The human immunodeficiency virus (HIV) infects thousands of people per year but findings of a new study may pave way for new treatments that could effectively fight the virus that causes AIDS.
In a new study published in the journal PLOS Pathogens on May 28, researcher from Northwestern University and Vanderbilt University reported that HIV has a sincere weakness: it has sweet tooth and that this could be its Achilles' heel.
The researchers reported that they have identified a way of blocking HIV from feeding on an infected person's bloodstream, which could eventually kill it off.
When HIV invades an activated immune cell, it needs the cell's sugar and nutrients so it could replicate and fuel its own growth in the body.
Researchers used an experimental compound to block the switch responsible for turning on the immune cell's nutrient and sugar pipeline, shutting this down and starving the virus to death. In vitro, researchers found that HIV was not able to replicate in human cells.
Besides withholding nutrients from the harmful cells, treatment with the experimental compound also left the healthy cells alone marking the first time that a study successful blocked HIV's source of nutrition and energy.
Current treatments stop the growth of HIV but do not have effect on the growth and excess activation of immune cells that were triggered by the virus and known to cause inflammation that leads to premature organ damage in HIV patients.
The researchers said that the discovery may have potential application in cancer treatment as cancer is also known to have huge appetite for sugar and nutrients from cells necessary for its growth and spread.
"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 study author Harry Taylor, from Northwestern University Feinberg School of Medicine.
Taylor added that it is important to identify new means of blocking HIV growth because the virus constantly mutates. He cited that a drug capable of targeting HIV today may no longer be as effective in the next few years because the virus mutates and evades the drug.
"These findings uncover a unique mechanism of action for PLD1 inhibitors and support their further development as part of a therapeutic combination for HIV-1 and other viral infections dependent on host nucleotide biosynthesis," Taylor and colleagues wrote in their study.
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