It’s easy to dismiss the idea of a war against sneezes as an unlikely outcome.
It is, after all, a relatively easy disease to fight.
But for decades, scientists have tried to identify its causes and understand why people develop the condition.
A team led by Professor Jonathan Parnell of the University of Sydney has now shown that sneezable bacteria can be turned on or off by a chemical called COVID-19.
This chemical triggers the release of certain proteins that are secreted by the immune system to fight the infection.
This suggests that COVID may trigger an immune response that causes the sneezer to develop a resistance to the toxin.
Parnells research was published in the journal Proceedings of the National Academy of Sciences.
The team used a genetically modified mouse to model the sneezy-resistance gene.
When the gene was introduced into the mouse, the mice developed resistance to COVID.
But this was only the first step in the gene’s development.
Poyson says the researchers are still working out exactly what happens when a gene is turned on and off.
The scientists want to see if it can activate other genes that are involved in sneezs.
This is likely to reveal clues to the pathophysiology of the condition, and possibly reveal new drugs.
The team is also studying whether the COVID infection can be treated by drugs that target the sneaker-resisting protein, a process that has been previously tried.
Poyson and his colleagues have also developed a model of the COV-19 immune system, in which it secures a specific type of molecule that can be produced by the cells in the immune cells.
When this molecule is released, the immune response is triggered.
“We’re working on figuring out what that molecule is and what it does,” he says.
Professor Poysen, who is also an associate professor of medicine at the University the University at Albany, New York, says that the current model of COVID is a “very preliminary and crude” one.
He notes that the mouse model was based on two genetic conditions, and that there is still much to be learnt about how sneezers respond to COV and other conditions.
“This model needs to be tested in a larger animal model that has multiple conditions, because it’s not clear yet how the immune responses of these different mouse models differ,” he explains.
“If you look at the human genome, you have genes for several different things that can affect sneez.
For example, we have a protein called COX-7 that regulates the sneer, and we have genes that control the immune reaction, and a number of other genes.”
Poyds work could help the understanding of more complex diseases, such as obesity, COPD, and asthma.
He adds: “If we can identify the genes that make these different sneez-related proteins, then we might be able to target those genes and have better treatments for these conditions.”
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