The SARS-CoV-2 Alpha (B.1.1.7) variant mutated to evade our immune system, helping establish it as the world’s first ‘Variant of Concern’, finds a new study led by researchers at UCL and the Quantitative Biosciences Institute, University of California San Francisco.
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Published in the journal Nature, the study shows the Alpha variant, first identified in the UK, evolved to make more of its ‘antagonism proteins’ that nullify the body’s first line of defense, known as the ‘innate immune system’.
The Alpha variant was first detected in November 2020 from a sample taken in September in the United Kingdom and began to spread quickly by mid-December. It was discovered that the variant, also known as lineage B.1.1.7, had one or more mutations on its spike protein.
CTV News Canada notes that the Alpha variant has since its discovery, evolved to include subsequent variants, like Delta and Omicron. By studying Alpha’s structure and function, scientists can better understand how virus variants evolve.
Scientists discovered the Alpha variant upped the production of specific proteins called ‘antagonism proteins’ that could help it suppress how infected cells signaled the immune system.
Every cell in the nose, throat, and lungs (airways) has a network of sensors that detect incoming viruses. These cells produce the protein interferon, which acts like a “burglar alarm,†eliciting a blanket anti-viral response, across both non-immune and immune cells (T cells and antibodies) to avert infection.
But it is the antagonism proteins that can help the virus to evade these sensors. And this is what the researchers wanted to study. It led to the discovery that antagonism proteins can help the virus to evade these sensors.
In the laboratory, researchers looked at lab grown cells infected by this variant to monitor protein levels and look deeper into how the variant worked. They then compared the data to how cells responded to infection with the original strain of COVID-19 from Wuhan, China.
The study was the first to identify the evolution of enhanced antagonism protein expression in any virus and the first to implicate mutations in SARS-CoV-2 that increase infectiousness but do not involve the ‘spike’ protein. ■