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IMAGE: A genome deletion removes 27 protein building blocks, called amino acids, from the SARS-CoV-2 ORF7a accessory protein. The protein is very similar to the SARS-CoV 2003 ORF7a / X4 immune antagonist …
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Credit: Efrem Lim, ASU Biodesign Institute
As the coronavirus pandemic has spread throughout the United States. In addition to tracking the number of daily COVID cases, there is a worldwide scientific community dedicated to tracking the SARS-CoV-2 virus.
Efrem Lim leads an ASU team that looks at how the virus can spread, mutate, and adapt over time.
To track the virus’ trail around the world, Lim’s team is using a new technology called next-generation sequencing at the ASU Genomics Facility to quickly read the 30,000 chemical letters in the SARS-CoV-2 genetic code, called genome.
Each sequence is deposited in a global gene bank, run by a non-profit scientific organization called GISAID. To date, more than 16,000 SARS-CoV-2 sequences have been deposited in GISAID’s EpiCoVTM database. Sequence data shows that SARS-CoV-2 originated from a single source in Wuhan, China, while many of the first Arizona cases analyzed showed that traveling from Europe was the most likely source.
Now, using a group of 382 nasal swab samples obtained from potential COVID-19 cases in Arizona, Lim’s team has identified a SARS-CoV-2 mutation that had never been found before —- where 81 of the letters they have vanished, permanently removed from the genome.
The study was published in the online version of the Journal of Virology.
Lim says that as soon as he made the manuscript data available on a medRxiv preprint server, it has sparked worldwide interest from the scientific community, including the World Health Organization.
“One of the reasons this mutation is of interest is because it reflects a large deletion that arose in the 2003 SARS outbreak,” said Lim, an assistant professor at the ASU Biodesign Institute. During the middle and late phases of the SARS epidemic, SARS-CoV accumulated mutations that attenuated the virus. Scientists believe that a weakened virus that causes less severe disease may have a selective advantage if it is able to spread unintentionally through populations by infected people.
Separating what exactly this means is of deep interest to Lim and his colleagues. ASU’s research team includes LaRinda A. Holland, Emily A. Kaelin, Rabia Maqsood, Bereket Estifanos, Lily I. Wu, Arvind Varsani, Rolf U. Halden, Brenda G. Hogue, and Matthew Scotch.
The ASU virology team had been set up to conduct research on seasonal influenza viruses, but when the third case of COVID-19 was found in an individual from Arizona on January 26, 2020, they knew they had all the skills. and scientific techniques to quickly pass the exam The spread of SARS-CoV-2.
“This was the scientific opportunity of a lifetime for ASU to help understand how this virus is spreading in our community,” said Lim. “As a team, we knew we could make a significant difference.”
All positive cases show that the SARS-CoV-2 viral genomes were different from each other, which means that they were independent of each other. This indicates that the new cases were not linked to the first Arizona case in January, but the result of recent travel from different locations.
In the case of the 81 base pair mutation, since it had never been found in the GISAID database before, it could also provide a clue as to how the virus makes people sick. It could also form a new starting point for other scientists to develop antiviral drugs or formulate new vaccines.
SARS-CoV-2 produces accessory proteins that help it infect its human host, replicate, and eventually spread from person to person. Genome deletion removes 27 protein building blocks, called amino acids, from the accessory protein SARS-CoV-2 ORF7a. The protein is very similar to the SARS-CoV 2003 ORF7a / X4 immune antagonist.
The ASU team is now working hard to conduct more experiments to understand the functional consequences of the viral mutation. The viral protein is believed to help SARS-CoV-2 evade human defenses, and ultimately destroy the cell. This releases the virus to infect other cells in a cascade chain reaction that can quickly cause the virus to make copies of itself throughout the body, causing severe symptoms of COVID-19 8-14 days after the initial infection.
Lim notes that only 16,000 SARS-CoV-2 genomes have been sequenced to date, which is less than 0.5% of the circulating strains. There are currently more than 3.5 million confirmed cases of COVID-19 worldwide.
Lim’s group has partnered with TGen, UA, and Northern Arizona University to continue tracking different genetic strains of the new coronavirus. Together, the newly formed Arizona COVID-19 Genomics Union (ACGU) hopes to use big data analytics and genetic mapping to give Arizona health care providers and public policy makers an advantage in fighting the growing pandemic.
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The work was supported by NSF STC Award 1231306, NIH awards R01 LM013129, R00 DK107923, One Water One Health from the J.M. Kaplan, Arizona State University Foundation Project 30009070), and the ASU Central Facility Seed Fund.
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