Researchers at a British university have released new findings which could shed light on why the UK variant of the novel coronavirus is more infectious.
The B.1.1.7 variant of SARS-CoV-2 was discovered in Kent, UK in December 2020, and has since spread across the globe, contributing to the increase in cases being seen in Europe and Britain’s own second wave of the pandemic earlier in the year, Shefield University said in a press release on Friday.
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SARS-CoV-2 is the strain of the coronavirus that causes COVID-19.
Frequently Asked Questions
A vaccine works by mimicking a natural infection. A vaccine not only induces immune response to protect people from any future COVID-19 infection, but also helps quickly build herd immunity to put an end to the pandemic. Herd immunity occurs when a sufficient percentage of a population becomes immune to a disease, making the spread of disease from person to person unlikely. The good news is that SARS-CoV-2 virus has been fairly stable, which increases the viability of a vaccine.
There are broadly four types of vaccine — one, a vaccine based on the whole virus (this could be either inactivated, or an attenuated [weakened] virus vaccine); two, a non-replicating viral vector vaccine that uses a benign virus as vector that carries the antigen of SARS-CoV; three, nucleic-acid vaccines that have genetic material like DNA and RNA of antigens like spike protein given to a person, helping human cells decode genetic material and produce the vaccine; and four, protein subunit vaccine wherein the recombinant proteins of SARS-COV-2 along with an adjuvant (booster) is given as a vaccine.
Vaccine development is a long, complex process. Unlike drugs that are given to people with a diseased, vaccines are given to healthy people and also vulnerable sections such as children, pregnant women and the elderly. So rigorous tests are compulsory. History says that the fastest time it took to develop a vaccine is five years, but it usually takes double or sometimes triple that time.
As well as mutations to the spike protein’ the virus uses to hijack our cells, researchers at Sheffield University have found that an additional mutation in the nucleocapsid gene could affect the viruses subgenomic RNA production which could make it more effective at evading our immune systems, allowing more replication and resulting in the higher-viral load and increased transmissibility of this variant.
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The research team, one of the first nationally to publish sequenced genomes of the COVID-19 virus, also discovered an entirely new subgenomic RNA, which contains the instructions for what could be a protein called ORF9b.
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Present in increased amounts in the UK variant, ORF9b has previously been shown to regulate our immune response.
Our analysis also detected a new subgenomic RNA message in the B.1.1.7 variant which contains the instructions for a protein (ORF9b) that has been shown to regulate our immune system’s response to the virus.
"If B.1.1.7 is better at regulating our immune response it could explain why it spreads faster than other variants, and why it may be associated with a higher-viral load, said scientist Matthew Parker from the University of Sheffield’s Department of Neuroscience."
Since the start of the pandemic, the whole genome sequencing of SARS-CoV-2 has been critical to form part of a worldwide emergency response to the outbreak, and allow scientists around the world to develop vaccines by understanding how the virus spreads and mutates.
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