生物学家shocked by covid. creepy.

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Inside the body, the coronavirus is even more sinister than scientists had realized
An electron microscopy image of a cell infected by the coronavirus that causes COVID-19.

An electron microscopy image of a cell infected by the coronavirus that causes COVID-19.
(UC San Francisco )
By MELISSA HEALYSTAFF WRITER
JUNE 26, 2020
8 AM
The new coronavirus’ reputation for messing with scientists’ assumptions has taken a truly creepy turn.
Researchers exploring the interaction between the coronavirus and its hosts have discovered that when the SARS-CoV-2 virus infects a human cell, it sets off a ghoulish transformation. Obeying instructions from the virus, the newly infected cell sprouts multi-pronged tentacles studded with viral particles.
These disfigured zombie cells appear to be using those streaming filaments, or filopodia, to reach still-healthy neighboring cells. The protuberances appear to bore into the cells’ bodies and inject their viral venom directly into those cells’ genetic command centers — thus creating another zombie.
The authors of the new study, an international team led by researchers at UC San Francisco, say the coronavirus appears to be using these newly sprouted dendrites to boost its efficiency in capturing new cells and establishing infection in its human victims.

Their research was published Friday in the journal Cell.
The scientists also believe they have identified several drugs that could disrupt the viral takeover of cells and slow the process by which COVID-19 takes hold. These compounds, many of which were designed as cancer treatments, seem likely to work because they block the chemical signals that activate filopodia production in the first place.
Among the seven drugs they identified as potentially useful against COVID-19 are Silmitasertib, a still-experimental drug in early clinical trials as a treatment for bile duct cancer and a form of childhood brain cancer; ralimetinib, a cancer drug developed by Eli Lilly; and gilteritinib (marketed as Xospata), a drug in use already to treat acute myeloid leukemia.
The new research emerges from an ambitious effort to identify promising COVID-19 treatments using the science of “proteomics,” the interactions among proteins. Scientists set out to identify the chemical signals and cascading chain of events that take place when a virus meets and overtakes a host cell. Then, they look for drug compounds that could scramble those chemical signals and disrupt the process of infection.



Until now, the process by which the coronavirus was thought to infect cells was pretty run-of-the-mill for a virus: It found receptors on the surface of the cells that line humans’ mouth, nose, respiratory tract, lungs and blood vessels.
Like space invaders in a science fiction tale, the tiny virus was known to dock on the surface of the much larger cell. A viral landing party came aboard and hijacked the cell’s usual function, making it a factory for its replication.
Tendrils reach out from a coronavirus-infected cell.

Tendrils reach out from a coronavirus-infected cell.
(UCSF)
The discovery that the coronavirus initiates the sprouting of filopodia in infected cells suggests that it has, at some point in its evolution, developed more than one way to ensure it gets passed quickly from cell to cell.

Typically, a rapid rise in infected cells will raise a victim’s viral load, make her feel sick and promote the transmission of the virus to other people. UC San Francisco’s Nevan Krogan, one of the paper’s senior authors, said there is much about the coronavirus that doesn’t match scientists’ expectations.
But the discovery of filopodia in coronavirus-infected cells suggests that this virus has developed more than one way to wheedle its way into cells and establish itself as a force to be reckoned with.
“It’s just so sinister that the virus uses other mechanisms to infect other cells before it kills the cell,” Krogan said. Other researchers include scientists from Mt. Sinai in New York, Rocky Mountain Labs in Montana (where these electron microscopy images were made), the Pasteur Institute in Paris and the University of Freiburg in Germany.
Another cell infected by the coronavirus.

Another cell infected by the coronavirus.
(UC San Francisco )

Cells sprouting filopodia not only look creepy. They keep some pretty nasty company as well.
Vaccinia, a member of the poxvirus family that causes smallpox, uses filopodia that sprout from infected cells to “surf” toward those cells and inject them with more viral particles, a 2008 study found. HIV and some influenza viruses have been known to use filopodia to enhance their ability to break and enter into cells. Many viruses alter the exoskeleton of the cells they infect, and inducing filopodia is one way they do it, said Columbia University virologist Angela L. Rasmussen. And while enhancing infection is one role they often play, there are many others.
But Krogan said even those viruses do not seem to set off the prolific growth of filaments that was seen by his colleagues on coronavirus-infected cells. The branching tentacles protruding from those cells were highly unusual, he said.
A coronavirus-infected cell reaches out to new hosts.

A coronavirus-infected cell reaches out to new hosts.
(UC San Francisco)

Columbia University microbiologist Stephen P. Goff urged caution in assuming that filopodia are necessarily behaving as a second mode of infecting cells with virus.
“It’s intriguing and a really cool observation,” Goff said. The study’s striking images show that the filopodia contain a lot of virus and that in the lab, inhibiting their growth seemed to reduce viral replication. This strongly suggests that filopodia are somehow amping up the virus’ ability to infect cells, he acknowledged.
“But we don’t yet know what stage [of infection] is affected” by the strange protrusions, he said. “It will be great fun to find out.”
 
福奇称新冠疫苗有效率仅为70%至75% 福奇称美国或无法实现群体免疫】在美国政府的支持下,预计3种新冠病毒疫苗将在未来三个月内投入到大规模临床试验研究中。但是,美国流行病学专家安东尼·福奇认为,新冠疫苗的有效率大约只有70%-75%左右,而且由于许多美国人不愿意接种,美国可能无法达到群体免疫的效果。“我们做得最好的是麻疹,有效率为97%-98%。”福奇说,“如果现在我们能达到那种程度就非常好了,但我认为不可能。我觉得有效率是70%-75%。”(@中国日报网,LS)



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美疾控中心公布数据:美国新冠死亡病例年龄明显偏低

“将新冠肺炎死亡病例按年龄进行分析时,美国处在一个异常值。”24日,美国《经济学人》以此为题报道称,美国疾控中心发布的最新数据显示,美国新冠死亡病例年龄明显偏低。



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报道称,在大家的普遍意识里,年纪大的人在被感染新冠肺炎后面临的风险最大。在一些被新冠肺炎影响的国家中,约60%死亡病例年龄在80岁以上。

然而,美国却是个例外。

报道援引美国疾病控制中心(CDC)6月16日发布的数据称,美国新冠肺炎死亡病例的年龄“明显偏年轻”。数据显示,在美国新冠死亡病例中,80多岁的人仅占不到一半,与此同时,40岁至60岁的人占绝大多数。不仅如此,报道还提到,美国新冠肺炎患者的平均年龄是48岁,但意大利是63岁。

对此,《经济学人》表示,与欧洲国家相比,美国新冠确诊及死亡病例的年龄均更低。如果将新冠肺炎死亡病例按年龄进行分析时,美国处在一个“异常值”。“而这一点有着严峻的影响。”

为什么美国会出现这种情况?对此,《经济学人》分析称,部分原因在于美国的人口平均年龄比欧洲小。报道称,美国人口平均年龄为38岁,意大利是45岁。而该报提到的另一个原因则是,美国中年人相比欧洲同龄人普遍“更不健康”。例如,他们往往更肥胖。
 
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