New research from the School of Medicine has unveiled unexpected insights into how COVID-19 infiltrates cells, shedding light on why coronaviruses possess a remarkable ability to jump between different species. Throughout the pandemic, discussions centered around the virus’s utilization of the ACE2 protein, found on human cells, to gain entry into cells. However, the latest findings challenge this notion, revealing that infection doesn’t necessarily hinge on ACE2.
Contrary to the previous understanding, the virus showcases a degree of versatility by employing alternative mechanisms for cell invasion. This newfound adaptability offers a potential explanation for coronaviruses’ adeptness at infecting various species. In the words of Peter Kasson, MD, Ph.D., from UVA’s Departments of Molecular Physiology and Biomedical Engineering, “The virus that causes COVID-19 uses ACE2 as the front door to infect cells, but we’ve found that if the front door is blocked, it can also use the back door or the windows.” This observation implies that the virus can continue to propagate by exploiting different entry points when confronted with resistance.
This phenomenon highlights the virus’s capacity to persistently spread while adapting to the entry mechanisms of new host species. Such adaptability raises concerns about the potential for emerging viruses to employ similar strategies in infecting humans. As our understanding evolves, scientists stress the importance of vigilance and preparedness to counteract the strategies employed by novel viruses.
The global toll of COVID-19 stands at nearly 7 million lives lost. Thankfully, vaccines and rising population immunity have diminished its threat for most individuals, although it remains a concern for vulnerable groups. While the U.S. Public Health Emergency ended in May, and life for most Americans resembles pre-pandemic times, scientists remain vigilant as COVID-19 continues to mutate. Vigilance is crucial to swiftly address any potential dangerous variants. Monitoring extends to other coronaviruses, ready to thwart the next public health crisis.
Kasson and team aimed to comprehend how SARS-CoV-2, responsible for COVID-19, enters human cells. ACE2 proteins serve as entry points, particularly abundant in the respiratory system. Yet, the virus can also engage other proteins. Could it exploit these alternative pathways? Indeed, ACE2 was optimal but not exclusive. Remarkably, the virus can invade cells lacking ACE2 receptors entirely.
This revelation might elucidate the virus’s adeptness at species transitions, reinforcing the necessity of continuous scrutiny. Kasson underscores, “Prior instances of SARS-CoV-2 and similar viruses causing outbreaks highlight the need to grasp their propagation and potential threats.”
These findings are documented in the journal Chemical Science.