May 30, 2024

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New Discovery Explains How COVID-19 infection Jumps Species

New Discovery Explains How COVID-19 infection Jumps Species



 

New Discovery Explains How COVID-19 infection Jumps Species

New insights are bolstering scientists’ efforts to stay ahead of COVID-19 and the next major pandemic.

An unexpected discovery regarding the way COVID-19 infects cells may unveil the virus’s capacity to adeptly jump from one species to another, aiding scientists in more accurately predicting its evolution.

New Discovery Explains How COVID-19 infection Jumps Species

 

Recent research suggests that COVID-19 can infect cells lacking the ACE2 protein through alternative infection methods, highlighting the virus’s adaptability and its ability to infect a variety of species. This variability underscores the necessity of ongoing monitoring and research to understand and mitigate the potential risks posed by the virus and its variants.

The mechanism by which COVID-19 invades cells has sparked widespread debate in the field of epidemiology, primarily centered on COVID-19’s utilization of a human cell protein called ACE2. However, the latest study from the University of Virginia School of Medicine suggests that ACE2 is not an absolute requirement for infection. Instead, the virus can employ other means to infect cells.

 

New Discovery Explains How COVID-19 infection Jumps Species

 

This multifaceted capability indicates that coronaviruses can utilize multiple “doors” to access cells, potentially explaining why they are so proficient at infecting different species.

Peter Kasson, a medical doctor and researcher at the University of Virginia’s Departments of Molecular Physiology and Biomedical Engineering, explains, “The virus causing COVID-19 uses ACE2 as the front door to infect cells, but we found that if the front door is blocked, it can also use the back door or a window. This means the virus can continue to spread when infecting new species until it adapts to using the front door of a specific species. Therefore, we must be cautious about new viruses infecting us in the same way.”

COVID-19 has resulted in nearly 7 million deaths worldwide. Fortunately, with the widespread distribution of vaccines and increased population immunity, the virus is no longer a significant threat to most people (though it remains a concern for immunocompromised individuals and the elderly). As the official public health emergency in the United States expired in May, most Americans have returned to a lifestyle resembling the pre-2019 pandemic era. However, COVID-19 continues to evolve and change, and scientists are closely monitoring its developments to act swiftly in the presence of more dangerous variants. They also continue to monitor other coronaviruses in case they cross over to humans, potentially becoming the next major public health threat.

As part of this work, Kasson and his team seek to gain a better understanding of how the virus SARS-CoV-2, responsible for COVID-19, enters human cells. Scientists have known that the virus essentially opens the cell’s door by binding with the ACE2 protein, which is abundant on the surface of cells lining the nasal passages and lung walls.

 

New Discovery Explains How COVID-19 infection Jumps Species

 

However, SARS-CoV-2 can also bind with other proteins. Scientists wondered if SARS-CoV-2 might use these other proteins to infiltrate cells. The answer is affirmative. While ACE2 is the most efficient pathway, it is not the only one. This suggests that the virus can still bind to and infect cells even when ACE2 receptors are absent.

Kasson suggests that this unexpected finding may help explain why coronaviruses are so adept at species jumping. He notes that this underscores the increased importance of scientists’ close attention to coronaviruses, saying, “As far as we know, coronaviruses like SARS-CoV-2 have caused one pandemic and several near misses. This suggests that there are more coronaviruses out there, and we need to understand how they spread and what to watch out for.”

(source:internet, reference only)


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