, a face mask will reduce our shedding of infected secretions, but not completely. But standard face masks give us little protection from the tiny airborne viruses distributed from an infected person. If viruses are caught on the mask and we then adjust the mask, our hands become contaminated. We could be making things worse, not better — hence the recommendation that the general population does not use masks.
What happens to us after we are infected?
When I started training in immunology in the late 1960s, the cause of the symptoms which follow infections was not certain. If you have a cold, is the virus itself responsible for the symptoms – the fever, headaches, chills, cough and so on – or is it the infection-fighting chemicals released by our immune systems?
We now know that, in most cases, the immune response is the culprit. Our immune systems recognise "foreignness" and take steps to eliminate invaders. Cells which recognise the problem release chemicals which activate other cells to fight off the invader. Those chemicals, such as interferon – used to treat a number of serious infections – can make us feel unwell as they activate some cells to make antibodies and others to kill infected cells.
Antibodies are proteins with a three-dimensional structure that allows them to bind to their target, again like a key and a lock. In the case of the coronavirus, we must produce antibodies to the "crown" proteins. Blocking them stops them from invading our cells. A successful vaccine against COVID-19 will probably involve the production of antibodies to these "crowns".
Crucial to a satisfactory immune response is the axiom, the punishment must fit the crime. Evolutionary biology has provided us with the ability to regulate our immune responses. Under and over-responding can both be disastrous. How important is this for our understanding of the seriousness of the risks associated with COVID-19 infections?
Clinical manifestations of COVID-19 infections
Much controversy characterises discussion about this coronavirus’ mortality rate. We can’t be sure, but it is probably in the 1-3% range. Uncertainty is inevitable, as we do not and cannot know the total number of infected people. We do know that, for most people, the infection will be minor, akin to that from the common cold virus.
What is really important, however, is the reality that, for some groups, the death rate is between 10% and 15%. Understanding much more about these vulnerable people is essential for developing tactics to minimise their exposure to the virus and for planning their needed health care services.
Young, apparently healthy individuals can die (Dr Li Wenliang, who alerted the world to the emerging crisis, was 35 when he died). The two common factors which appear to be associated with severe illness and fatal outcomes are ageing and the co-existence of other compromising illnesses, such as heart, lung and kidney disease. Emerging data suggest that older men are at greater risk than older women.
We are not yet certain, but there is strong evidence that individuals older than 70 – but otherwise healthy – have poorly regulated immune responses to COVID-19. This can result in an excessive immune response, damaging the lungs and other tissues. The same phenomenon, plus comorbidities, might be in play with older, sicker individuals.
Given the above priority must be given to tactics to minimise the chances of older, sicker Australians encountering the virus, it is important for the infected (but relatively well) to stay out of circulation for two weeks. We are asking for an unusual degree of societal responsibility from such individuals and for those who, in so doing, would suffer financial hardship (for example casual workers), an emergency payment would be appropriate. Similarly, we need employers to be flexible when schools and childcare facilities are closed as a precaution, disrupting arrangements that allow parents to work.
Much deserved criticism has descended on U.S. President Trump’s ignorant advice that people with mild infections could still go to work. Their first encounter for the morning with a vulnerable colleague at the coffee pot could result in a fatality.
Also unconscionable was Trump’s refusal to allow 3,500 passengers on a cruise ship known to have a number of infected guests, to disembark because he did not want the number of U.S. infections to rise. Experience with the Diamond Princess off the coast of Japan demonstrated that the conditions on such ships ensure that the infection rate among passengers will steadily increase, with deaths to be expected, given the average age of cruise passengers. Fortunately, disembarkation has now occurred.
It is reasonable, at the moment, to suggest that older Australians limit unnecessary exposure to the broader community (meetings, travel, shopping centres and so on), while special attention is given to infection-control strategies in nursing homes and aged care facilities. These have a serious shortage of trained health care professionals; staff often having little or no knowledge of the infection control measures necessary for the protection of older residents.
Suggestions for "FaceTime" family visits make sense. While total control of all risk is impossible, harm reduction is not — this is being pursued vigorously and appropriately, if not as quickly as one would like.
Professor John Dwyer is an immunologist and Emeritus Professor of Medicine at UNSW. This article was originally published by 'Pearls and Irritations' and is republished with permission.
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