Mechanism for Inhibiting Retroviruses Found

During research on retroviruses, a doctoral student currently at the University of British Columbia, in Canada, discovered a never-before-observed mechanism of inhibiting this class of organisms. This family of viruses contains that dreaded, and often fatal, human immunodeficiency virus (HIV), the one that promotes the development of AIDS. The new research could allow experts to produce a variety of drugs for a wide range of medical conditions that retroviruses cause.

In addition to being very resilient, retroviruses are also prone to triggering fatal mutations in the DNA information of the hosts they infect. The pathogens themselves are nothing but segments of genetic material (RNA), which can be enveloped in a nearly-impenetrable envelope of lipids. Breaching through it using standard drugs has proven to be extremely difficult, and it's precisely this resilience that made this field of research nearly grind to a halt. The new investigation, published yesterday, April 7, in the esteemed journal Nature, may provide a much-needed breath of fresh air into this line of studies, experts say.

Its many possible applications include the development of new cancer therapies that could be targeted specifically at tumor site, leaving surrounding healthy tissue intact. The study was conducted by UBC Faculty of Medicine Department of Medical Genetics graduate student Danny Leung, 27. He was working in assistant professor Matthew Lorincz's lab, when he discovered a protein that appears to be crucial for inhibiting the activity of endogenous retroviruses inside mouse embryonic stem cells. The use of the ESET protein may therefore be translated in humans as well. Similar types of retroviruses are mainly responsible for human breast and skin cancers.

The expert also discovered that the mechanisms ESET employs in silencing the pathogen are different from the ones the process known as DNA methylation uses. The latter method is generally used to promote the spread of retroviruses, and it involves attaching a chemical group to the host cell's DNA, so as to prevent the virus from bonding with it, and replicating. Researchers at the Kyoto University, in Japan, also collaborated on the new investigation.