Genetics Research May Help Identify More Dangerous Strains of the Virus That Causes COVID-19

Genetic Sequencing Concept

New research has examined the genetic code of SARS-CoV-2 viruses that have infected patients, looking for links between different mutations and patient deaths.

Viral mutations during the COVID-19 pandemic could cause the SARS-CoV-2 virus to become more dangerous. A new study published in the journal Genetic Epidemiology has examined the genetic code of SARS-CoV-2 viruses that have infected patients, looking for links between different mutations and patient deaths.

For the study, investigators analyzed 7,548 SARS-CoV-2 genomes of COVID-19 patients worldwide and looked for an association between genomic variants and mortality. In total, 29,891 locations in the viral genome were assessed.

One location was significantly linked with patient mortality. Mutations at this location cause changes in part of the SARS-CoV-2 spike protein, which plays a key role in viral entry into host cells.

“When, in the fall of 2020, we applied methodology from genome-wide association studies to COVID-19 genomes, we noticed one locus in the COVID-19 genomes from Brazil that was associated with mortality and that later became part of the definition of the P.1 strain from Brazil,” said co-lead author Georg Hahn, PhD, of Harvard University. The P1. strain was behind a deadly COVID-19 surge in the Latin American country. It’s more contagious and more resistant to antibodies than the original strain.

For more on this research, see Genome-Wide Association Studies Accurately Flag More Deadly COVID-19 Variants.

Reference: “Genome-wide association analysis of COVID-19 mortality risk in SARS-CoV-2 genomes identifies mutation in the SARS-CoV-2 spike protein that colocalizes with P.1 of the Brazilian strain” by Georg Hahn, Chloe M. Wu, Sanghun Lee, Sharon M. Lutz, Surender Khurana, Lindsey R. Baden, Sebastien Haneuse, Dandi Qiao, Julian Hecker, Dawn L. DeMeo, Rudolph E. Tanzi, Manish C. Choudhary, Behzad Etemad, Abbas Mohammadi, Elmira Esmaeilzadeh, Michael H. Cho, Jonathan Z. Li, Adrienne G. Randolph, Nan M. Laird, Scott T. Weiss, Edwin K. Silverman, Katharina Ribbeck and Christoph Lange, 22 June 2021, Genetic Epidemiology.
DOI: 10.1002/gepi.22421

2 Comments on "Genetics Research May Help Identify More Dangerous Strains of the Virus That Causes COVID-19"

  1. Howard Jeffrey Bender, Ph.D. | June 27, 2021 at 10:19 am | Reply

    All the talk is about the spike proteins, but the real problem is in the virus and how coronaviruses may attack cells and why two of the most dangerous, MERS and Covid-19, are so infectious. My independent research has found multiple one-in-a-million nucleotide sequence matches between all the coronaviruses and the human genome. Those sequences are the same as some of the DHU loops of human tRNA. Using those loops and their anticodon matches, viruses may be able to fool the nucleus membrane in cells to allow the virus to enter and associate with the human DNA, creating more opportunities for further infection. Our immune system may be compromised and may no longer be able to stop the virus and other diseases from attacking organs throughout the body. Vaccines that attack the virus protein shells while ignoring their contents are doomed to failure from the Darwin effect, but recognizing these DHU loops suggests a possible approach to successful coronavirus vaccines. For MERS, eliminating the nucleotide sequence CAGTGGTAG from the virus may make it less infectious and stimulate the body to create antibodies to attack the entire virus. And eliminating the nucleotide sequence TAGTGGTGAG from Covid-19 may do the same thing. Only the infection process is considered in my work, not the innate virulence of the virus. For more info, check out this YouTube: https://www.youtube.com/watch?v=pd4OD4GpsJI

  2. I really hope that science advisors are not starting to receive dissertations in youtube form.

Leave a Reply to Neil B Cancel reply

Email address is optional. If provided, your email will not be published or shared.