Some background and a few thoughts on evolution, phylogeny and new variants of SARS-CoV-2.

BACKGROUND

From the NEXTSTRAIN website…

“This phylogeny shows evolutionary relationships of hCoV-19 (or SARS-CoV-2) viruses from the ongoing novel coronavirus COVID-19 pandemic. This phylogeny shows an initial emergence in Wuhan, China, in Nov-Dec 2019 followed by sustained human-to-human transmission leading to sampled infections. Although the genetic relationships among sampled viruses are quite clear, there is considerable uncertainty surrounding estimates of specific transmission dates and in reconstruction of geographic spread. Please be aware that specific inferred transmission patterns are only a hypothesis.

“There are thousands of complete genomes available now and this number increases by hundreds of every day. This visualization can only handle ~3000 genomes in a single view for performance and legibility reasons. Because of this we have to subsample available genome data for these analysis views. Our primary global analysis subsamples to 120 genomes per admin division per month. This will result in a more equitable global sequence distribution, but it hides samples available from regions that are doing lots of sequencing.

“To mitigate against this, we’ve set up separate analyses to focus on particular regions. They are available on the “Dataset” dropdown on the left or by clicking on the following links: AfricaAsiaEuropeNorth AmericaOceania and South America.

“Site numbering and genome structure uses Wuhan-Hu-1/2019 as reference. The phylogeny is rooted relative to early samples from Wuhan. Temporal resolution assumes a nucleotide substitution rate of 8 × 10^-4 subs per site per year. Full details on bioinformatic processing can be found here.

“Phylogenetic context of nCoV in SARS-related betacoronaviruses can be seen here.

“We gratefully acknowledge the authors, originating and submitting laboratories of the genetic sequence and metadata made available through GISAID on which this research is based. A full listing of all originating and submitting laboratories is available below. An attribution table is available by clicking on “Download Data” at the bottom of the page and then clicking on “Strain Metadata” in the resulting dialog box.”

EVOLUTION AND PHYLOGENY

This first paper from authors at Iowa (2016) is necessary for a fundamental understanding, it seems, to the origins of the SARS-CoV-2 in SARS-CoV – all beta coronaviruses, and its potential for reeking havoc in mammals and humans.

The second paper is telling. It is 5 years old, but discusses the potential for a community of coronaviruses in bats jumping from that mammalian species to humans, specifically. Was it ignored?

Both papers are under HHS public access and/or free access.

I wish to to quote extensively from the first paper, page 8-9, here…

Human Coronaviruses

“Prior to the SARS-CoV outbreak, coronaviruses were only thought to cause mild, self- limiting respiratory infections in humans. Two of these human coronaviruses are α- coronaviruses (HCoV-229E and HCoV-NL63) while the other two are β-coronaviruses (HCoV-OC43 and HCoV-HKU1). HCoV-229E and HCoV-OC43 were isolated nearly 50 years ago [74,75] [76] while HCoV-NL63 and HCoV-HKU1 were only recently identified following the SARS-CoV outbreak [77,78].

“These viruses are endemic in the human populations, causing 15–30% of respiratory tract infections each year. They cause more severe disease in neonates, the elderly, and in individuals with underlying illnesses, with a greater incidence of lower respiratory tract infection in these populations. HCoV-NL63 is also associated with acute laryngotracheitis (croup) [79]. One interesting aspect of these viruses is their differences in tolerance to genetic variability. HCoV-229E isolates from around the world have only minimal sequence divergence [80] while HCoV-OC43 isolates from the same location but isolated in different years show significant genetic variability [81]. This likely explains the inability of HCoV-229E to cross the species barrier to infect mice while HCoV-OC43 and the closely related bovine coronavirus, BCoV, are capable of infecting mice and several ruminant species.

“Based on the ability of MHV to cause demyelinating disease, it has been suggested that human CoVs may be involved in the development of multiple sclerosis (MS). However, no evidence to date suggests that human CoVs play a significant role in MS…”

A FEW THOUGHTS

Remember, they are discussing SARS-CoV, the pregenitor of SARS-CoV-2. The link between the two beta viruses is close. Actually less than generation, so what may apply in evolutionary terms will apply to both. These viruses are endemic in human populations, meaning the are everywhere humans are found on the globe. Second, they arose from bats, as we now understand it – from a community of coronaviruses – one strain became SARS-CoV-2.

Now humanity is confronted with three reported variants. On reported in Italy, which is more contagious but less pathogenic. One in South Africa, which again is more contagious. and the third in the UK, which is also more contagious, yet of unknown level of pathogenicity.

That we have three viable variants in humans should not be a surprise. There are, at this writing, 34 mutations or evolutions of the SARS-CoV-2 mRNA genome (Figure 2, above from NEXTSTRAIN). Obviously, not every evolution is viable.

Do these variants ONLY arise from the UK, Italy, and South Africa? No. They do not. They are evolutions of the same virus. They have occurred elsewhere, and will occur in the future. It’s evolutionary now that the virus is endemic in humans.

Can we shut them out, by stopping interactions with the UK, Italy, and South Africa? No, we cannot. They are here already, no doubt, or will evolve here until we, as a society decide to stop the spread of the virus itself, through isolation, vaccination, and following the public health officials advice whom we have selected.

The vaccines, based on the mRNA of the S-protein (the Spike protein) of SARS-CoV-2 will work against ALL variants, no doubt. It is the S-protein that makes coronaviruses unique and is one of four proteins that the coronavirus needs to survive.

However, it is up to us, to stop the pandemic. Pandemics are socially-mediated.

These are my thoughts as of 25DEC20.

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