There are a couple of misapprehensions here. First, the S glycoprotein (the ‘spike’) is what facilitates the virion entering a cell but it is not what makes the virus pathogenic (causing symptoms and illness); the nucleaocapsid (N) protein is the structure that contains the RNA genome of the virus which allows it to replicate by hijacking the host cell’s transcription machinery, and the open reading frame (ORF) proteins, particularly ORF8, appear to be largely dictating the pathogenicity of the virus while the envelope (E) and membrane (M) proteins seem to regulate intercellular production and transport of the S-proteins, helping to form and export new viral particles, likely contributing to the increased viral loads observed from patients infected with the more aggressive variants.
There is a common misperception that ‘Omicron’ and newer variants are less pathogenic than the ‘Alpha’ and ‘Delta’ variants that drove early waves and so many deaths in developed countries. However, there is no direct evidence (based on in vivo testing or assays of active virus in living tissue) and the epidemiological evidence is suspect because the statistics on testing and hospitalization are focused on developed countries through which early variants already raged, killing swaths of the most vulnerable people prior to vaccine availability and producing natural immune response plus the additional protections against severe morbidity and mortality once vaccines were widely available. Where the ‘Omicron’ variants have spread through novel (previously unexposed) populations that also have poor vaccination levels or poor efficacy vaccines, e.g. North Korea, China, Taiwan, they have produced similar or potentially even higher rates of mortality.
Even having endured an infection by an earlier variant is not a guarantee of mild disease from a subsequent infection; not only do variants appear to operate differently from their predecessors in their preferred tropism (type of cells it infects) but the degree to which they escape prior inoculation varies from patient to patient, with some tolerating reinfection with little effect while others experiencing far more severe infection the second time around. And there is, of course, still the wide unknowns about the duration of ‘long Covid’ effects; I’ve pointed out to people that polio patients have suffered Post-Polio Syndrome decades after the original and often mild infection.
Well, that is the discussion, and as it happens, there is a lot you can do, from wearing a good quality respirator mask, avoiding crowded indoor gatherings and poorly ventilated buildings, being cautious about transmitting the pathogen to immunocompromised or elderly people, et cetera. The reality is that this virus is not going to go away in the foreseeable future nor is it mutating to a benign variant that produces essentially no mortality the way that most ‘common cold’ viruses do (for anyone who is not severely immunocompromised).
I have a friend to is an epidemiologist and molecular biologist trained in virologist working in a nationally recognized university-affiliated research lab who is pretty convinced that we’re going see the emergence of a variant with an order of magnitude greater case fatality rate (something on the order of 3% to 5% instead of 0.3-0.4 %) based upon comparisons with the SARS-CoV(-1) and MERS betacoronavirus genomes and patterns of mutation and genetic shift seen in these variants, and we are in no way prepared for that kind of catastrophic mortality, either in our overstrained medical system and burned out responders, our economic system built on a fragile web of global interdependencies, or our social and educational nets that were already failing long before a mild pandemic illness came along and strained them to the breaking point. You should of course make decisions that are right for you in terms of risks and protections, but also bear in mind that there are larger effects for the spread of contagion than your own personal state of health.
Stranger