How to Create a Less Dangerous (or More Dangerous) Covid-19 Virus.
What we can learn from evolution and other infectious diseases.
Evolution isn’t occasional huge jumps. It is tiny differences which give some members of a species a higher likelihood of more offspring that live to reproduce. Whatever is able to survive does. Whatever survives in the greater numbers is more common.
Most DNA organisms tend to mutate slowly, because they have a “proof-reading” system which catches many of their copying mistakes, RNA viruses like Covid 19 don’t have that mutation correction, so they mutate more frequently, perhaps thousands of times more frequently. The vast majority of those mutations soon die off, but a tiny percentage of them work better at reproducing themselves, and they soon dominate. Because of these mutations Covid 19 now includes a huge number of minor variations, and at least one significant one: Covid 19 strain (SG614) is felt to be about 10 times as transmissible (contagious), but not necessarily more virulent (severe), than the older (SD614) type.
Scientists have found excellent correlation between how a disease is spread and how dangerous it is. Diseases spread by vectors such as mosquitoes (eg Malaria, Dengue, Yellow Fever, Encephalitis), or by contaminated water (Cholera, Typhoid etc) or other vectors, tend to be much more serious than those which need their hosts to be up and around for its spread (eg Rhinoviruses, the common cold). Sexually transmitted diseases tend to be less severe where most people with them rarely have a new sexual partner than where new sexual partners are frequent. It makes sense. The longer it takes to pass to a new host, and the more transmission requires the host to be up and around, the more successful will be the strains of a disease which do not kill or immobilize the host too quickly.
Covid 19 has proven much more dangerous than its cousins SARS and MERS in spite of their considerably higher mortality, because Covid 19 is contagious before the hosts know they are ill.
According to Johns Hopkins Corona Resource Center, countries throughout the world have reported very different case fatality ratios — the number of deaths divided by the number of confirmed cases. Differences in mortality numbers can be caused by:
- Differences in the number of people tested: With more testing, more people with milder cases are identified. This lowers the case-fatality ratio.
- Demographics: For example, mortality tends to be higher in older populations.
- Characteristics of the healthcare system: For example, mortality may rise as hospitals become overwhelmed and have fewer resources.
- Other factors, many of which remain unknown.
One of those unknown factors may be inaccurate numbers reported.
But another may be that in different areas, different strains of Covid 19 dominate, and some of those strains may be more, or less, dangerous. The more careful we are about social distancing, mask use, contact tracing, etc, the slower and more difficult it is for Covid19 to be transmitted, the less severe Covid 19 is apt to be. Careless behavior allowing easy spread encourages more serious strains.
New technologies are allowing development of Covid 19 vaccines at an unprecedented pace, a small fraction of the time needed for previous vaccines. Hopefully effective vaccines will soon be readily available, and end the pandemic. But it is difficult to predict how effective Covid 19 vaccines will be.
Despite billions of dollars and decades of effort, there is still no effective vaccine for HIV, nor any expectation of one in the foreseeable future..
Flu vaccines have also been disappointing. Flu viruses quickly create many new serotypes — mutations different enough to need different antibodies, and therefore different vaccines, to protect against them. Each year researchers try to guess what serotypes to cover, (there are too many possibilities to cover them all) and their success has been variable and suboptimal. Although Flu and Covid 19 are both RNA viruses, previous corona viruses mutate more slowly to different serotypes than Flu does. But no one knows for sure what Covid 19 will do. Covid 19 viruses replicate very quickly. Each time the virus replicates is an opportunity for mutation, and the more viruses per host, the more hosts infected, the more people who get Covid 19 before vaccinations, and the fewer people able or willing to get the vaccines, the more chance the vaccines will not work perfectly.
One thing we can learn from previous vaccine success stories, is that for diseases with many variations, it is better to protect against whatever makes the disease dangerous, rather than against the organism itself. This works extremely well against bacteria like Diphtheria and Tetanus, which form potent toxins. Vaccinating against the toxin, makes producing the toxin a cost, rather than a benefit to the more dangerous strains. The harmless cousins infect and immunize people, which is why we have almost no Diphtheria cases in spite of less than half the adult population vaccinated against it.
But Covid 19 does not create a toxin, and so far, exactly how it kills patients is extremely puzzling and poorly understood. If and when those mechanisms can be understood, and if vaccines against Covid 19 turn out to be limited by mutations of surface antigens, as flu vaccines are, aiming vaccines at the source of harm may allow harmless versions of Covid 19 to finally end this pandemic. Until then, our treatment options and success against those mechanisms of harm will probably continue to improve, unless we are careless and foolish enough to let Covid 19 spread so quickly that its mutations race ahead of our vaccines and treatment.
So wear your masks, be careful, social distance, stay safe, help slow down the spread, and help push the virus toward less virulence.
Also, please pay attention to Science, and support its recommendations, along with public health and research. Although most doom and gloom predictions, luckily, prove false, a major pandemic just like Covid 19 has been predicted for some time. And the animal kingdom teems with pathogens to which we have no immunity. Some, not infrequently, spillover to other species including ours. So there are a startling number of possible Next Big One contenders for the pandemic after this one. Hopefully we will be better prepared next time.
Suggestions for further reading:
Spillover: Animal Infections and the Next Human Pandemic, by David Quammen
wwnorton.com › books › spillover
and
Evolution of Infectious Disease, by Paul W. Ewald
https://www.amazon.com/Evolution-Infectious-Disease-Paul-Ewald-ebook/dp/B000VDGQO0
