Encouraging Health

A team of researchers from the University of Rochester Medical Centre and Princeton University has discovered that existing anti-obesity drugs can be used to treat infections like flu, hepatitis or HIV.

Metabolism refers to a process by which living things break down nutrients to produce energy. For instance, the breakdown glucose and its conversation via chain reactions into adenosine triphosphate, the energy-storing currency of cellular life.

Glucose can also be converted into fatty acids - the lipid building blocks of human hormones and cell membranes - that are used by influenza, HIV and hepatitis viruses to build their viral cover and hijack human cells.

During the study, the researchers developed a new technique to analyse the mechanisms regarding how such viruses penetrate the metabolic building blocks from their cellular hosts.

They also studied the fluxes or concentration and turnover, of interchangeable molecules within the metabolic reactions that convert sugars into fatty acids.

“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,” Nature magazine quoted Dr. Joshua Munger, assistant professor of Biochemistry and Biophysics at the University of Rochester Medical Centre, and a study author, as saying.

“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,” Munger added.

The new technique enabled the researchers to measure the changes in metabolic flux in human cells as they became infected by human cytomegalovirus (HCMV), an enveloped virus of the b-herpes family that infects most human adults and that causes severe disease in those with weakened immune systems.

The team used drugs known to inhibit enzymes that build fatty acids, acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS), used in the treatment of obesity and high cholesterol, to determine whether HCMV-induced fatty acid production was necessary for enveloped viruses to make copies of themselves.

They found that treatment with TOFA, an ACC inhibitor, led to a more than thousand-fold reduction in HCMV replication, while C75, an inhibitor of FAS, resulted in a more than 100-fold reduction.