Is it possible to halt the coronavirus’ infection cycle? A VCU study is exploring the possibility.
For a person to become infected with SARS-CoV-2, the virus first needs to get inside the body’s cells. Once that occurs, the infected cells replicate the virus, which then goes on to infect other cells in the body. Once enough virus is produced that symptoms develop, it can be shed by an infected person and go on to infect others.
A new study at Virginia Commonwealth University is aiming to explore whether it’s possible to stop SARS-CoV-2, the virus that causes COVID-19, from entering cells, thereby possibly breaking the infection cycle.
“If we can find ways to prevent the virus from getting into cells in the first place, we might be able to prevent people from becoming infected, reduce the severity of the disease, or reduce person-to-person transmission,” said Derek Prosser, Ph.D., an assistant professor in the Department of Biology in the College of Humanities and Sciences.
Prosser is one of 31 researchers launching projects under VCU’s COVID-19 Rapid Research Funding Opportunity, led by the Office of the Vice President for Research and Innovation with support from the C. Kenneth and Dianne Wright Center for Clinical and Translational Research. The program awarded nearly $350,000 in funding this spring to VCU research that seeks to address the impact of the coronavirus.
Prosser’s study, “Inhibition of Viral Uptake as a Mechanism for Reducing SARS-CoV-2 Infection,” could lead to a better understanding of how the virus works and how to fight it.
“As a rule, viruses can’t replicate on their own,” he said. “Instead, they ‘hijack’ the cells they infect and use them to create copies of themselves. The virus and its genome needs to get inside of a host cell for this to happen, so if we can prevent the internalization step, it could be an important way to prevent infection and disease.”
The project builds on Prosser’s research into how cells internalize material, a process called endocytosis. Prosser’s lab has previously focused on understanding how different endocytic pathways work at a molecular level.
“In the early days of the pandemic, I learned that the SARS-CoV virus responsible for the SARS outbreak in 2003 is internalized using a pathway that is very similar to one that we’ve studied extensively,” he said. “SARS-CoV-2 is internalized using the same receptor on the surface of host cells, called ACE2, so it seems reasonable that the two viruses use similar mechanisms to get inside of cells. Since we were already studying this endocytic pathway, we decided to turn our efforts toward understanding how it applies to SARS-CoV-2.”
Prosser hopes the project contributes to the worldwide effort to understand how the virus infects cells and causes disease, how it spreads, and what can be done to manage and prevent infections.
“While developing a vaccine is the most effective way to manage COVID-19, there are other important pieces to the puzzle that can help to prevent infection or reduce its severity,” he said. “Designing drugs that block specific steps in the infection cycle could be really useful in that regard.”
For example, he said, a drug that blocks specific steps in the infection cycle could be delivered via inhaler to the lungs.
“Something like that could be helpful for people at the front lines of the pandemic, such as health care workers who are at high risk because they routinely encounter and treat COVID patients,” he said.
The findings of the study may prove useful even beyond the coronavirus, Prosser said.
“I think it’s interesting that many pathogenic bacteria and viruses use similar internalization pathways to get inside of host cells,” he said. “They have adapted this strategy because it helps them to evade the immune system. So while our research is currently focused on COVID-19, the discoveries we make might also be applicable to other infectious diseases.”