There is talk of a second lockdown on the way as reported in The Telegraph https://www.telegraph.co.uk/news/2020/09/28/lockdown-second-wave-new-rules-uk-national-boris-update/ but on reading this I was reminded of a story I came across a short while ago regarding a mutation in the disease.
A study earlier this year has found that SARS-CoV-2’s ability to mutate has been quite seriously underestimated.
A group of researchers at Zhejiang University, a reputable research university situated in Hangzhou, the capital of the eastern coastal Chinese province of Zhejiang, have made what just might be a critical breakthrough in our understanding of the wide range of symptoms that patients face.
Studies have suggested that as up to half of those who have been infected with the virus might be “asymptomatic”, a category that includes those who experienced extremely mild symptoms, often resembling a bad cold, in some cases no discernible symptoms at all. This team of scientists has discovered 31 new mutated strains of the virus that might explain the stubbornly high mortality rates in parts of Europe and USA.
According to the South China Morning Post, some of the mutant strains exhibited a much more dangerous capacity to invade human cells, implying that certain strains might be much more lethal than others. These strains were found to be “genetically similar” to samples isolated in New York and places like Italy in Europe.
Critically, the study, led by Professor Li Lanjuan, the first Chinese academic to recommend a complete shutdown to fight the virus, showed for the first time a probable link between the type of strain that infects a patient and the severity of the symptoms they face.
This is a breakthrough – though it’s being underplayed in the mainstream press, probably because health journalists are grappling with a confusing paradox: Dr. Fauci has said that there was “no evidence” of deadly mutations, but these researchers have found exactly that!
“Sars-CoV-2 has acquired mutations capable of substantially changing its pathogenicity,” Li and her team wrote in their non-peer-reviewed paper which was published by themedRxiv.org, another top research for non-peer-reviewed research, along with the Lancet.
Li took an unusual approach to investigate the virus mutation. She analyzed the viral strains isolated from 11 randomly chosen Covid-19 patients from Hangzhou in the eastern province of Zhejiang, and then tested how efficiently they could infect and kill cells.
The deadliest mutations in the Zhejiang patients had also been found in most patients across Europe, while the milder strains were the predominant varieties found in parts of the United States, such as Washington state, according to their paper.
A separate study had found that New York strains had been imported from Europe. The death rate in New York was similar to that in many European countries, if not worse.
But the weaker mutation did not mean a lower risk for everybody, according to Li’s study. In Zhejiang, two patients in their 30s and 50s who contracted the weaker strain became severely ill. Although both survived, the elder patient needed treatment in an intensive care unit.
Li’s study involved a notably small number of strains, only a few dozen were investigated, as opposed to hundreds or thousands of strains in some major studies of new viruses. However, she still managed to find what appears to be a definite link that could shed new light – or unearth new complications in the quest to finding a cure or a vaccine. Li’s team attributed these “functional changes” in the different strains to variations in the “viral-spike protein” – aka the “spikes” on the “ball” used to represent SARS-CoV-2.
Li’s team detected more than 30 mutations and about 60 per cent were new.
They found some of these mutations could lead to functional changes in the virus’ spike protein, a unique structure over the viral envelope enabling the coronavirus to bind with human cells. Computer simulation predicted that these mutations would increase its infection capability.
The fact that such unexpectedly intense variations could arise from a sample of less than a dozen patients means the variability of this virus might be much higher than initially expected. It may have mutated since the outbreak began, which of course could create complications in the quest for a vaccine. Alarmingly, some of the mutated strains carried as much as 270 times the viral load as the weakest strains.
To verify the theory, Li and colleagues infected cells with strains carrying different mutations. The most aggressive strains could generate 270 times as much viral load as the weakest type. These strains also killed the cells the fastest.
It was an unexpected result from fewer than a dozen patients, “indicating that the true diversity of the viral strains is still largely underappreciated,” Li wrote in the paper.
The projection that a virus could take 18 months to 2 years to develop is based on not much more than guesswork inspired by wishful thinking. Because of this, waiting until a vaccine or cure is in hand could lead us to wait much longer than expected. Both Boris Johnson and Matt Hancock have optimistically hinted at a vacine by Christmas. I, for one, do not share that view.
After all, it was only four months ago that China was worrying about a fresh outbreak https://www.theguardian.com/world/2020/may/11/now-it-starts-again-new-coronavirus-outbreaks-spark-unease-in-china
Then of course there is the unfortunate gas explosion in Wuhan, site of the original Covid19 outbreak, that has wrought so much trouble onto the world https://www.express.co.uk/news/world/1341164/China-news-explosion-wuhan-five-dead-chemical-plant-Hubei-tianmen Do you believe in coincidence?
I think skepticism is justified what we have been told so far.
Image by Darko Starjanovic