Ebola: Guinea Health Agency declares 'pandemic' in February

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The team, led by scientists at the University of Utah Health and The Rockefeller University, found a genetic mutation in the animals that interferes with deadly viruses. The gene, called retroCHMP3, appears to disrupt the ability of certain viruses to exit an infected cell and prevents it from going on to infect other cells. Normally, some viruses encase themselves in cell membranes and then make an exit by budding off from the host cell.

RetroCHMP3 delays that process long enough that the virus can no longer escape.

Dr Nels Elde, a senior author of the study, said: “This was an unexpected discovery.

“We were surprised that slowing down our cell biology just a little bit throws virus replication off its game.”

The team say the finding could eventually lead to the development of medical interventions in humans.

RetroCHMP3 originated as a duplicated copy of a gene called charged multivesicular body protein 3, or CHMP3.

While some monkeys, mice, and other animals have retroCHMP3 or other variants, humans only have the original CHMP3.

The gene is known for playing a key part in cellular processes that are vital for maintaining cellular membrane integrity, intercellular signalling, and cell division.

But HIV and certain other viruses hijack this pathway to bud off from the cellular membrane and infect other cells.

Dr Elde and his colleagues believe that this from happening as protection against viruses like HIV and other viral diseases.

They then began to explore whether variants of the gene could be used as an antiviral.

And in a lab experiment a shorter, altered version of human CHMP3 successfully prevented HIV from budding off cells.

But there was an issue.

The modified protein also disrupted important cellular functions, causing the cells to die.

So they were forced to try a different approach.

Using genetic tools, they coaxed human cells to produce the version of retroCHMP3 found in squirrel monkeys.

Then, they infected the cells with HIV and found that the virus had difficulty budding off from the cells, essentially stopping them in their tracks.

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This occurred without disrupting metabolic signalling or related cellular functions that can cause cell death.

Dr Wes Sundquist, a co-corresponding author of the study, added: “We’re 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 that could happen without interfering with other very important cellular functions.”

Dr Elde has hailed the breakthrough.

He added: “We thought the ESCRT pathway was an Achilles heel that viruses like HIV and Ebola could always exploit as they bud off and infect new cells.

“RetroCHMP3 flipped the script, making the viruses vulnerable. Moving forward, we hope to learn from this lesson and use it to counter viral diseases.”

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