A recent study conducted by the University of Virginia School of Medicine, and published in the journal Chemical Science, unveils the alternative infection methods used by coronaviruses, showcasing its adaptability and explaining their capacity to infect various species.
The new research challenges the conventional belief that COVID-19 solely relied on the ACE2 protein for cell infection. Contrary to previous assumptions, ACE2 is not a prerequisite for infection; the virus employs alternative pathways to infiltrate cells.
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The study’s chief author, Peter Kasson, an MD and PhD at the Departments of Molecular Physiology and Biomedical Engineering, argues that coronaviruses possess the capability to utilize multiple "doors" for cell entry, if the primary one is obstructed.
SARS-CoV-2, the virus causing COVID-19, primarily targets ACE2 proteins, abundant on respiratory cell surfaces. However, the virus can also bind with other proteins, potentially infiltrating cells even without ACE2 receptors.
Exploring alternative entry points, they adapt to new hosts’ conditions whether the same or different species, and evolve to strengthen their resilience to treatments. Ultimately, coronaviruses multiply to create their own diversity (variants).
This unexpected finding contributes to understanding why coronaviruses exhibit such adeptness at jumping between species, emphasizing the need for sustained vigilance and research to preempt and manage future threats.
This newfound versatility underscores the necessity for ongoing monitoring and research to comprehend and mitigate potential risks posed by the coronaviruses and their evolving variants.
The research was funded by entities such as the Commonwealth Health Research Board and the Knut and Alice Wallenberg Foundation to provide valuable insights into the virus's entry mechanisms.
COVID-19, responsible for more than 7 million deaths globally, has seen a decline in threat levels due to vaccines and increasing population immunity. But its legacy is vast.
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