A virus is essentially information, a packet of data that you can benefit from sharing.
The information in question is genetic. Instructions for increasing the virus. Unlike truly living organisms, viruses cannot replicate on their own. It cannot move, grow, persist, or endure. You need a host. The viral code invades living cells, hijacks the genetic machinery and commands it to produce a new code, the new virus.
President Donald Trump characterized the response to the pandemic as a “medical war,” describing the viruses behind it as “geniuses,” “hidden enemies,” and “monsters.” It is more accurate to say that it is in conflict with a micrograph copier. Even that: copy machine assembly instructions, model SARS-CoV-2.
The virus has replicated among us for at least six months from now. The toll was catastrophic. Officially, more than 6 million people have been infected worldwide and 370,000 have died. (Actual numbers are certainly high.) America, which experienced the largest share of incidents and casualties, recently exceeded 100,000 deaths. The company was shut down, over 40 million Americans lost their jobs in 10 weeks, and the food bank was overrun. The virus fueled widespread frustration and revealed our most serious shortcomings in color, class, and privilege between carriers.
Still, summer-summer! — Everything has arrived. We look out, breathe, and breathe. Pausing is an illusion. Incidents are declining in New York, the epicenter of the United States, but are steadily increasing in Wisconsin, Virginia, Alabama, Arkansas, North Carolina, South Carolina, and other states. A recent revival was seen in China and South Korea where the pandemic broke out. Health officials are afraid of another major wave of infectious diseases in the fall, which is beyond the potential of that wave.
“We are in the early stages of this illness,” Dr. Ashisher of the Harvard Global Health Institute recently told the New York Times. “If this is a baseball game, it will be twice.”
There may be trillions of virus species in the world. They mainly infect bacteria, but also abalone, bats, beans, beetles, blackberries, cassava, cats, dogs, hermit crabs, mosquitoes, potatoes, pangolins, ticks, and Tasmanian devils. They give the birds cancer and blacken the bananas. Of the trillions, hundreds of thousands of viruses are known, and less than 7,000 have names. Only about 250, including SARS-CoV-2, have an infection mechanism.
In our information age, we have become accustomed to computer viruses and memes getting infected by viruses. The real thing is here now to remind you what the metaphor means. Just a tiny fraction of the data has landed more than half of the world’s commercial aircraft, significantly reducing global carbon footprint and doubling Zoom’s share price. It permeated our words “social distance,” “immunocompromised shopper,” and our dreams. It has postponed the premiere of sports, political competitions, and the upcoming Spider-Man, Black Widow, Wonder Woman, and James Bond films. Because of the virus, the US Supreme Court ruled over the phone and the boar roams the empty streets of Barcelona, Spain.
And unlike other species, it encourages a cooperative response. Cross-border teams of scientists are competing to understand the weaknesses of the virus, develop treatments and vaccine candidates, and accurately predict their next move. Healthcare professionals endanger their lives to make them more susceptible to illness. Here’s what we can do at home: Share the steps on how to make a surgical mask from a pillowcase. Sing or cheer from the window or front door. Please accept my sincere condolences. Provide hope
Dr. Melanie Ott, director of the Gladstone Institute of Virology in San Francisco, said:
So far, the game has reached a dead end. Collection, analysis, dissemination, research: what is this? What should i do? When can life return to normal? And we hide and advance ourselves at our expense while the latest iterations of ancient biochemical codes are ticking.
Horrible envelope
No one knows when the virus first came out. Perhaps, as one theory holds, they started as free-living microbes and were eliminated by natural selection into parasites. Perhaps they started out as genetic gears within the microorganism, then gained the ability to invade and invade other cells. Alternatively, the virus came first, shuttled and replicated in a primitive protein soup, increasing the shadow of complexity-enzymes, adventitia-cells, and ultimately us. They are bags of code (double-stranded or single-stranded, DNA or RNA) and are sometimes called capsid-encoding organisms or CEOs.
SARS-CoV-2 grows as the virus progresses. Its genome is more than twice the size of the average influenza virus, about half the size of the Ebola virus. But it’s still small. One tenth of a millimeter, almost one thousandth of the width of human hair, is less than the wavelength of light from germicidal lamps. If the person is the size of the earth, the virus is the size of the person. Imagine human lung cells as a cramped office large enough for a desk, chair or copier. SARS-CoV-2 is an oil-based envelope attached to the door.
It was officially confirmed by Chinese scientists on January 7. Since a few weeks ago, a mysterious respiratory disease has spread to Wuhan. Health officials worried that it could be a severe acute respiratory syndrome or a relapse of SARS, a surprising viral disease that suddenly emerged in 2002, with more than 8,000 people infected and months later. Nearly 800 people were killed in the country and then forcibly forgotten.
Scientists collected fluid samples from three patients and used a nucleic acid extractor and other tools to compare the pathogen’s genome to a known genome. Transmission electron microscopy has revealed the cause: a spherical, “quite unique spike” reminiscent of a crown or sun corona. It was a coronavirus and was new.
In later-colored images, the virus resembles a small shiny orb of lint or a paper-like egg of certain spiders, with dozens attached to much larger cells. Recently, a visual team working closely with researchers created the “most accurate model of the SARS-CoV-2 viral particle currently available”: a multicolored glove of barbed wire from Dr. Sousse. A sunk navy mine whose fine moss texture is covered with algae and sponge.
Once upon a time, our pathogens were loosely named: Spanish cold, Asian cold, yellow fever, and black death. You now have a code for H1N1, MERS (Middle East Respiratory Syndrome), HIV, a string, code that is as efficient as the virus itself. The new coronavirus was temporarily named 2019-nCoV. On February 11, the International Commission on Taxonomy of Viruses officially renamed SARS-CoV-2 and showed that it was very closely related to another coronavirus, the SARS virus.
Prior to the advent of the original SARS, coronavirus research was a specialized backwater. “There’s been a lot of attention to coronavirologists,” said Susan R. Weiss, a virologist at the University of Pennsylvania. “It’s in sharp contrast to what was previously largely ignored.”
There are hundreds of coronaviruses. Two, SARS-CoV and MERS-CoV, can be fatal. Four cause one third of common colds. It infects many human-related animals, including camels, cats, chickens, and bats. All RNA viruses. Our coronavirus, like all others, is a string of approximately 30,000 biochemical building blocks called nucleotides surrounded by both protein and lipid membranes.
“I’ve always been impressed by the coronavirus,” said Anthony Fehr, a virologist at the University of Kansas. “They’re very complex in that they move and start hijacking cells. They produce more genes and proteins than most other RNA viruses, giving you more options to shut down your host cells. .”
The core code of SARS-CoV-2 contains genes for up to 29 proteins. This is an instruction to copy the code. One protein, S, provides a spike on the surface of the virus, opening the door to target cells. Others, when entering the room, separate their tasks and pay attention: turn off the cell’s alarm system. Command the copy machine to make new viral proteins. Folds the viral envelope, helping new viruses bubble thousands of cells.
“I usually imagine it as an entity that enters a cell, and then it falls apart,” Ott of the Gladstone Institute said. “It needs to fall apart in order to build some mini-factories within the cell to replicate itself, and finally assemble as entities to infect other cells.”
For medical researchers, these proteins are key to understanding why the virus succeeds and how it is neutralized. For example, to enter cells, the S protein binds to a receptor called angiotensin-converting enzyme 2, or ACE2, like the doorknob’s hand. This coronavirus S protein is similar in structure to the original SARS S protein (the “SARS classic”), but data suggest that it binds much more strongly to the target enzyme. Some researchers think this may partly explain why the new virus infects humans so efficiently.
All pathogens evolve along a pathway between impact and stealth. It is mild and the disease is not transmitted from person to person. Those who are too visible and sick and aware will stay at home or be avoided — the disease will not spread. “SARS was quickly contained because it infected 8,000 people, some of which did not spread before the symptoms appeared,” Weiss said.
By comparison, SARS-CoV-2 seems to have achieved a good balance. “No aspect of the virus is unusual,” said Pardis Sabeti, a computational geneticist at the Broad Institute who helped Ebola virus sequencing in 2014.
The SARS Classic not only colonized human lung cells quickly and coughed, but announced its presence. In contrast, successors tend to settle first in the nose and throat and may experience fewer initial symptoms. It is believed that some cells are rich in the surface enzyme ACE2 — the doorknob is swiveled by SARS-CoV-2. The virus grows quietly and spreads quietly. According to one study, people who carry SARS-CoV-2 are most likely to be infected 2-3 days before they realize they may become ill.
From there, the virus can travel to the lungs. Delicate alveoli, which collect essential oxygen for the body, become inflamed and struggle to do their jobs. The texture of the lungs changes from air leaf loss to gummy marshmallow. Patients can develop pneumonia. Some are drowned internally, desperate for oxygen, have acute dyspnea, and need ventilators.
The virus is even more subdued. Damages the muscle wall of the heart. Attacks the inner walls of blood vessels to cause blood clots; causes stroke, stroke, inflammation; damages the kidneys. In many cases, the greatest damage is not by the virus, but by attempts to repel it with dangerous “cytokine storms” of immune system molecules.
The result is an illness with an embarrassing array of faces. Initially a dry cough and low fever. Shortness of breath or difficulty breathing, sometimes. Maybe you lose your smell and taste. It may be that your toes are red and inflamed, as if you had frostbite. For some patients, it feels like a heart attack and causes delusions and disorientation.
In many cases, you don’t feel anything at all. According to Centers for Disease Control and Prevention, 35% of people infected with the virus have little or no symptoms, but they can spread it. “The virus behaves like a pathogen humans have never seen,” says Science.
In addition, pathogens are almost gone. “It has these perfect traits that spread throughout the human population,” Fehr said. “If you don’t know what the virus is, and if you don’t take proper precautions, it will infect almost every human on Earth. It may still do it.”
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Data and data
On January 10, China’s Wuhan Health Commission reported last week that 41 people had a disease caused by a coronavirus and one died.
That same day, Chinese scientists published the complete genome of the virus. The blueprints that can be simulated and synthesized in the lab are similar to physical samples, and were readily available to researchers around the world. The analyzes were displayed on journals, preprint servers such as bioRxiv, and sites such as nextstrain.org and virological.org. A clue to the origin, error and weakness of the virus. Since then, the new coronavirus has started to replicate not only physically in human cells, but figuratively, and perhaps even in its own mind, to its own harmful effects.
Ott entered medicine in the 1980s, when AIDS was still new and horribly unknown. “If you compare that time to today, there are many similarities,” she said. “New viruses, rushes to understand, cures or vaccines. What’s fundamentally different now is the creation of this community of collaboration and data sharing. It’s really moving.”
Three hours after the virus’ code was published, San Diego-based Inovio Pharmaceuticals set out to research a vaccine against it—now one of more than 100 such efforts worldwide. Sabeti’s lab immediately set about developing diagnostic tests. Ott and Weiss were able to quickly get a sample of the live virus and “look up what’s really going on” when they infected cells in the lab, Ott says ..
“The cells are starting a serious battle to prevent the virus from entering, or to alert everyone around them when they enter and prevent the virus from spreading,” she said. “The purpose of the virus is to overcome this first surge of defenses and set up a shop long enough to replicate and spread itself.”
Because the toolkit contains so many proteins, viruses have many ways to counter our immune system. They also provide potential vaccine and drug targets. Researchers work at every angle. Most vaccine efforts focus on destroying spike proteins that allow them to enter cells. The drug lemdecivir targets the viral replication machinery. Fehr is studying how the virus can kill the immune system.
“I use the analogy of’Star Wars’,” he said. “The virus is the dark side. We have a cellular defense system of hundreds of antiviral proteins.”-Jedi Knight-“To protect ourselves. In our lab, one specific weapon I’m investigating one specific Jedi that uses a virus and how the virus fights back.”
These battles in the field of biochemistry put a strain on the alphabet they describe. This analogy of the Jedi is a specific enzyme (poly-ADP-ribose polymerase, or PARPS) produced by infected cells and that swings a molecule that attaches to a specific invading protein. Yet,” Fehr said—and confuses them. Correspondingly, the virus has its own enzyme that cleans the sand crawler out of the Jedi like dust.
Carolyn McHumer, a cell biologist at Johns Hopkins School of Medicine, is studying later stages of the process to learn how the virus can navigate, assemble, and shed itself within host cells. The research topics on her university webpage include not only coronaviruses, but also intracellular protein transport and exocytosis of large cargo.
Once in the cell, the viral components are placed in a small area or organelle. This is called the Golgi complex, which is similar to a stack of pancakes and acts as the cell’s mail classification center. Machamer has been working to understand how the virus directs the unit and routes all newly replicated viral bits scattered throughout the cell for final assembly.
She admitted that the subject was “insufficiently studied.” Most drug research focuses on the early stages. For example, they block infections very first or interfere with intracellular replication. “It’s not getting as much attention as I said,” she said. “But I think that’s the case now. I think there are some very interesting targets that could create new types of drugs.”
The inquiry line dates back to her postdoctoral era. She was studying the Golgi complex — “Organelles are really strange” — even then. “It follows what you are interested in. It’s the basic science. It’s like you follow your nose, not actually undertaking to cure the world or something.”
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For every note the virus received, it is still new to science and rich in unknowns. “I’m still very focused on the question. How do viruses get into the body?” Ott said. “Which cells are infected in the upper respiratory tract? How does it enter the lower respiratory tract and from there to other organs? It is not clear what the path is or what kind of vulnerable path it is. There is none.”
And the most pressing: why are many of us asymptomatic? “The virus manages this without leaving any trace, but some people have a huge reaction,” she said. “It’s the biggest problem right now and the most urgent.”
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Mistakes are made
Even copiers are imperfect, and SARS-CoV-2 is no exception. Whenever a virus tells a host cell to copy itself, mistakes occur, for example, the wrong nucleotide is replaced with the correct nucleotide. Theoretically, these mutations or their accumulation can reduce the infectivity and lethality of the virus, but in most cases it does not affect virus performance.
The important thing to note is that the process is random and continuous. Humans describe the battle between the host and the virus as war, but the virus is not in war. Our enemies have no agents. It does not develop a “strategy” to escape the activity of our drugs or our immune system.
Unlike some viruses, SARS-CoV-2 has a proofreading protein (NSP14) that eliminates mistakes. Still, the error slips through. On average, the virus gets two mutations a month. This is less than half the flu error rate, increasing the likelihood that a vaccine or drug treatment once developed will not soon become obsolete. “So far, it’s been relatively loyal,” Ott said. “It’s good for us.”
By March, at least 1,388 variants of coronavirus had been detected worldwide, all functionally identical to the knowledge of scientists. Arranged as an ancestor tree, these strains reveal where and when the virus spread. For example, the first confirmed case of COVID-19 in New York was published on March 1st, but analysis of the sample revealed that the virus began to spread in the region a few weeks ago. .. Unlike the earlier cases on the West Coast, which were inoculated by people arriving from China, these cases were inoculated from Europe and in many parts of the country.
The roots can be traced back further. The first known patient was hospitalized in Wuhan on December 16, 2019 and became sick for the first time on December 1. The first infection would have occurred much earlier. Sometime before that, the virus or its precursors were in the bat-the genome is 96% similar to the bat virus. It is unknown how long ago it did the jump and acquired the mutations needed to do so. In all cases, contrary to certain conspiracy theories, SARS-CoV-2 was not designed in the laboratory.
“These scenarios are very unlikely to be impossible,” said Dr. Robert Garry, a microbiologist at Tulane University and an emerging disease expert. In March, a team of researchers including Garry published a paper in Nature Medicine that compared the genome and protein structure of the novel virus with those of other coronaviruses. They conclude that the new differences are “most likely the result of natural selection.” “Our analysis clearly shows that SARS-CoV-2 is not a laboratory construct or a deliberately engineered virus.”
In our species, the virus has found a major habitat. Garry appears to do most of the replication in the upper respiratory tract, Garry says. “It may make it easier to spread in your voice, so you may have more chances to spread it by chance, and perhaps early in the course of the disease.”
And we have it: whatever creature, or the correct word, ideally adapts to human conversation, the louder it gets. Our communication is that communication. Consider where so many outbreaks began, such as funerals, parties, call centers, sports arenas, meat packing plants, dorm rooms, cruise ships, and prisons. A medical conference in Boston in February generated more than 70 cases in two weeks. In Arkansas, several incidents were associated with “a high school swimming party that I’m sure everyone is convinced is innocuous,” Governor Asa Hutchinson said. After the choir rehearsal in Mount Vernon, Washington, 28 choir members became ill. Even the song is no longer safe.
The virus has no problem finding us. But we are still struggling to find it. A recent model by a Columbia University epidemiologist estimates that an additional 12 people will not be detected for all infections recorded in the United States. Who has it, who had it, who doesn’t? Having a firm grasp of the whereabouts of the virus using diagnostic tests, antibody tests, and contact tracking is essential to our bid to return to a normal life. However, human immune response is not uniform.
In an open letter in late May, a group of former White House scientific advisors say the federal government will immediately prepare to avoid an “abnormal supply shortage” in preparation for a possible pandemic recurrence later this year. I warned that I needed it that happened this spring.
“The virus is here and everywhere,” Dr. Rick Bright, former director of the Office of Advanced Biomedical Research and Development, told the US Senate in mid-May. “We need to unleash the voices of scientists in the US public health system so they can hear,” he said, “the Master Coordination Plan on how to respond to this outbreak is No,” he added.
The SARS-CoV-2 virus has no plans. there is no need. Without the vaccine, the virus will remain.
“This is a fairly efficient pathogen,” Garry said. “It’s very good at what it does.”
Next wave
“The virus spreads because of the intrinsic and latent nature of culture,” recently wrote media theorist Douglas Rashkov, who coined the word “get viral” 20 years ago. 「生物学的ウイルスとメディアウイルスはどちらも、自分たちのホストよりも自分たちのことをあまり言いません。」
SARS-CoV-2を知ることは、自分自身を熟考することです。それは、機械的で、無反射で、一貫してメッセージ上にあります—地球上で見られる、データ管理の最も純粋に近い生きた表現。あり、あり、さらにあります。ウイルスには「私」は存在しません。
私たちはその正反対です。人間とそれが意味するすべてのもの。情報の達人、誤った情報のための吸盤;感情、自我、希望的な思考の奴隷。しかしまた：探究的、故意、楽観的。私たちの最高の瞬間に、私たちは学び、私たち自身よりも進歩するよう努めています。
「このパンデミックから抜け出すための最良のことは、誰もが何らかの方法でウイルス学者になったことです」とオットは言いました。彼女はズームで家族とドイツで定期的に雑学クイズをします。最近、トピックはウイルスを中心にしていて、彼女は彼らがどれだけ知っているかに感銘を受けました。 「周りにはもっと多くの知識があります」と彼女は言った。 「周りにも間違った情報がたくさんあります。しかし、私たち全員がそれを廃止したいと考えているため、人々は非常に読み書きができるようになりました。」
Sabetiはある程度まで同意した。彼女はウイルスについて深い好奇心を示した—それらは「理解するための明白な反対者」である—と言ったが、今度は、彼女は純粋に知的追求への関心を失ったと述べた。
「今のところ、私がいる場所です。私は本当にこのウイルスを止めたいだけです」と彼女は言った。 「控えめに言っても、私たちが社会を遠ざけてきたこの地位にいることは、とても苛立たしくて失望します。社会的距離を作り出しました。準備されていませんでした。
「私はそれを理解したくありません」と彼女は言った。 「私にとって、それは…私は朝起きて、私の動機はただ、このことをやめ、これが二度と起こらないようにする方法を見つけ出すことです。」
