However, once the virus enters the human respiratory tract, it hijacks our cells to create millions more versions of itself.
The way this coronavirus pathogen works has a certain evil genius: it can easily be bought in humans without knowing it. Before his first host even develops symptoms, he already spreads his replicas everywhere and passes on to his next victim. It is powerfully lethal in some cases, but mild enough in others to avoid containment. And at the moment we have no way to stop it.
While researchers are running to develop medicines and vaccines for the disease that has already made 350,000 people ill and killed more than 15,000 people, this is a scientific portrait of what to expect.
Between chemistry and biology
Respiratory viruses tend to become infected and multiply in two places: in the nose and throat, where they are highly contagious, or deeper in the lungs, where they spread less easily but are much more deadly.
This new corona virus, SARS-CoV-2, reduces the difference. It lives in the upper airways, where it sneezes or coughs easily on its next victim. However, in some patients, it can get deep in the lungs, where the disease can be fatal. This combination gives him the contagion of some colds and the lethality of his close molecular cousin SARS, which caused an outbreak in Asia from 2002-2003.
Another insidious feature of this virus: if you give up this piece of lethality, its symptoms appear less quickly than with SARS, which means that people often pass it on to others before they even know they have it.
Viruses like this have been responsible for many of the most destructive outbreaks of the past 100 years: the 1918, 1957, and 1968 river; and SARS, MERS and Ebola. Like the corona virus, all of these diseases are zoonotic – they sprang from an animal population in humans. And all of them are caused by viruses that encode their genetic material in RNA.
This is no accident, say scientists. The zombie-like existence of RNA viruses makes them easy to catch and difficult to kill.
Viruses rest outside a host. They do not have any of the traditional characteristics of life: metabolism, exercise, reproductive ability.
And so they can last quite a long time. Recent laboratory tests have shown that although SARS-CoV-2 is usually broken down outside of a host within minutes or a few hours, some particles are viable up to 24 hours on cardboard and up to three hours on plastic and stainless steel – potentially infectious – can stay days. In 2014 a Virus frozen in permafrost for 30,000 years The scientists found were able to infect an amoeba after it was revived in the laboratory.
When viruses encounter a host, they use proteins on their surfaces to unlock and penetrate their unsuspecting cells. Then they take control of the molecular machinery of these cells to produce and assemble the materials needed for more viruses.
"It alternates between alive and not alive," said Gary Whittaker, professor of virology at Cornell University. He described a virus as "between chemistry and biology".
Coronaviruses – named after the protein spikes that adorn them like crown points – are unique among RNA viruses because of their size and relative sophistication. They are three times the size of the pathogens that cause dengue, West Nile and Zika, and can produce additional proteins that support their success.
"Let's say dengue has a tool belt with just a hammer," said Vineet Menachery, a virologist at the University of Texas Medical Department. This corona virus has three different hammers, each for a different situation.
These tools include a proofreading protein that corona viruses can use to fix some bugs that occur during the replication process. They can still mutate faster than bacteria, but are less likely to produce offspring that are so harmful that they cannot survive.
The ability to change helps the germ to adapt to new environments, be it a camel intestine or a person's airway that unwittingly grants access with an accidental scratch on the nose.
Scientists believe that the SARS virus originated as a bat virus that reached humans through civet cats sold in animal markets. It is believed that this current virus, which can also be attributed to bats, may have had an intermediate host an endangered scaly anteater called pangolin.
"I think nature has told us over the past 20 years that & # 39; hey, corona viruses that start in bats can cause pandemics in humans, and we have to consider them as influenza, a long-term threat. & # 39 ; " said Jeffery Taubenberger, virologist at the National Institute of Allergy and Infectious Diseases.
Funding for coronavirus research increased after the SARS outbreak, but funding has dried up in recent years, Taubenberger said. Such viruses usually cause colds and are not as important as other viral pathogens, he said.
The search for weapons
In a cell, a virus can make 10,000 copies of itself in just a few hours. Within a few days, the infected person carries hundreds of millions of virus particles in every teaspoon of their blood.
The attack triggers an intense reaction from the host's immune system: defensive chemicals are released. Body temperature rises and causes fever. Armies of germ-eating white blood cells swarm in the infected region. It is often this reaction that makes a person sick.
Andrew Pekosz, a virologist at Johns Hopkins University, compared viruses to particularly destructive burglars: they break into your house, eat your food and use your furniture and have 10,000 babies. "And then they leave the place devastated," he said.
Unfortunately, people have little resistance to these burglars.
Most antimicrobial agents interfere with the functions of the germs that they target. For example, penicillin blocks a molecule that bacteria use to build their cell walls. The drug works against thousands of bacteria, but since human cells don't use this protein, we can absorb it without harming it.
But viruses work through us. Without their own cellular machinery, they are intertwined with ours. Your proteins are our proteins. Your weaknesses are our weaknesses. Most of the medication that could hurt them would hurt us too.
For this reason, antiviral drugs must be highly targeted and specific, said Stanford virologist Karla Kirkegaard. They tend to target proteins produced by the virus (using our cellular machinery) as part of its replication process. These proteins are unique to their viruses. This means that the drugs that fight one disease generally don't work on several.
And because viruses develop so quickly, the few treatments that scientists develop don't always last long. For this reason, scientists are constantly developing new drugs to treat HIV, and patients are taking a “cocktail” of antivirals that viruses have to mutate several times to resist.
"Modern medicine has to constantly look for new viruses," said Kirkegaard.
SARS-CoV-2 is particularly puzzling. Although his behavior differs from that of his cousin SARS, there are no obvious differences in the spiky protein keys of the viruses that allow them to enter host cells.
Understanding these proteins could be key to developing a vaccine, said Alessandro Sette, director of the Center for Infectious Diseases at the La Jolla Institute for Immunology. Previous research has shown that the spike proteins on SARS trigger the protective response of the immune system. In an article published this week, Sette found that this also applies to SARS-CoV-2.
According to Sette, this gives scientists reason to be optimistic. This confirms the researchers' assumption that the spike protein is a good target for vaccines. Inoculating people with a version of the spike protein can teach their immune systems to recognize the virus and respond more quickly to the intruder.
"It also means that the novel corona virus is not that new," said Sette.
And if SARS-CoV-2 is not that different from its older cousin SARS, the virus is unlikely to develop very quickly, so scientists who develop vaccines have time to catch up.
In the meantime, Kirkegaard said, the best weapons we have against coronavirus are public health measures like testing and social distancing, as well as our own immune system.
Some virologists believe that we have another thing in our favor: the virus itself.
Despite his evil genius and efficient, deadly design, Kirkegaard said, "The virus doesn't really want to kill us. It's good for them, good for their people, if you walk around and are perfectly healthy."
Experts believe that the ultimate goal of viruses is to be contagious while protecting the host – a less destructive burglar and a more considerate house guest.
This is because highly lethal viruses like SARS and Ebola tend to burn themselves out, so nobody stays alive to spread them.
But a germ that only annoys can continue indefinitely. A 2014 study found that the virus that causes oral herpes has been in the human line for 6 million years. "This is a very successful virus," said Kirkegaard.
From this perspective, the novel corona virus, which kills thousands worldwide, is still at an early stage in its life. It replicates destructively without knowing that there is a better way to survive.
But bit by bit, his RNA will change over time. Until one day, not so far in the future, it will only be one of the few cold corona viruses that circulate every year and give us cough or runny nose and nothing else.