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New Strategy to Kill HIV- Starve its Sweet Tooth to Death

A new study has found a possible way to starve the HIV virus to death so that the immune cells do not grow. 

Published
Health News
2 min read
An illustration of a schematic depiction of the protein structure of the pre-fusion HIV spike. (Photo: Reuters)

Scientists have found a new strategy to starve the human immunodeficiency virus (HIV) to death - by blocking its sugar and nutrient pipeline.

HIV has a voracious sweet tooth, which will be its Achilles’ heel, according to researchers from Northwestern Medicine and Vanderbilt University.

After the virus invades an activated immune cell, it craves sugar and nutrients from the cell to replicate and fuel its wild growth throughout the body.

Scientists discovered the switch that turns on the immune cell’s abundant sugar and nutrient pipeline. Then they blocked the switch with an experimental compound, shutting down the pipeline and, thereby, starving HIV to death.

The discovery may have applications in treating cancer, which also has an immense appetite for sugar and other nutrients in the cell, which it needs to grow 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.
– Harry Taylor, Assistant prof in Medicine-Infectious Diseases

Northwestern and Vanderbilt scientists figured out that the first step in stocking the T-cell’s pantry involved turning on a cell component called phospholipase D1 (PLD1).

Then they used an experimental compound to block PLD1 and shut down the pipeline.

This is believed to be the first time scientists have targeted the virus’s ability to pilfer the cell’s pantry to stop its growth. The compound also slowed the proliferation of the abnormally activated immune cells, the study found.

Current HIV medications stop HIV growth but do not affect the abnormal excess activation and growth of immune cells triggered by HIV.

The study was published in the journal PLOS Pathogens.

(With inputs from PTI)

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