HIV has a voracious sweet tooth and is its downfall

If there was one thing in common between humans and HIV, it would be the craving for sugar. A new study has suggested that HIV pines for sugar and other nutrients once it invades an activated immune cell. Therefore, cutting its access to the sugar hinders its growth, and thus its proliferation.

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It appears that the deadly virus, HIV, seeks sugar together with other nutrients from the immune cell it has infected. It needs the sugar for its own growth and propagation throughout the body of its host.

The researchers of the new study discovered the link when they observed the death of the virus after they blocked the switch that causes the immune cell to provide an abundance of sugar and nutrients. HIV could not replicated when deprived of sugar.

HIV is not the only one with a voracious desire for sugar. Cancer cells also tend to consume lots of sugar and nutrients for its growth and spread. The new study might therefore be relevant in the treatment of cancer too.

 

The virus needs activated immune system T cells: activation triggers an increase in the cell’s sugar supply that is used up by the virus. How does the newly activated T cell stock up on sugar? This is what the scientists have discovered.

The first step in stocking sugar supplied entails turning on a cell component, a compound known as phospholipase D1 (PLD1). When the latter was blocked, the virus could not access sugar supplies, and thus could not grow well.

“This compound can be the precursor for something that can be used in the future as part of a cocktail to treat HIV that improves on the effective medicines we have today,” said corresponding study author, Harry Taylor, research assistant professor in medicine at Northwestern University Feinberg School of Medicine.

“It’s essential to find new ways to block HIV growth, because the virus is constantly mutating,” said Taylor, also a scientist at Northwestern Medicine’s HIV Translational Research Center. “A drug targeting HIV that works today may be less effective a few years down the road, because HIV can mutate itself to evade the drug.”

The team made use of a non-toxic way to block the HIV’s access to the supplies. Furthermore, the procedure also stops the abnormal activation and growth of immune cells that is caused by HIV. The new research is therefore considered to be extremely promising.

“Perhaps this new approach, which slows the growth of the immune cells, could reduce the dangerous inflammation and thwart the life-long persistence of HIV,” Taylor said.

“This discovery opens new avenues for further research to solve today’s persisting problems in treating HIV infection: avoiding virus resistance to medicines, decreasing the inflammation that leads to premature aging, and maybe even one day being able to cure HIV infection,” said Dr. Richard D’Aquila, director of Northwestern’s HIV Translational Research Center. He also is the Howard Taylor Ricketts Professor of Medicine at Feinberg and a physician at Northwestern Memorial Hospital.

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