The study was carried out by Professor Li Lanjuan and colleagues from Zhejiang University in Hangzhou, China, and published in a non-peer reviewed paper released on website medRxiv.org on Sunday.
By ALEX WINSTON
A new study in China has found that the novel coronavirus has mutated into at least 30 different variations. The results showed that medical officials have vastly underestimated the overall ability of the virus to mutate, in findings that different strains have affected different parts of the world, leading to potential difficulties in finding an overall cure.
The study was carried out by Professor Li Lanjuan and colleagues from Zhejiang University in Hangzhou, China and published in a non-peer reviewed paper released on website medRxiv.org on Sunday.Li’s team analyzed the strains from 11 randomly chosen coronavirus patients from Hangzhou, where there have been 1,264 reported cases, and then tested how efficiently they could infect and kill cells.More than 30 different mutations were detected, of which 19 were previously undiscovered.“Sars-CoV-2 has acquired mutations capable of substantially changing its pathogenicity,” Li wrote in the paper.The team discovered that some of the mutations could lead to functional changes in the virus’ spike protein, the South China Morning Post reported. Spike protein is the protein that the coronavirus uses to attach itself to human cells.
TOP ARTICLES2/5READ MOREGantz at Independence Day ceremony: Israel must prepare for tough timesLi ‘s team infected cells with COVID-19 strains carrying different mutations, of which the most aggressive strains were found to generate as much as 270 times as much viral load as the weakest strains. The aggressive strains also killed the human cells the fastest. The results indicated “that the true diversity of the viral strains is still largely underappreciated,” Li wrote. The study could have future implications on the treatment of coronavirus, as several different strains have been found throughout the world. The United States, which has the world’s worst death toll at 42,897, and 799,515 overall cases, has been struck by different mutations. New York, which itself had the worst death rate in the US, and the eastern coast show a strain of coronavirus similar to that found in Europe, whereas the western US has shown similarities with strains found in China. Coronavirus has so far been treated in hospitals worldwide as one disease and patients receive the same treatment regardless of the strain. It has been suggested by the team at Zhejiang University that defining mutations in different regions may change the way we approach combating the virus.“Drug and vaccine development, while urgent, need to take the impact of these accumulating mutations into account to avoid potential pitfalls,” the scientists said.
We’ve never made a successful vaccine for a coronavirus before. This is why it’s so difficult
For those pinning their hopes on a COVID-19 vaccine to return life to normal, an Australian expert in vaccine development has a reality check — it probably won’t happen soon.
The reality is that this particular coronavirus is posing challenges that scientists haven’t dealt with before, according to Ian Frazer from the University of Queensland.
Professor Frazer was involved in the successful development of the vaccine for the human papilloma virus which causes cervical cancer — a vaccine which took years of work to develop.Coronavirus questions answeredBreaking down the latest news and research to understand how the world is living through an epidemic, this is the ABC’s Coronacast podcast.Read more
He said the challenge is that coronaviruses have historically been hard to make safe vaccines for, partly because the virus infects the upper respiratory tract, which our immune system isn’t great at protecting.
And while we have vaccines for seasonal influenza, HPV and other diseases, creating a new vaccine isn’t as simple as taking an existing one and swapping the viruses, said Larisa Labzin, an immunologist from the University of Queensland.
“For each virus or different bacterium that causes a disease, we need a different vaccine because the immune response that’s mounted is different,” Dr Labzin told ABC Science.
“Just because we’ve got a really good vaccine against polio doesn’t mean the same thing will work with coronavirus, because it’s so different.”
The challenge of respiratory infections
There are several reasons why our upper respiratory tract is a hard area to target a vaccine.
“It’s a separate immune system, if you like, which isn’t easily accessible by vaccine technology,” Professor Frazer told the Health Report.
Despite your upper respiratory tract feeling very much like it’s insideyour body, it’s effectively considered an external surface for the purposes of immunisation.
“It’s a bit like trying to get a vaccine to kill a virus on the surface of your skin.”
Your skin, and the outer layer of cells in your upper respiratory tract act as a barrier to viruses, stopping them getting into the body.
And finding a way to neutralise the virus “outside” of the body is very difficult.
This is partly because only the outer layer of cells (the epthelial cells) get infected, which, compared to a severe infection of internal organs doesn’t produce the same immune response, so is harder to target.
It’s hard to produce a successful vaccine if the virus isn’t activating a strong immune response.
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And if a vaccine elicits an immune response that misses the target cells, the result could potentially be worse than if no vaccine was given.
“One of the problems with corona vaccines in the past has been that when the immune response does cross over to where the virus-infected cells are it actually increases the pathology rather than reducing it,” Professor Frazer said.
“So that immunisation with SARS corona vaccine caused, in animals, inflammation in the lungs which wouldn’t otherwise have been there if the vaccine hadn’t been given.”
What’s the story with antibodies?
Antibodies are proteins that are released by the immune system to neutralise a threat, like a virus.
We’ve so far found with coronavirus that those infected have had different antibody responses, some weak, some strong.
The ABC has received many questions around how long immunity lasts and whether someone can be reinfected.
So is antibody response critical to whether or not a vaccine is going to work?
To answer this we have to go back to what we know about coronaviruses that cause the common cold, according to Professor Frazer.
“Yes, you get antibodies after a [cold] infection, and yes it lasts for a while, but it’s not lifelong… sort of months rather than years,” he said.
“I think it would be fair to say that the natural immunity that you get after infection from this coronavirus is probably going to turn out like the coronaviruses we’ve seen in the past.
“There will be some natural protection over a period of months, maybe even years, but it won’t be lifelong.
“The good news is that if you get reinfected with the virus a second time some months down the track, there will probably be enough immunity there to stop you becoming seriously ill.”
What are the vaccine options?
At the moment, teams around the world are deploying different technologies in vaccine development, from killing the virus and using it in the vaccine like we do with influenza, to using messenger RNA to prompt the infected cells to produce antibodies.
But the reality of vaccine development is that many fail before a successful one is developed.
Professor Frazer’s prediction is that the most likely candidate will be a vaccine that uses a part of the virus attached to a chemical to induce an immune response, or “subunit” vaccine.
“That [vaccine type] has been successful in animal models for coronaviruses in the past and that is of course where the money is being put in large measure at the moment,” he said.
“Another sort of vaccine would be just antibody transferred from somebody who had been infected already and had got rid of the infection.
“Which would be an immunological means of preventing infection, and could probably be more quickly developed than an actual vaccine.”
This sort of vaccine was tested with SARS in 2003 and resulted in reinfected lab monkeys having a nasty immune response, which is why many groups working on a vaccine for Sars-CoV-2 are going for a very specific antibody response.
Professor Frazer said the narrow, targeted approach is fine, unless you pick the wrong specific antigen — the substance that stimulates an immune response which antibodies bind to — in which case you could end up with the same problem.
Will we ever get a vaccine?
We don’t yet have vaccines against any coronaviruses in humans, in part due to the challenges of developing vaccines for viruses that infect the upper respiratory tract.
There are a lot of vaccine experiments going on around the world at the moment trying to change that though, including some in human trials.
While this gives us the best possible chance of getting a successful vaccine, it also highlights that there isn’t an obvious winner yet, said Professor Frazer.
“I think it would be fair to say even if we get something which looked quite encouraging in animals, the safety trials in humans will have to be fairly extensive before we would think about vaccinating a group of people who have not yet been exposed to the virus.
“They might hope to get protection but certainly wouldn’t be keen to accept the possibility of really serious side effects if they actually caught the virus.”
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American health care, as we call it today, and for all its high-tech miracles, has evolved into one of the most atrocious rackets the world has ever seen. By racket, I mean an enterprise organized explicitly to make money dishonestly.
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