After claiming that cancelling Christmas would be “inhuman”, Scrooge Johnson promptly cancelled Christmas. Then Hancock cancelled Boxing Day just to make sure. Why? Because of a supposedly “70% more transmissible” new strain of Covid which was spreading like wildfire in London and Kent – and now it seems, Norfolk, Cambridgeshire, Essex and Oxforshire. Next year it will probably be everywhere and we’ll all have to suffer the economic and social catastrophe of Tier 4 lockdowns until we beg to be vaccinated (and probably long after that too). The name given to this ‘new strain’ is VUI 202012/01 (Variant Under Investigation, year 2020, month 12, variant 01), or B.1.1.7. Firstly, as the name suggests, it’s not a ‘new strain’, it’s a new variant – and it’s not that new. It was first reported in mid October when two samples from Kent and London sent to the Milton Keynes Lighthouse Lab were genetically sequenced by COG-UK. The dates of the samples were 20th September (Kent) and 21st September (London). Nothing much seems to be known about these ‘patients’. Were they asymptomatic (tested in the community) or did they have symptoms or were they in hospital? I can find no information at present. Had they recently arrived from abroad? That would mean the origin of the new variant might not even be the UK. Who knows.
The other thing is, it’s not a ‘new strain’ as claimed by our clueless politicians and media. To qualify for that status, it would have to have conclusively demonstrated a distinct clinical difference from other dominant strains in circulation, i.e. increased transmissibility and/or enhanced or even lower virulence. So far, despite the claims by NERVTAG and the government, no such evidence has been demonstrated. The claim of ‘70% more transmissible’ is based on modelling and is not backed up by hard data. This virology Professor explains in detail why he is not too worried by the new variant and why the claims by NERVTAG and the government are scare-mongering hype not backed up by hard science and data.
It’s a pretty damning video. He forensically dismantles the claims made by NERVTAG about this being a distinct new strain which has gained an evolutionary advantage over other, less contagious strains, basically stating that you cannot infer biological properties of a virus from limited epidemiological data only and that you must perform experiments in the field. For example, the apparent rapid spread of this new variant may simply be down to super-spreader events as it is well known that 80% of transmissions are caused by 10% of infectious individuals. He also goes through all the changes in the amino acid proteins (in particular the spike amino acid proteins) which are incorrectly called ‘mutations’ – even by the experts – and points out that the ORF8 changes may actually mean that this variant is less virulent. So even if it does turn out to be more contagious and does spread through the community, it may actually be a good thing because it will mean that a greater number of people become infected at less risk and natural herd immunity is attained that much quicker.
The government doesn’t see it this way of course. Nor does the WHO. It’s just an excuse to keep us all locked up for longer, with even more restrictions upon our personal liberty until we are forced to accept vaccination for a disease which to the vast majority does not present a major threat and is about 99.96% survivable. Ferguson doesn’t see it that way either. He was supposed to have resigned from all government advisory roles after he broke the rules of the lockdown which he was instrumental in implementing back in May. But he has now popped back up in NERVTAG and suddenly he’s the darling of the media again and the government are hanging on his every word. He’s warning us about the ‘threat’ of this new variant being transmitted by schoolchildren, bringing kids further under the jackboot of the psychopaths who are intent on controlling our lives. So don’t be surprised if schools are closed in a new lockdown in January on the ‘recommendation’ of Pants Down Ferguson who, it seems, is a turd which just cannot be flushed. The very same Ferguson responsible for the unnecessary slaughter of millions of innocent farm animals in the 2001 Foot and Mouth Epidemic and who predicted 150,000 deaths from BSE, among other catastrophic failures. Being wrong is his speciality it seems, an expertise which apparently qualifies him to give advice to the government on policies which affect all our lives, including voicing his opinion on how other peoples’ kids should have their lives seriously disrupted yet again.
Something which Prof. Vincent Racaniello neglected to mention and which is pertinent is the fact that this new variant has a large number of changes and deletions in the genome (14 changes and 3 deletions) which, on the face of it, mark it out as unique. They all ‘appeared’ at once, which is ‘unprecedented’, given the estimated mutation rate of approximately 1 or 2 per month. Lots of ‘mutations’ have been tracked, but never have 17 been recorded simultaneously in a newly discovered variant. It is also notable that a total of 8 changes occur in the critical spike region of the virus, when only 44 have been recorded previously. So it is perhaps unsurprising that the appearance of this new variant and its apparent rapid spread has caused some to worry, but is that concern justified enough to further destroy people’s lives? I think not and I will attempt to explain why not.
When I say lots of mutations have been tracked I do mean lots; in fact 12,706 ‘mutations’ up until 21 September 2020. What is remarkable is that none of those mutations have proven to have had any significant effect upon transmissibility or pathogenicity of SARS-CoV-2. It’s a rather odd coincidence that this paper, published on 25th November, authored by our old friend Francois Balloux and others, only covers up to the exact date that the new variant was discovered in Kent and London. So presumably, the ‘new strain of Covid’ is not included in this analysis. But here is what the study says:
The most plausible mutations under putative natural selection are those which have emerged repeatedly and independently (homoplasies). Here, we formally test whether any homoplasies observed in SARS-CoV-2 to date are significantly associated with increased viral transmission. To do so, we develop a phylogenetic index to quantify the relative number of descendants in sister clades with and without a specific allele. We apply this index to a curated set of recurrent mutations identified within a dataset of 46,723 SARS-CoV-2 genomes isolated from patients worldwide. We do not identify a single recurrent mutation in this set convincingly associated with increased viral transmission. Instead, recurrent mutations currently in circulation appear to be evolutionary neutral and primarily induced by the human immune system via RNA editing, rather than being signatures of adaptation.
We informally estimated the mutation rate over our alignment as 9.8 × 10−4 substitutions per site per year, which is consistent with previous rates estimated for SARS-CoV-21,2,3,4 (Figs. S1 and S2). This rate also falls in line with those observed in other coronaviruses25,26 and is fairly unremarkable relative to other positive single-stranded RNA viruses, which do not have a viral proof-reading mechanism.
Across our data set, we identified a total of 12,706 mutations, heavily enriched in C→U transitions, of which we identified 398 strongly supported recurrent mutations (Supplementary Data 3 and Supplementary Figs. 4 and 5). Employing a phylogenetic index (RoHO) to test whether these recurrent mutations contribute to a change in transmission, we found no candidate convincingly associated with a significant increase or decrease in transmissibility (Figs. 2 and 3 and Supplementary Data 4).
A much discussed mutation in the context of demographic confounding is D614G (nucleotide position 23,403), a non-synonymous change in the SARS-CoV-2 Spike protein. Korber et al. suggested that D614G increases transmissibility but with no measurable effect on patient infection outcome21. Other studies have suggested associations with increased infectivity in vitro18,40 and antigenicity41. Here we conversely find that D614G does not associate with significantly increased viral transmission (median log10(RoHO) = 0, paired t test p = 0.28; Supplementary Data 4), in line with our results for all other tested recurrent mutations.
These apparently contrasting results for D614G should be considered carefully. What is, however, indisputable is that D614G emerged early in the pandemic and is now found at high frequency globally, with 36,347 assemblies in our data set (77.8%) carrying the derived allele (Fig. 1a and Supplementary Data 3). However, D614G is also in linkage disequilibrium (LD) with three other derived mutations (nucleotide positions 241, 3037, and 14,408) that have experienced highly similar expansions, as 98.9% of accessions with D614G also carry these derived alleles (35,954/36,347). It should be noted that the D614G mutation displays only five independent emergences that qualify for inclusion in our analyses (fewer than the other three sites it is associated with). While this limits our power to detect a statistically significant association with transmissibility, the low number of independent emergences suggests to us that the abundance of D614G is more probably a demographic artefact: D614G went up in frequency as the SARS-CoV-2 population expanded, largely due to a founder effect originating from one of the deepest branches in the global phylogeny, rather than being a driver of transmission itself.
To summarise, what Balloux et al are saying is that they’ve examined thousands of changes in the genome of SARS-CoV-2 since it first emerged and they have found none that significantly alter the biology of the virus in terms of transmissibility or pathogenicity. One ‘mutation’ in the spke protein, D614G, which first appeared in February, was thought to increase transmissibility and virulence but turned out to be largely neutral and its spread around the globe was attributed largely to the Founder Effect, which Prof . Racaniello discusses in the video above.
Matt Ridley has a opinion piece in the Telegraph on the subject of this new variant and he makes much of the fact that it suddenly appeared with an unprecedented number of changes in the amino acid proteins, suggesting, he says, that those changes occurred artificially, not randomly, as occurred with the 12,706 mutated genomes which Balloux et al analysed. He tends to paint an alarming picture:
This number of changes would normally take months to emerge at the rate the virus typically evolves: it is less prone to random mutation than an influenza virus. What caused such a burst of evolution within perhaps a single body?
Here the story gets alarming. According to analysis by Andrew Rambaut at Edinburgh University and colleagues for the Covid-19 Genomics Consortium UK, such high rates of mutation have happened in people with suppressed immune systems who get a Covid infection that persists for months and are treated with “convalescent plasma” – essentially blood extracted from those who have recovered from Covid.
In a person with a deficient immune system, a large population of viruses can proliferate, mutate and diversify, and then the treatment selects a new strain from among this diversity.
Essentially, the virus has a crash course in evolution. If so, this casts doubt on the wisdom of convalescent-plasma treatment, pitting the possibility that it might save a life against the possibility that it might help the virus become more infectious or lethal.
As Matt points out, he is referring to a theory of the origin of this new variant put forward by a team of academics lead by Andrew Rambaut of the University of Edinburgh, in conjunction with the Universities of Birmingham, Oxford, Imperial College, Cambridge, Cardiff, The Wellcome Trust Sanger Institute and the MRC-University of Glasgow Centre for Virus Research. What they say is this:
What evolutionary processes or selective pressures might have given rise to lineage B.1.1.7?
High rates of mutation accumulation over short time periods have been reported previously in studies of immunodeficient or immunosuppressed patients who are chronically infected with SARS-CoV-2 (Choi et al. 2020; Avanzato et al. 2020; Kemp et al. 2020). These infections exhibit detectable SARS-CoV-2 RNA for 2-4 months or longer (although there are also reports of long infections in some immunocompetent individuals). The patients are treated with convalescent plasma (sometimes more than once) and usually also with the drug remdesivir. Virus genome sequencing of these infections reveals unusually large numbers of nucleotide changes and deletion mutations and often high ratios of non-synonymous to synonymous changes. Convalescent plasma is often given when patient viral loads are high, and Kemp et al. (2020) report that intra-patient virus genetic diversity increased after plasma treatment was given.
Under such circumstances, the evolutionary dynamics of and selective pressures upon the intra-patient virus population are expected to be very different to those experienced in typical infection. First, selection from natural immune responses in immune-deficient/suppressed patients will be weak or absent. Second, the selection arising from antibody therapy may be strong due to high antibody concentrations. Third, if antibody therapy is administered after many weeks of chronic infection, the virus population may be unusually large and genetically diverse at the time that antibody-mediated selective pressure is applied, creating suitable circumstances for the rapid fixation of multiple virus genetic changes through direct selection and genetic hitchhiking.
These considerations lead us to hypothesise that the unusual genetic divergence of lineage B.1.1.7 may have resulted, at least in part, from virus evolution with a chronically-infected individual. Although such infections are rare, and onward transmission from them presumably even rarer, they are not improbable given the ongoing large number of new infections.
Although we speculate here that chronic infection played a role in the origins of the B.1.1.7 variant, this remains a hypothesis and we cannot yet infer the precise nature of this event.
It’s basically just a speculative hypothesis about the origin of the ‘new strain’. By their own admission, they don’t have any solid evidence it would seem and it would also appear to be the case that the two people who initially tested positive for this ‘new strain’ are not immuno-compromised patients who have suffered Covid for a long period, otherwise we would have heard about it now, I’m sure. The authors refer to several examples of enhanced viral evolution in immuno-compromised patients to back up their theory and there is an example of an immuno-compromised patient suffering recurrent bouts of Covid-19 over several months who sadly died. A series of changes in the genome of the virus were observed over the course of the treatment, but they appear to be nothing like the changes recorded for this new variant, so obviously, this particular patient was not the source of the new variant. I quote:
Phylogenetic analysis was consistent with persistent infection and accelerated viral evolution (Figures 1A and S6). Amino acid changes were predominantly in the spike gene and the receptor-binding domain, which make up 13% and 2% of the viral genome, respectively, but harbored 57% and 38% of the observed changes (Figure 1B).
Although most immunocompromised persons effectively clear SARS-CoV-2 infection, this case highlights the potential for persistent infection5 and accelerated viral evolution associated with an immunocompromised state.
So, though it is a possibility that the new variant may have arisen as a result of prolonged treatment of an immuno-compromised patient, in the absence of any patient fitting the profile, it remains just a theory. The actual origin of these synchronously appearing ‘mutations’ thus remains a mystery. It’s a possibility but we cannot definitely blame plasma convalescent therapy for the emergence of this new variant. So what else might explain where it came from?
We maybe have a clue as to the origins of this virus from the following article:
After the first official records of the virus in September, progress was slow, and it wasn’t until England’s second wave took hold in late October that cases exploded.
This, scientists say, could be because the virus strain is faster spreading and made cases rise quicker – or it could be that it was simply found more often as cases surged naturally.
At the time of the first sample the UK was averaging just 3,700 positive coronavirus tests per day. By the start of November, when samples were coming in thick and fast, the average number of positive results had skyrocketed to 23,000 per day.
Professor Loman said there was ‘no evidence’ the strain had come from any other countries, adding: ‘It’s sort of come out of nowhere.
‘We have a long gap between the first cases we saw with this variant in late September [and recent surge in cases]… It’s more likely to have evolved in the UK but we don’t know that.
‘There are very few examples of this variant in other countries at the moment – it’s really a kind of UK phenomenon.’
Well, sorry, but “It’s sort of come out of nowhere” is not adequate. We need explanations, if only tentative explanations. It’s the first time apparently, as noted above, that a virus has been discovered with so many (17) changes in the genome. These changes accumulate slowly in SARS-CoV-2 at a rate of 1-2 per month and none have so far proved to be significant in terms of transmission or virulence. So if these changes happened naturally, they might have taken several months and the question arises as to how they managed to remain unobserved until September 20th?
The first thing to note is that COG-UK first started sequencing Covid viruses back in March 2020. It should be pointed out though that until July, all sequenced positive samples were from the limited number of Pillar 1 tests in hospitals. So initially, not many samples were being sequenced. Then Pillar 2 testing got going and the number of tests rose rapidly from July onwards, as did the number of positives. In concert with the rising number of positives, more and more samples were sent for sequencing. I believe at some point, the Wellcome-Sanger Institute (who do a lot of the sequencing for COG-UK) automated their processes so they could handle a lot more samples. Also, when national and international travel restrictions were relaxed in July and August, there appeared many more SARS-CoV-2 lineages in the UK, which most likely were imported from other countries. This analysis from the Welsh Government confirms that fact:
While we have seen increases over the summer, the numbers of UK lineages remain less than in mid-March.
The graphs demonstrate the two types of lineage that are currently causing disease in Wales.
Firstly, UK lineages such as UK5 and UK2243 have been long term causes of disease in Wales. UK5 is the largest UK lineage and was probably introduced into the UK multiple times in February/March, and became rapidly established in community transmission. As one of the largest lineages, it has continued to transmit in the community as other smaller lineages have died out. Secondly, we see a new wave of lineages arriving in Wales over the summer. Lineages such as UK389 and UK395 have never been seen before in Wales and have arrived in the August-September timescale to cause considerable numbers of cases in multiple locations, simultaneously. Examining these new arrival lineages reveals that they have arrived in many parts of the UK simultaneously, presenting a signature that is consistent with the idea that these lineages have been seeded by multiple simultaneous imports from outside Wales/the UK.
So, after the initial epidemic, which saw many different lineages, they tailed off into late spring/early summer, then genetic diversity increased once again going into late summer/early autumn, as people jetted off on their holidays and returned to the UK. Concurrent with that, we have a large increase in the number of sequencing being done from positive tests across the UK. Is it beyond the realms of possibility that the variant discovered with 17 ‘mutations’ in Kent and London in mid October, from samples donated at the end of September, could have arrived in the UK during September and have evolved naturally in another country, unnoticed, because that particular country was doing very little sequencing? Those two people carrying the virus get tested, their samples get sequenced by COG-UK and hey presto, a ‘new variant’ with an ‘unprecedented number of ‘mutations’ suddenly appears. A few months later, when it starts spreading in the community, for reasons which may have nothing whatsoever to do with the claimed ‘70% increased transmissibility’, Johnson, Hancock, Ferguson, Whitty and Vallance realise they’re onto a winner and use the new ‘mutant Covid strain’ as a perfect excuse to cancel Christmas in the UK with just a few days’ notice.