By IANS,
Washington : Viruses dramatically increase cellular metabolism, and existing anti-obesity drugs may be a new way to block these metabolic changes and inhibit viral infection.
Metabolism refers to all the reactions by which living things break down nutrients to produce energy, along with those by which they rebuild broken-down nutrients into complex molecules such as DNA.
A significant example is the breakdown of blood sugar (glucose) and its conversion via chain reactions into adenosine triphosphate, the energy-storing currency of cellular life.
As an important offshoot of that process, glucose can also be converted into fatty acids, the lipid building blocks of human hormones and cell membranes.
Many viruses, including influenza, HIV and hepatitis, use those same fatty acids to build their viral envelopes, outer coatings that help them penetrate human cells.
Going into the study, little was known about the mechanisms through which viruses hijack metabolic building blocks from their cellular hosts, with older techniques providing a limited picture.
In the current study, a team of researchers from the University of Rochester Medical Centre and Princeton University created a new technique to clarify these mechanisms, and found that the technique could identify anti-viral therapeutic targets, according to a Rochester press release. The study was published in Nature Biotechnology Sunday.
Researchers combined drug discovery technologies to capture for the first time the exact concentrations and turnover of interchangeable molecules within the metabolic chain reactions that convert sugars into fatty acids.
The fields of metabolomics and fluxomics have emerged to measure these patterns, and to provide insight into diseases with a metabolic component, from diabetes to infectious diseases to cancer.
“Using new fluxomic techniques, our study reveals that viral infection takes control of cellular metabolism and drives, among other things, marked increases in fatty acid synthesis,” said Joshua Munger, assistant professor of biochemistry at Rochester Medical Center, and a study author.
“We also found that if you target these increases in fatty acid metabolism using existing anti-obesity and anti-metabolism drugs, you inhibit viral replication.”