By Mariana G. Bego
Independent surveillance programs examining sequences of the SARS-CoV-2 virus associated with COVID- 19 cases, simultaneously detected several distinct variants carrying amino acid substitutions or mutations in the same genetic position on the Spike protein.
The first mutation was designed Q677P, as the amino acid in position 677 of the Spike protein changed from a glutamine to a proline, which are abbreviated as Q and P, respectively. The second and more predominant mutation was designed Q677H, as glutamine in position 677 changed to a histidine (abbreviated as H). These mutations seemed to have risen independently, providing strong evidence of viral adaptation. Often, this is observed when a mutation confers some advantage to the virus. The viruses carrying these mutations were first detected at the end of October 2020, predominantly in the Southcentral and Southwest of the United States (US). By mid-January 2021, these variants represented over 27% of all COVID-19 cases detected in the state of Louisiana.
The variant carrying the Q677P mutation was named Pelican. The Pelican variant, which was first detected in Oregon, can be now found in 12 US states and four other countries, namely Australia, Denmark, Switzerland and India.
Several variants carry the same Q677H mutation but differed in other regions of the virus; these were named Robin, Mockingbird, Bluebird, Yellowhammer and Quail. The Robin variant was found in over 30 US states but predominates in the Midwest. Yellowhammer can be detected mostly in the Southeast, Bluebird mostly in the Northeast, Quail mainly in the Southwest and Northeast, and Mockingbird mainly in the Southcentral and East Coast states. Other variants carrying the mutation Q677H were identified in Egypt, Denmark and India as well. Some of these also carry the N501Y substitution, a hallmark of the highly virulent variants originally described in the United Kingdom. These results were released in a recent pre- print.
The Spike protein is responsible for binding to receptors found on the surface of human cells, which is the first step required in order for the virus to enter and infect cells. The position of this mutation on the Spike protein implies a potential functional relevance during cell entry, which may confer an added advantage for transmission in viruses carrying this substitution. Studies to confirm this hypothesis are warranted.