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Many things have changed in the five months since the world found out about Sars-CoV-2, the long name for the little virus that has had a massive impact on economies and societies.
And there may be more surprises, or shocks, to come.
Scientists, detectives in the microbial world, are still learning more about the virus, so tests, medications, and vaccines can be developed to identify and treat those who are infected and inoculate those who are not.
But as the layers of the unknown peel off, it may appear that this virus is constantly changing, leading to changes in public health policy.
At first, it seemed unlikely that people without symptoms could transmit the virus, so only the unwell were asked to wear a mask in Singapore. In April, it became clear that people asymptomatic with Covid-19 were more common than previously thought, and could go out and infect others.
Now, anyone caught in public without a mask faces a $ 300 fine.
There are still several other questions about the virus.
For example, although this virus belongs to the same family that caused the outbreak of severe acute respiratory syndrome (Sars) in 2003, why is it so much more contagious?
And why do some Covid-19 patients develop a severe form of the disease while others do not?
Safe distancing measures can give us some time while waiting for a vaccine.
As the chief health scientist at the Ministry of Health, Professor Tan Chorh Chuan, said in the early days of the outbreak: “To fight a war, you must know your enemy.”
The Straits Times highlights what we know about the virus and the gaps that remain.
IMAGE OF A MURDERER
Joining the profile of a murderer requires, first of all, knowledge about his identity.
And once that identity has been finalized, the next step is to counter it.
COLLECTIVE FAILURE
Seventeen years have passed since the Sars outbreak, and although there has been a scattered investigation of coronaviruses since then, there was little coordination between the research groups, and there was no useful medication or vaccine for that … It was there that we collectively failed.
It’s great now that everyone is working on this, and the pandemic illustrates the need for real, international collaboration in the future.
PROFESSOR JULIEN LESCAR, expert in infectious diseases at the Nanyang Technological University.
The virus first appeared in Wuhan, China in late December, infecting workers at a wildlife market in China and causing them to display pneumonia-like symptoms.
In its early stages, it was simply known as the new 2019 or 2019-nCoV coronavirus, a nod to how new and unknown this virus was.
But on January 12, scientists around the world received an important clue when Chinese scientists uploaded the coronavirus genome into a public database.
An organism’s genome is unique and helps scientists distinguish it from other viruses.
The genome of this coronavirus is made up of a single-stranded genetic material known as RNA, which is made up of an “alphabet” of molecules known as nucleotides.
There are four different nucleotide bases that function as the basic building blocks for all RNA viruses: adenine (a), cytosine (c), guanine (g), and uracil (u). The way these four nucleotide bases are organized is unique to each virus.
From this, scientists were able to say that the virus was closely related to the one that caused Sars in 2003.
The official name of the virus, Sars-CoV-2, which was announced in February by the World Health Organization (WHO) about a month after the genome was released, reflects this relationship.
But unlike Sars, which caused around 800 deaths, Covid-19 has caused a much higher death toll, with nearly 300,000 dead so far.
Scientists are still trying to figure out why. And its genome can provide important clues.
Infectious diseases expert at Nanyang Technological University (NTU), Julien Lescar, said: “Genome availability is a very important step and this information is used constantly.”
Genes refer to a specific nucleotide sequence throughout the genome.
In humans, genes determine how we look and behave, as genes direct the type of protein, an important component of cells, tissues, and organs, that is produced.
This is the same for viruses.
For example, specific genes in the viral genome direct the production of proteins that are used to hijack a human cell.
Under a microscope, the virus that causes Covid-19 is spherical.
At the center is its genome, which is surrounded by an oily membrane that has a “crown” of sugar-coated spike proteins protruding from it, hence the name “crown” or crown.
It is these pointy proteins, or S proteins, that help the virus infect its host by hooking into the receptors of the human cell, the way a key fits into a lock.
This could have implications in the real world.
“Some candidate vaccines target this part of the virus to elicit a protective immune response,” said associate professor Lescar.
“In principle, antibodies to protein S should be enough to prevent infection.”
Antibodies are elements of the human immune system.
By “capturing” S proteins before they bind to human cell receptors, these antibodies can prevent invasion, Professor Lescar said.
But viruses are prone to mutation, which occurs when the virus makes imperfect copies of itself, introducing variations along the way.
Until now, mutations in the coronavirus have made little difference in its ability to infect humans, said Dr. Sebastian Maurer-Stroh, deputy executive director for research at the Institute for Bioinformatics at the Agency for Science, Technology and Research (A * Star), who is involved in the surveillance of the viral genome.
Instead, the various “types” of coronaviruses observed so far were like similar vehicles with different plates, he added.
MODUS OPERANDI
So when does a coronavirus invasion start?
Does it start when virus-laden respiratory drops enter the mouth, nose, or eyes? Or can you contract the disease by inhaling virus particles into the air? If the virus can be found in stool samples, can it be spread through the fecal-oral route?
Scientists have raised all these possibilities.
But the WHO is clear.
“Based on current evidence, the Covid-19 virus is primarily transmitted between people through respiratory drops and contact routes,” it said on its website.
And in an analysis of 75,465 cases of Covid-19 in China, transmission by air was not reported, the global health agency added, saying that to date there have also been no reports of fecal-oral transmission of the virus.
But once in the human body, the virus can cause disease, and scientists are now trying to figure out exactly how.
The virus begins its invasion by using its S proteins to bind to receptors in the human cell. The ACE2 receptor on the surface of the human cell is a likely entry point.
Once inside, the virus releases its RNA into the human cell and uses its host’s cellular machinery to replicate. Once replication is complete, new viral particles are released from the host cell. Active replication and the release of viral particles cause the host cell to die.
“Assuming there is no immune response, the virus would invade cells in the lungs and multiply exponentially, killing the cells as it infects them. This would cause great damage to the lungs,” said Dr. Poh Chek Meng, researcher at A * Star’s Singapore Immunology Network.
This is why people with compromised immune systems can easily contract serious bacterial and viral infections.
However, in the case of most people, the immune system responds to fighting the virus, Dr. Poh said. “Unfortunately, sometimes the immune system itself can cause damage to the lungs,” he added.
When a human host cell dies from viral invasion, it releases molecular “distress signals” that trigger the formation of cytokines, an element of the immune system that signals the presence of a pathogen.
Cytokines cause inflammation so that the immune system responds to potential danger and recruits more help.
Explained Dr. Matthew Tay, also a researcher with the A * Star Singapore Immunology Network: “Cytokines instruct the body’s immune ‘soldiers’ to come to the area and look for pathogens to eliminate them.” This also causes the blood vessels in the area to dilate, allowing more fluid to pass.
“This is often helpful because it allows soldiers to come more quickly,” said Dr. Tay, adding that bloating is a by-product of this process. These responses generally work together to clear the infection from the body.
But sometimes, the immune system goes into overdrive, causing the overproduction of cytokines that could eventually damage the lung infrastructure.
This cytokine storm can also circulate to other organs, causing damage to multiple organs or muscle and joint pain and fatigue, as well as abdominal pain, vomiting, and diarrhea.
Although cytokines are first produced at the site of infection, they can spread to other sites in the body, Dr. Tay explained.
“This could occur when the virus multiplies too much, or the host’s immune response to infection becomes dysfunctional, causing cytokine production to become uncontrollably high,” he said.
Both Dr. Poh and Dr. Tay are part of a team of scientists who last month published an article in the journal Nature Reviews Immunology on how Sars-CoV-2 causes disease in the body and possible ways to treat it.
One strategy proposed in the document was to administer high concentrations of a soluble form of ACE2, the receptor found on the surface of the human cell, which could reduce the entry of virus into target host cells.
Dr. Poh said such decoy strategies are already being used against other diseases, such as rheumatoid arthritis. “This decoy strategy may work against Covid-19, especially if soluble ACE2 receptors encounter the virus when injected into the body, and if they are injected early enough in the infection, before inflammation becomes get out of control. “
But more work is needed, he said, since the stability of the soluble ACE2 receptor in the human body is unclear at this time.
DEFEND YOURSELF
But humanity has more than one tool in its arsenal to fight the virus.
Antibody therapy, which involves injecting laboratory-produced antibodies into a patient as a substitute for those generated by the immune system, is a promising area.
When antibodies detect the presence of a virus, they bind to the infected cell, signaling the presence of the pathogen so that other elements of the immune system can intervene to destroy it.
A * Star, for example, is working with the Japanese pharmaceutical company Chugai Pharmabody Research on a therapeutic antibody for Covid-19. This antibody targets the virus S protein, preventing it from attaching to a human host cell.
But in the long term, vaccines are also being developed to help inoculate the population before they become infected. They work by injecting a small amount of a less or non-infectious strain of the virus into a person, awakening the body’s protective response.
Homegrown biomedical company Esco Aster, for example, is working on a “chimeric vaccine” in collaboration with US biotech company Vivaldi Biosciences.
This vaccine is produced by binding antigens, the part of the virus that antibodies detect, from the coronavirus, to flu virus proteins. The hope is that the vaccine, if successfully implemented within the next year, could confer immunity against both Covid-19 and influenza.
The Duke-NUS School of Medicine is also working on a vaccine in collaboration with the American firm Arcturus Therapeutics.
The vaccine works by first injecting some of the virus’s genetic material into the patient’s body.
This initiates a series of molecular processes, including the manufacture of viral parts that the human immune system remembers.
This allows the immune system to “recognize” the virus, causing the production of antibodies without exposing the patient to the risk of infection.
But NTU professor Lescar said it could be a year or more before a vaccine can be developed and put into practice, due to the need for rigorous controls to ensure it is safe for use in people.
While rapid diagnostic tests and antiviral drugs could be accomplished sooner, he emphasized that scientific research is a marathon, not a race.
“It has been 17 years since the Sars outbreak, and although there has been scattered research on coronaviruses since then, there was little coordination between research groups, and there was no useful medicine or vaccine from that,” he said.
“It was there that we collectively failed. It is great now that everyone is working on this, and the pandemic illustrates the need for real and international collaboration in the future.”
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