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An effort led by Lin Li, Ph.D., assistant professor of physics at the University of Texas at El Paso, working with students and faculty at Howard University, identified key variants that help explain the differences between viruses that cause COVID -19 and severe acute respiratory syndrome (SARS).
A team of researchers from UTEP and the historically black research university in Washington, DC, have uncovered valuable data by comparing the fundamental mechanisms of severe acute respiratory syndrome coronavirus (SARS-CoV) and SARS-CoV -2 – also known as COVID-19 – to better understand how these viruses attack the human body. Their results are published in an article titled “Advanced proteins of SARS-CoV and SARS-CoV-2 use different mechanisms to bind to human ACE2” which recently appeared in the scientific journal. Frontiers in molecular biosciences.
“We are very excited and interested in the timely work that Dr. Li and his collaborators have reported,” said Robert Kirken, Ph.D., Dean of the College of Science at UTEP. “As SARS-COV2 continues to evolve through passage through infected humans, the rapid identification and evaluation of these mutants using the research and testing approaches they have established will be of importance. crucial for the development of new vaccines and therapeutics. “
When comparing the viruses, the researchers found that the two were very similar in sequence and almost identical in structure. Using computational approaches, they were also able to identify mutations in SARS-CoV that make SARS-CoV-2 much more contagious and likely to cause serious infections.
“We found that due to the mutations, the binding of SARS-CoV-2 to the human cell is much stronger than that of SARS-CoV,” Li said. “Perhaps this is one of the reasons why SARS-CoV-2 spreads much faster and is difficult to control. SARS-CoV-2 also uses a much smarter strategy to attack the human cell than SARS-CoV. For example, when SARS -CoV infects or binds to the human cell, it uses several key residues or amino acids to do this, while SARS-CoV-2 uses more residues, which makes it more robust and easier. to completely divert from the human cell.
“We have identified the most important residues for SARS-CoV-2 to bind to the human cell. This type of data is essential in the development of drugs to cure or treat infections caused by these types of viruses. These rules and basic characteristics can also be used. for future disease control, maybe 10 years from now there will be SARS-CoV-3 or 4. “
Researchers at both universities focused on examining one of the virus’ four main proteins, known as the spike protein, which initiates infection in the human body. They found that from SARS-CoV to SARS-CoV-2, there is an interesting change in the mechanism of the spike protein binding domain.
“The binding domain has to be flipped in order to bind to the human cell, but we have found some strange mutations that have occurred. Like the hinge of a gate, the binding domain can affect the flipping mechanism of SARS -CoV-2 It can be more flexible, which makes it easier to bind to the human cell, ”Li said.
The team included an interdisciplinary mix of undergraduate and graduate students, postdoctoral researchers and faculty from UTEP and Howard University. Yixin Xie, UTEP graduate student and research assistant, was the first author of the document and led the calculation and analysis parts of the project while working closely with other students from UTEP and the Howard University remotely due to the pandemic.
Going forward, the team’s goal is to expand their research to study the mechanisms of the four proteins to gain even better understanding of the inner workings of these viruses to help fight COVID-19 and related viruses.
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Material provided by University of Texas at El Paso. Note: Content can be changed for style and length.
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