A new study published by Northwestern Medicine and Vanderbilt University revealed that the HIV virus is affected by a lack of sugar. The HIV virus uses the immune system by replicating in specific types of immune cells called CD4+ T cells and scientists used a compound with a high amount of sugar to test the research hypothesis.
Previous studies have implicated sugar as a fuel for viruses and bacteria. The inability to access sugar and other nutrients after invading a cell affects the ability of the virus to replicate.
“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 Harry Taylor, research assistant professor in medicine at Northwestern University Feinberg School of Medicine.
The scientists blocked the cell’s sugar supply and turned off the phospholiapse D1 enzyme, which is required to signal T cells to increase their supply of sugar and vital nutrients. HIV triggers the excess activation and growth of T cells which can lead to inflammation in the body, causing premature organ damage in patients with HIV even when the virus is suppressed by medicine.
“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,” said Prof. Taylor.
“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,” he states.
Phospholipase D1 couples CD4+ T cell activation to c-Myc-dependent deoxyribonucleotide pool expansion and HIV-1 replication, Harry E. Taylor et al., PLOS Pathogens, doi: 10.1371/journal.ppat.1004864, published online 28 May 2015.