Researchers from King's College London in the UK say the gene, called MX2, could lead to new effective and less toxic treatment against HIV - the virus that causes acquired immunodeficiency syndrome (AIDS).
For the study, the researchers conducted experiments on human cells, in which they introduced the HIV virus to two different cell lines. One cell line had the MX2 gene "switched on," while the other cell line had no MX2 expression.
On observing the effects, the researchers found that in the cells in which the MX2 gene was expressed, the HIV virus was unable to replicate, therefore stopping new viruses from being produced.
In the cell line in which the MX2 gene was switched off, the HIV virus replicated and spread.
Professor Mike Malim of the Department of Infectious Disease at King's College London, says:
"This is an extremely exciting finding which advances our understanding of how HIV virus interacts with the immune system and opens up opportunities to develop new therapies to treat the disease.
Until now, we knew very little about the MX2 gene, but now we recognize both its potent anti-viral function and a key point of vulnerability in the life cycle of HIV."
|Researchers say a gene called MX2 may prevent the HIV virus (pictured) from spreading once in the body. |
Photo credit: King's College London
However, many of these drugs can cause serious side effects, including abnormal heartbeats, shortness of breath, skin rash, weakened bones and even bone death.
"Although people with HIV are living longer, healthier lives with the virus thanks to current effective treatments, they can often be toxic for the body, and drug resistance can become an issue with long-term use," says Prof. Malim.
He notes that it is important to continue finding new ways of mobilizing the body's natural defense system, and the MX2 gene appears to play an important role in initiating viral control in HIV sufferers.
"Developing drugs to stimulate the body's natural inhibitors is a very important approach because you are triggering a natural process and therefore won't have the problem of drug resistance," he adds.
"There are two possible routes - it may be possible to develop either a molecule that mimics the role of MX2 or a drug which activates the gene's natural capabilities."