I learn’t a new word yesterday … “quasispecies”

I learn’t a new word yesterday … “quasispecies”

This post is really personal notetaking but I’m putting it out here anyway…

So expect no start, beginning or end or indeed any sense here.

I did some reading on the B.1.617 strain that is currently extant in India.

Apparently it’s not too dissimilar to the B.1.427 and B.1.429 “variants of concern” circulating in California presently.

These carry 3 mutations in the spike protein, including an L452R substitution.

“In the current study, we describe the spread of a novel B.1.427/B.1.429 variant in California carrying a characteristic triad of spike protein mutations (S13I, W152C, and L452R) that is predicted to have emerged in May 2020 and increased in frequency from 0% to >50% of sequenced cases from September 2020 to January 2021.”

This L452R substitution, together with others, forms a hydrophobic patch on the surface of the spike that assists the viral binding to the cell wall.

And it’s been around for more than a year but due to other, previously more competitive strains, it is only now finding its place in the limelight.

Ironically, the USA – with no joined up genome sequencing network – has been late to spot this. This may be one of the reasons why apparently (according to this paper) no one knows where the mutation came from.

“The evolutionary mechanism underlying the unusual genetic divergence of these emerging variants, with the accumulation of many mutations over a short time period, remains unexplained, but this divergence may potentially be due to accelerated viral quasispecies evolution in chronically infected patients (Avanzato et al., 2020; Choi et al., 2020; Kemp et al., 2021). Another possible explanation for the absence of genomes directly ancestral to B.1.427/B.1.429 is the aforementioned limited genomic sampling of SARS-CoV-2 in California and the US to date.”

Well that’s enough of that. It’s where my new word came from.

The other thought I had – which I think I’ve solved now – was…. how do the mRNA vaccines get into your cells (in order to co-opt your cellular ribosomes to become spike producing factories) in the first place – seeing that they don’t actually have a spike themselves?

I think the answer is because the mRNA fragments are tiny and encapsulated in a fatty membrane –  much like your cells membrane – and therefore bind and easily incorporate into the cell walls and gain access that way..

Other vaccines use an adenovirus shell (which is adept at gaining cellular entry) to get in and deliver their payload.

Finally, some older vaccinated friends of mine in the UK are reporting that their arthritis is much better pending vaccination which struck me as odd because vaccination produces an inflammatory response rather than the other way around.

And after all, arthritis is an inflammatory disease.

But also a physical one in that small bubbles of air trapped in bones expand on days of low air pressure (bad weather generally) causing pain in joints.

And in March (ie., recently when old gimmers like me were being invited to have our vaccine) we set a record for the hottest day in 53 years … that’s got to help your arthritis – else why would so many old UK expats be living in Spain?

PS.. just in case anyone still thinks i’m a faxxer I’m closing in on a top 1000 (1017 of 225783) ranking on folding at home 😁.

Notes for a new post ….

Good news – vaccines produce a memory T-cell response to SARS-CoV-2 – even if antibodies can be sidestepped by new variants.

There are 7 coronaviruses for humans – 4 cause common colds – 3 cause serious illness – (i) SARS-CoV-1, (ii) MERS-CoV and (iii) SARS-CoV-2

It also appears that T-cells in unvaccinated people (the following study was published before vaccines were widely available) who have recovered from (i), (ii) or (iii) may also confer immunity against (iii).

Finally memory T-cells in people who have NOT been infected with (i), (ii) or (iii) ALSO show some efficacy at tackling (iii) and the hypothesis is that prior coronavirus infections (we’ve all had a cold!) prime memory T-cells to target homologous (similar or of common ancestry) coronavirus proteins.


T-cells from recovered victims of (i) and (ii) attack the structural (nucleocapsid (N) protein) regions of (iii)

T-cells from circa 50% of uninfected volunteers attack the non-structural (NSP7 and NSP13 of ORF1) regions of SARS-CoV-2.