After billions of years of evolution, virus have learned how to “survive without life” – a terrifyingly effective strategy to make them endure, constantly threatening humans.
The deadly SARS-CoV-2 virus has brought to a standstill that the global life is only a cluster of genetic material, surrounded by protruding proteins with a thickness of 1/1000 thick eyebrow, which looks like a crown. (hence the name “corona”, meaning crown).
They are like zombies pretending to be (zombies), almost no sign of living things. But as soon as they enter the human airway, the virus activates, attacks the cell, multiplying millions of copies.
The mode of action of SARS-CoV-2 can be considered a “genius”, according to the Washington Post ‘s comment : penetrate into the human body and before humans have symptoms, they reproduce quickly and spread to other people.
They cause harm, devastate the lungs, cause death in some patients, but only cause mild symptoms in others, so they can always spread.
Researchers are racing to find a cure and a vaccine, but they stand in front of a formidable virus.
Outside “fake death”, the body is activated again
Respiratory virus often enter and reproduce in two places in the body. Either in the nose or throat, where they spread more strongly, or in the lower part of the lungs, where they will be less easily spread but easily fatal.
But the new strain of SARS-CoV-2 coronavirus as the two types combined. They live in the upper part of the airway, from which they can easily spread to the next victim after coughing or sneezing. But in some patients, the virus can go deep into the lungs, leading to death.
Thus, SARS-CoV-2 has both the potential for spread of common influenza and the death of its “relative” SARS, which caused an epidemic in Asia in 2002-2003.
But unlike SARS, SARS-CoV-2 has a lower death rate. In turn, symptoms will manifest less, longer than SARS. Thus, an infected person with SARS-CoV-2 often spreads it to others before he or she is infected.
In other words, SARS-CoV-2 has enough stealth to spread to the whole world.
The virus that are responsible for the most dangerous epidemics in the past 100 years: the 1918, 1957 and 1968 influenza, SARS, MERS and Ebola. Like the corona virus, the viruses all have animal origin, all encode genetic material in the RNA chains.
Outside the host’s body, such RNA viruses are often “inactive”. They have no signs of life such as metabolism, movement or reproduction. And they can “sit still” so long.
SARS-CoV-2 usually degrades for a few minutes or hours outside the host, but some particles may still be able to spread longer – such as 24 hours on the surface of the cover, or even to Three days on plastic and stainless steel surfaces.
In 2014, a virus that froze for 30,000 years, discovered and revived by scientists, could still infect an amoeba (a form of unicellular life).
On – off between live and not live
After entering the host, they use proteins to surround themselves to “unlock” and invade cells, then use intracellular mechanisms to assemble the necessary material and then continue doubling.
“They seem to have the ability to turn on and off between living and not living,” Gary Whittaker, a professor of virology at Cornell University, told the Washington Post . He described the virus as a hybrid of chemicals and biology.
The coronavirus strains such as SARS-CoV-2 are one of many families of RNA viruses. Among RNA virus, coronavirus are larger in size and have more complex mechanisms.
One of these “preeminent” mechanisms includes the “error proofing” proteins, which allow the coronavirus to correct errors during its replication. As a result, they reproduce faster than normal bacteria, but still do not duplicate the error and then “die prematurely”.
The general adaptability helps pathogens adapt to new environments, spread from one species to another. Scientists believe that SARS originates from bats and spreads to humans through the plow sold in the market. The SARS-CoV-2 virus can also now be derived from bats, and is thought to infect humans through intermediate hosts.
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Fight SARS-CoV-2 with the immune system and antiviral drugs
nce inside a cell, the virus can replicate 10,000 on its own within hours. After a few days, the infected person will have hundreds of millions of virus molecules in just a few drops of blood.
The strong proliferation of the virus makes the immune system counterattack, secreting chemicals. Increased body temperature, causing fever. Leukemia “legions” are drawn to the infected area. These reactions make people sick.
Andrew Pekosz, a virologist at John Hopkins University, compared the virus to a vandal.
He comes into your home, eats your food, uses your tables and chairs, and gives birth to 10,000 babies. “Destroy the house,” he said.
The battle between the virus and the immune system is extremely fierce, the surrounding cells are “plagued”.
Unfortunately, people do not have many ways to combat these bandits.
Currently, for bacteria, most antibacterial drugs work by interfering with the mechanism of the bacteria. For example, penicillin, the world’s most popular antibiotic, will “block” the type of molecule bacteria use as a cell wall.
Thanks to that, penicillin had a miraculous effect when it was brought to the front during World War II, fighting thousands of bacteria. In addition, human cells do not use this type of molecule, so we can safely use penicillin.
But viruses are different from bacteria. They do not have their own machinery and cells, so they work through human cells. Their protein is also human protein. Drugs that can kill viruses will also harm us.
For this reason, antiviral drugs often have to be “targeted” in a very specific and accurate manner, according to virologist at Stanford University Karla Kirkegaard.
Antiviral drugs need to target the proteins that the virus needs to use during copying. These proteins are specific to each virus, meaning that the virus is difficult to use for other viruses.
Worse, because the virus evolves quite quickly, if scientists find a cure, it is also unlikely to have a lasting effect. That’s why scientists have to constantly develop new drugs to treat the HIV virus, and why patients must take a “cocktail”, that is, mix a few antiviral drugs, to treat at the same time. several virus variants.
“Modern medicine must constantly keep up with the virus variants,” Ms. Kirkegaard said.
Particularly SARS-CoV-2 is still a question mark. Although the behavior of this strain differs from its cousin, SARS, there does not seem to be a difference between the surrounding spiny protein outside SARS-CoV-2 and SARS.
Understanding these proteins is key in vaccine development, according to Alessandro Sette from the La Jolla Immune Institute in California.
Previous research on SARS has shown that the protein surrounding SARS is what triggers the immune system to respond. In a study published this week, Sette showed that the same holds true for SARS-CoV-2.
More SARS-CoV-2 resembles SARS, the more optimistic the scientific community
That brings optimism, Sette said, because it shows that the current direction of scientists is targeting proteins to study vaccines is right. Specifically, if a person is exposed to a version, the body will be “trained” to identify and respond earlier.
“As such, the new strain of coronavirus is not so ‘new,'” Sette said.
Another positive point is that if SARS-CoV-2 is not much different from the SARS relative, it means that SARS-CoV-2 does not evolve too quickly. This gives scientists time to develop the vaccine and catch up.
In the meantime, the best weapon we have against coronavirus is community health measures, such as testing and maintaining social distance, along with diligent “gatekeepers”. our own immune system, says Kirkegaard from Stanford University.
Some scientists are even more optimistic about one thing: the virus itself.
Despite the mechanism of “genius” and effective, even potentially lethal, “viruses do not really want to kill us. (If not fatal) then it will be better for them, better for the virus number, when we are still healthy, ”according to Ms. Kirkegaard.
Experts say that, from an evolutionary perspective, the ultimate goal of the virus is to spread but only mildly affect the host – making an unwelcome but polite “guest” instead of a name ” vandalism “. The reason is that if the host dies as much as SARS or Ebola, the virus will no longer have a host to spread.
Virus are not fatal, only minor harm is the kind that can exist forever. A 2014 study found that the virus that causes herpes sores (cold sores) has existed with humans for 6 million years. “It was a very successful virus,” said Ms Kirkegaard.
If viewed from such an evolutionary perspective, the new strain of coronavirus SARS-CoV-2 seems to be quite “innocent” when spreading and causing many deaths, without knowing that there is another “softer” way for long-term survival, the Washington Post comments.
But over time, the viral RNA will gradually change. Maybe one day, not far, it will become one of the common seasonal flu strains, emerging every year, making us cough, sneeze, but nothing more serious, according to the Washington Post .