Bird flu is just four mutations away from being able to infect humans and cause a pandemic, experts warn.
The virus has ravaged bird and mammal populations worldwide and has been given ample opportunity to spread in recent years.
Each time it starts replicating in a new host, it can mutate and acquire one of these lethal traits.
Mutations that could pose risks to humans include the ability to survive in the air and the ability to optimize themselves to infect human cells.
Experts highlight four key features that bird flu can acquire through mutation. Two of the mutations must occur in hemagglutinin, the outer part of the virus responsible for binding the virus to human cells.These mutations allow it to move through the air and bypass the body’s natural defenses. includes matching itself to optimize for
Dr Mathilde Richard, a virologist at the Erasmus Medical Center in the Netherlands, said: told science magazine“This is a threat that will keep knocking on our doors until it actually causes a pandemic.
“Because there is no way back.”
Before a virus can harm humans, it must first reach humans.
Currently, a person can become infected with bird flu when virus particles enter the body through the mouth, nose, or eyes.
Usually this happens when someone touches an infected surface and then wipes their face.
However, these cases are rare, with only about 1,000 cases detected in humans.
In a landmark 2012 studyDutch researchers produced H5N1 bird flu to spread airborne infections among ferrets.
This kind of research falls under the controversial “gain-of-function” label and is restricted in most of the world.
Through their research, however, the team identified alterations in the binding of the virus that allow it to move through the air and attach to human cells. It is the RNA code that allows viruses to infect more efficiently and escape natural barriers.
Viral pathogens such as COVID-19, influenza, and respiratory syncytial virus are most effectively transmitted through the air.
But bird flu is difficult to spread through aerosol particles.
Like other pathogens, avian influenza attaches to host cells via a moiety called hemagglutinin. These are small proteins in the outer layer of the virus.
When the virus infects an animal’s cells, the hemagglutinin fuses with fluid inside the cells called vesicles.
Due to the high acidity of the liquid, it fuses with it. This allows the virus to integrate inside the cell and infect the cell’s protective inner layer, the membrane.
Once inside the membrane, the virus attacks cells with little resistance, infects them completely, and propagates itself once replication begins.
Viruses can survive on surfaces for long periods of time because the pH of water and other surfaces is relatively balanced.
But it’s a different story when particles move through the air after a person sneezes or coughs.
Carbon dioxide in the air makes the air slightly acidic. As a result, the hemagglutinin begins to dissolve and cannot reach its new host.
Scientists say that if the avian flu hemagglutinin mutates to resemble that of the new coronavirus or influenza, it will be able to move through the air.
Once the virus reaches the host, it must infect.
A second mutation optimizes influenza binding to human cells.
Birds are classified as “birds” in the animal kingdom, whereas humans are considered mammals.
This means that they have different biological structures, and viruses that are adapted for animals are enough to cause problems in humans.
Avian influenza has mutated to optimize its ability to infect birds, and as a result struggles to find non-avian hosts. The virus was first detected in ducks in Europe and Asia, but it is unknown where it became infected.
However, this could change with a simple mutation in hemagglutinin.
Changes to amino acids called G228S and Q226L are necessary for this optimization to occur, the scientists say after reviewing data from previous outbreaks.
When these amino acids undergo this mutation, they become more suitable for binding carbohydrates in human cells.
These mutations have been detected in previous human outbreaks of the virus.
This includes the 1968 H3N2 outbreak that originated in the United States and killed about 1 million people worldwide.
The 1957 “Asian Flu” epidemic killed 1.1 million people worldwide.
It was later found to be caused by the H2N2 strain of bird flu, which also had these mutations.
Both strains of the virus have since disappeared from the human population, but their occurrence indicates that these dangerous mutations are possible.
After a sample taken from the market tested positive for influenza A(H3), the woman is believed to have contracted the virus from a wet market she spent before becoming ill.
The woman from Guangdong province first became ill on February 22, was hospitalized with severe pneumonia on March 3, and died on March 16.
Hemagglutinin isn’t the only part of the virus that needs to be altered.
A third mutation, which scientists believe is the most important evolution a strain of bird flu needs to pose a threat to humans, is within its RNA.
All influenza viruses are composed of single-stranded RNA rather than double-stranded DNA.
RNA is composed of four basic chemicals: cytosine, guanine, adenine, and uracil. In DNA, thymine is present instead of uracil.
All combinations of the three chemicals within the RNA chain form amino acids.
These acids are the building blocks of proteins, and their combinations make up numerous traits.
Unlike cells, viruses do not have both DNA and RNA. Most infections acquire their signature from their RNA structure.
Each trio of these chemicals on the RNA strand constitutes a protein-bearing chemical that helps the body function.
When some cytosines in these chains mutate to adenine instead, the output of some strains changes from a chemical called glutamine to a chemical known as lysine.
Scientists call this the E627K mutation. When glutamic acid is replaced by lysine, the virus is more likely to infect human protein cells than bird cells.
These three mutations make the virus potentially threatening to humans.
However, the fourth change could circumvent the final defenses humans have and start a deadly pandemic.
Myxovirus resistance gene A (MxA) is a protein in human cells engineered to destroy RNA viruses such as avian influenza.
Protein is triggered when viral RNA is detected in the cell. In most cases, it can disrupt pathogen binding and prevent infection.
Failing that, it signals the immune system that there is an intruder and triggers a flow of white blood cells to fight the virus.
Humans are more susceptible than other mammals to MxA, making bird flu less likely than foxes, sea lions, and others that have been infected over the past two years.
Dr. Richard states that the virus will inevitably undergo all four mutations, allowing it to attack humans, but the time it takes to do this varies greatly.
Due to the randomness of genetic mutations and the very specific changes that viruses require, it could be decades before one of the changes takes place.
For now, bird flu remains a human-observed threat, but we’re not particularly concerned.
However, human cases do occur from time to time. Officials have reported that a 56-year-old woman in southeastern China died of her H3N8 strain of the virus in March.
However, the strain she suffered was not tailored to humans. Only 3 cases of H3N8 strains in humans have been reported.
The strain most threatening to humans is the H5N1 virus.
Since it was first discovered in 1959, this strain has been documented about 870 times, and about half of the cases have resulted in death.
Over the past two years, wild bird populations around the world have been overwhelmed, causing sporadic infections among humans.
It has been shown to be capable of human-to-human transmission, unlike other strains of bird flu.
Human-to-human transmission was confirmed during an outbreak in Hong Kong in 1997 that stranded 18 people.