SALT LAKE CITY – A gene found in animals could be the key to stopping viruses, including HIV and Ebola, from dead in their tracks, according to a new study. The genetic mutation, nicknamed “retroCHMP3”, prevents certain viruses from spreading by trapping them inside the cell membrane, scientists say. While humans have the CHMP3 gene, we don’t have the “retro” variant, which is only found in monkeys, mice, and some other animals.
Most viruses lock themselves up in cell membranes before sprouting to infect other healthy cells in the body. Now researchers at the University of Utah Health and Rockefeller University have found a way to stop viruses from exploiting this “Achilles heel.” Their discovery could help provide people with immunity against certain viral diseases in the future.
“It was an unexpected discovery. We were surprised that slowing down our cell biology a bit disrupts the replication of the virus a bit, ”says Dr. Nels Elde, lead author of the study, in a commentary. declaration.
Scientists have known for some time that CHMP3 plays an important role in daily cellular processes. For example, it is vital for maintaining cell membrane integrity, intercellular signaling, and cell division. But HIV and some other viruses can hijack these processes in order to exit the cell membrane and infect other cells.
Laboratory experiments were carried out to see if any of the retroCHMP3 variants could function as an antiviral in humans. Shorter, modified versions of human CHMP3 were successful in preventing HIV from leaving the cell, the researchers found, but there was a problem. The variants also disrupted other important cell functions, eventually causing the cells to die.
To remedy this, the researchers used genetic tools to trick human cells to produce a version of retroCHMP3 found in squirrel monkeys. They then infected the cells with HIV and found that the virus was struggling to spread, except this time, no other process was affected.
“We are excited about the work because we showed some time ago that many different enveloped viruses use this pathway, called the ESCRT pathway, to escape cells. We always thought that this might be a point at which cells could defend themselves against such viruses, but we didn’t see how it could happen without interfering with other very important cellular functions, ”says Dr. Wes Sundquist, author. of the study.
From an evolutionary point of view, these genetic variations could represent a new type of immunity, which can arise quickly to counter short-lived threats. “We thought the ESCRT pathway was an Achilles heel that viruses like HIV and Ebola could still exploit when they sprout and infect new cells. RetroCHMP3 reversed the script, making viruses vulnerable. In the future, we hope to learn from this lesson and use it to counter viral diseases, ”said Dr Elde.
“This raises the possibility that an intervention that slows down the process may be harmless to the host, but provide us with a new antiretroviral,” adds study co-author Professor Sanford Simon.
The results are published in the journal Cell.
South West News Service writer Tom Campbell contributed to this report.