Коронавирус создан в американской лаборатории ещё в 2015 году! И не надо "лохматить бабушку"!!!
Листала старые рассылки по медицине и вот нашла...
Привожу статью на
русском из Российской газеты от 2015 года и ниже оригинал на английском языке из Nature. Того же 2015 года!
Ученые нашли новый смертельный вирус гриппа
Американские биологи создали смертельно опасный для человека коронавирус, экспериментируя с летучими мышами, сообщает журнал Nature.
По
данным издания, биологи создали вирус, способный напрямую заражать
человека и вызывать его смерть. Исследователи экспериментировали с
созданием гибрида коронавируса летучей мыши, обитающей в Китае. Они
скрестили поверхностный белок SHC014 с вирусом SARS, который взяли из
легких летучих мышей. В результате получился вирус-мутант. Тесты
доказали, что он способен очень быстро и активно развиваться в клетках
человеческого тела.
Авторы исследования считают свою работу значимой. Им удалось доказать,
что данный вирус смертельно опасен. Следовательно, человечество
предупреждено.
Однако открытие вызвало жаркие дебаты в научной
среде. Спорят больше не о его ценности, а о возможной утечке вируса из
лаборатории. Чем это грозит миру, можно только гадать. Ученые сходятся
во мнении, что вирус-мутант способен унести массу жизней. Критике
подвергается и тот факт, что эксперимент был проведен после того, как в
2014 году власти США ввели мораторий на финансирование исследований
таких вирусов гриппа, как SARS и MERS. В данном случае почему-то было
сделано исключение.
Копия статьи из Nature.
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An experiment that created a hybrid version of a bat
coronavirus — one related to the virus that causes SARS (severe acute
respiratory syndrome) — has triggered renewed debate over whether
engineering lab variants of viruses with possible pandemic potential is
worth the risks.
In an article published in Nature Medicine1
on 9 November, scientists investigated a virus called SHC014, which is
found in horseshoe bats in China. The researchers created a chimaeric
virus, made up of a surface protein of SHC014 and the backbone of a SARS
virus that had been adapted to grow in mice and to mimic human disease.
The chimaera infected human airway cells — proving that the surface
protein of SHC014 has the necessary structure to bind to a key receptor
on the cells and to infect them. It also caused disease in mice, but did
not kill them.
Although almost all
coronaviruses isolated from bats have not been able to bind to the key
human receptor, SHC014 is not the first that can do so. In 2013,
researchers reported this ability for the first time in a different
coronavirus isolated from the same bat population2.
The
findings reinforce suspicions that bat coronaviruses capable of
directly infecting humans (rather than first needing to evolve in an
intermediate animal host) may be more common than previously thought,
the researchers say.
But other virologists
question whether the information gleaned from the experiment justifies
the potential risk. Although the extent of any risk is difficult to
assess, Simon Wain-Hobson, a virologist at the Pasteur Institute in
Paris, points out that the researchers have created a novel virus that
“grows remarkably well” in human cells. “If the virus escaped, nobody
could predict the trajectory,” he says.
Creation of a chimaera
The
argument is essentially a rerun of the debate over whether to allow lab
research that increases the virulence, ease of spread or host range of
dangerous pathogens — what is known as ‘gain-of-function’ research. In
October 2014, the US government imposed a moratorium on federal funding of such research
on the viruses that cause SARS, influenza and MERS (Middle East
respiratory syndrome, a deadly disease caused by a virus that
sporadically jumps from camels to people).
The
latest study was already under way before the US moratorium began, and
the US National Institutes of Health (NIH) allowed it to proceed while
it was under review by the agency, says Ralph Baric, an
infectious-disease researcher at the University of North Carolina at
Chapel Hill, a co-author of the study. The NIH eventually concluded that
the work was not so risky as to fall under the moratorium, he says.
But
Wain-Hobson disapproves of the study because, he says, it provides
little benefit, and reveals little about the risk that the wild SHC014
virus in bats poses to humans.
Other
experiments in the study show that the virus in wild bats would need to
evolve to pose any threat to humans — a change that may never happen,
although it cannot be ruled out. Baric and his team reconstructed the
wild virus from its genome sequence and found that it grew poorly in
human cell cultures and caused no significant disease in mice.
“The
only impact of this work is the creation, in a lab, of a new,
non-natural risk,” agrees Richard Ebright, a molecular biologist and
biodefence expert at Rutgers University in Piscataway, New Jersey. Both
Ebright and Wain-Hobson are long-standing critics of gain-of-function
research.
In their paper, the study authors
also concede that funders may think twice about allowing such
experiments in the future. "Scientific review panels may deem similar
studies building chimeric viruses based on circulating strains too risky
to pursue," they write, adding that discussion is needed as to "whether
these types of chimeric virus studies warrant further investigation
versus the inherent risks involved”.
Useful research
But
Baric and others say the research did have benefits. The study findings
“move this virus from a candidate emerging pathogen to a clear and
present danger”, says Peter Daszak, who co-authored the 2013 paper.
Daszak is president of the EcoHealth Alliance, an international network
of scientists, headquartered in New York City, that samples viruses from
animals and people in emerging-diseases hotspots across the globe.
Studies
testing hybrid viruses in human cell culture and animal models are
limited in what they can say about the threat posed by a wild virus,
Daszak agrees. But he argues that they can help indicate which pathogens
should be prioritized for further research attention.
Without
the experiments, says Baric, the SHC014 virus would still be seen as
not a threat. Previously, scientists had believed, on the basis of
molecular modelling and other studies, that it should not be able to
infect human cells. The latest work shows that the virus has already
overcome critical barriers, such as being able to latch onto human
receptors and efficiently infect human airway cells, he says. “I don't
think you can ignore that.” He plans to do further studies with the
virus in non-human primates, which may yield data more relevant to
humans.
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