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特别报导:新冠病毒

Inside the Coronavirus

What scientists know about the inner workings of the pathogen that has infected the world

对于这一切仍然是未解之谜about the novel coronavirus and the COVID-19 disease it causes, scientists have generated an incredible amount of fine-grained knowledge in a surprisingly short time.

In the graphics that follow,亚博电子竞技presents detailed explanations, current as of mid-June, into how SARS-CoV-2 sneaks inside human cells, makes copies of itself and bursts out to infiltrate many more cells, widening infection. We show how the immune system would normally attempt to neutralize virus particles and how CoV-2 can block that effort. We explain some of the virus's surprising abilities, such as its capacity to proofread new virus copies as they are being made to prevent mutations that could destroy them. And we show how drugs and vaccines might still be able to overcome the intruders. As virologists learn more, we will update these graphics on our Web site (www.scientificamerican.com)。

对于此内容的静态版本,因为它出现在2020年七月刊亚搏竞彩官方合作伙伴亚博电子竞技请点击这里

Gene Machine

A SARS-CoV-2 virus particle wafting into a person's nose or mouth is about 100 nanometers in diameter--visible only with an electron microscope. It is a near sphere of protein (cross section shown) inside a fatty membrane that protects a twisting strand of RNA--a molecule that holds the virus's genetic code. Proteins called "S" form spikes that extend from the surface and grab onto a human cell, hundreds of times larger, so the particle, or virion, can slip inside; the crown, or corona, appearance gives the virus its name. Structural proteins--N, M and E--move inside the cell, where they help new virions form.

冠状病毒图文
  • 1.该病毒:在SARS-CoV的-2病毒颗粒是包裹在保护性脂肪包衣的蛋白质的一个球。
  • 2. RNA(red):这种RNA的扭曲链是蓝图病毒利用自我复制你的内心。
  • 3.参赛尖峰(Orange):该病毒利用其尖峰状蛋白S,它散布在表面上,以抢在人细胞。
  • 4.保护壳:这种脂质双层保护病毒的遗传货物因为它的旅行体内。
  • 4. N蛋白(Blue):这种蛋白质有助于保持病毒RNA稳定。
  • 6. E蛋白(Yellow):这种蛋白质有助于新的病毒颗粒的形式。
  • 7. M蛋白(Purple):这种蛋白质有助于新的病毒颗粒的形式。
How the Virus Invades

A SARS-CoV-2 particle enters a person's nose or mouth and floats in the airway until it brushes against a lung cell that has an ACE2 receptor on the surface. The virus binds to that cell, slips inside and uses the cell's machinery to help make copies of itself. They break out, leaving the cell for dead, and penetrate other cells.

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首先,它结合肺细胞 当病毒刺突蛋白的锁存器到一个ACE2受体,蛋白酶片断尖峰的头部。(ACE2通常有助于调节血压。)
接下来,它里面卡瓦 该版本融合机构,是在春天的状态下压缩穗的茎的一部分。病毒和肺细胞膜融合。斯派克斩首允许融合机构展开。
机械刀片本身到细胞膜和信道形式,允许Ñ蛋白质和RNA(遗传指令)进入肺细胞。 时间流逝:ABOUT 10 MINUTES
它复制 一旦病毒RNA是细胞内,它提出了二十几个基因细胞的核糖体,它的基因翻译成蛋白质。其中一些蛋白质的伸展,内质网,建立保护小泡,或囊。
病毒RNA复制机,使用自己的a polymerase, to make duplicates of RNA inside the vesicles. Some of the copies are utilized to make more viral proteins, such as the spike. Others are packaged into new virus particles, which break out of the lung cell.
N proteins link to RNA to help keep it stable.

Additional vesicles (that come from the endoplasmic reticulum and Golgi complex) assemble spike, M and E proteins.
Finally, It Breaks Out Vesicles carrying newly formed viruses merge with the cell membrane, opening a channel that allows the viruses to exit.
One cell can release hundreds of virus copies. It typically dies because its resources have been used up, or it is killed by the immune system. Some viruses head off to infect more cells. Others are exhaled into the air. 时间流逝:ABOUT 10 HOURS
How the Immune System Responds

Infected cells send out alarms to the immune system to try to neutralize or destroy the pathogens, but the viruses can prevent or intercept the signals, buying time to replicate widely before a person shows symptoms. When infection begins, the innate immune system tries to immediately protect lung cells. The adaptive immune system gears up for a greater response.

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The Innate Immune System Acts First:An infected cell releases interferon proteins that alert neighboring cells to create molecules that try to stop virus particles (red dots)from entering or reproducing. Interferon also beckons cells such as macrophages in the bloodstream that can engulf virus particles. 时间流逝:0–3 DAYS
The Adaptive Immune System Follows:Interferon also alerts B cells. They produce “neutralizing antibodies” that might recognize parts of the spike protein and bind to it, preventing the spike from grabbing onto a lung cell.
Interferon also recruits T cells, which can destroy viruses and also kill infected cells before viruses inside them burst out. Some B and T cells become memory cells that can quickly identify and fight a future invasion by the virus. 时间流逝:6–11 DAYS
The Virus Takes Countermeasures SARS-CoV-2 uses several tactics to thwart the immune system’s response.

Tactic 1:The virus spike may camouflage itself with sugar molecules. They flex and swing, potentially blocking antibodies from attaching to the virus, neutralizing it.
Normally, sensor proteins recognize incoming viruses as foreign and tell the cell nucleus to turn on genes for making messenger RNA molecules. The molecules deliver instructions to ribosomes to make interferon proteins that exit the cell to alert immune system cells.
Tactic 2:Several SARS-CoV-2 proteins are thought to block sensor proteins from acting or to interfere with instructions to the ribosome.
Drug and Vaccine Interventions

Commercial and university labs are investigating well over 100 drugs to fight COVID-19, the disease the SARS-CoV-2 virus causes. Most drugs would not destroy the virus directly but would interfere with it enough to allow the body's immune system to clear the infection. Antiviral drugs generally stop a virus from attaching to a lung cell, prevent a virus from reproducing if it does invade a cell, or dampen an overreaction by the immune system, which can cause severe symptoms in infected people. Vaccines prepare the immune system to quickly and effectively fight a future infection.

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Drug Target 1 Prevent the Virus from Entering the Cell:A drug or therapeutic antibodies could lock on to the spike protein, preventing it from binding to a lung cell’s ACE2 receptor. A drug could also attach to the protease enzyme and prevent it from cutting the spike protein so the virus cannot fuse with the cell.
Drug Target 2 Encourage Defective Viruses:A drug could interfere with the viral RNA polymerase enzyme, which works with another enzyme called ExoN (not shown) to fix mistakes in copied viruses that would disable those viruses,leading to more bad copies and fewer good ones.
Drug Target 3 Shut Down Virus:A drug could interfere with lung cell proteins the virus needs, such as those involved in making virus proteins or in making the vesicles the virus uses to copy its genome.
Drug Target 4 Reduce Hyperimmune Response:Immune cells can destroy too many lung cells, creating enough mucuslike waste to suffocate the lungs, forcing victims onto ventilators. Overproduction of an alarm protein, or cytokine, such as interleukin-6 can put immune cells into overdrive. Drugs could inhibit some of the cytokines by binding to them.
Vaccine Options A vaccine exposes the immune system to a safe version of a virus so it can practice making antibodies that will stop the pathogen and commit the exercise to memory so it is ready to fight the real virus during an infection. Vaccine makers are pursuing a variety of strategies for formulating and mass-producing vaccines.
How Vaccines Work Antibody Preparation:The vaccine version of a SARS-CoV-2 virus presents various molecules called antigens that belong to the real virus. Antigen-presenting cells grab them and provide them to helper T cells and B cells.
The T cells help B cells turn on to produce antibodies that could bind to the actual virus.
The helper T cells also tell killer T cells to devise ways to destroy lung cells that are infected.
Some of the B and helper T cells turn into memory cells that store the instructions so they can quickly spark B and T cells into action during an infection.
SARS-CoV-2 Vaccine Development Strategies Experts are exploring at least six strategies for making vaccine versions of the virus. Three of them involve injecting a modified version of the virus into people....
Three involve mapping genes from the virus, such as those for the spike protein, inserting the blueprints into DNA, RNA or a safe virus and injecting those into people.
The Remarkable and Mysterious Coronavirus Genome

在SARS-COV-2基因组是RNA的链是大约29,900个碱基长 - 为附近RNA病毒的极限。流感有大约13500个碱基,并引起普通感冒的鼻病毒有大约8,000。(A基是一对是RNA和DNA的积木化合物)。因为基因组是复制会削弱病毒期间可能发生如此之大,许多突变,但SARS-CoV的-2能够校对和正确拷贝。这种质量控制是在人细胞和DNA病毒共同但在RNA病毒极不寻常的。长基因组也有辅助基因,尚不完全清楚,其中一些可能会帮助它抵挡我们的免疫系统。

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校对 由于SARS-COV-2基因组是这么长时间,它可以编码一个巨大的信息量,使新型冠状病毒,创造更多的蛋白质和可能开展比其他RNA病毒更复杂的复制策略。其中一个有利的蛋白质是一种酶称为核酸外切酶(外显子),这有助于病毒校对无误的副本,因为它们制成。只有基因组病毒是长于约20,000个碱基使这种酶。
图像 图像
一旦SARS冠状病毒2型病毒已经感染了肺细胞,酶叫做聚合酶开始使其RNA拷贝,而另一种酶,外显子,发现随机突变和排出从这些复制基因错误。
图像 图像
附属基因 不寻常的,基因组的短位称为辅助基因与结构蛋白的基因聚类。研究人员还不确定他们做什么。一些被认为是帮助病毒逃避免疫系统编码蛋白质。
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