A single cell was infected with an HIV Tat model virus containing green fluorescent protein (GFP) and grown into a population of clones. The virus is integrated into a single identical genomic position in all cells, but the cells display highly variable levels of GFP, which are driven by random fluctuations in HIV-1 Tat protein.
Random fluctuations in gene expression can influence the fates of cells infected with human immunodeficiency virus (HIV) far more than previously thought, according to new research from Howard Hughes Medical Institute (HHMI) researchers at the University of California, Berkeley. By combining experimental and computational studies of HIV’s replication cycle, the researchers found evidence that the virus may become latent in some cells by harnessing the random molecular behavior of the cell.
HIV can hide in cells for years before reappearing to make new virus. Latency is considered one of the biggest reasons why drug therapy fails to eradicate HIV from patients. The new findings, which will be published in the July 29, 2005, issue of the journal Cell, could help scientists design new and more effective treatments to slow or halt the progression of HIV infection.
HIV normally replicates rapidly in the body’s white blood cells, but, in some cells, the virus stops replicating and becomes dormant. Researchers have long puzzled over how HIV makes the “decision” to become latent or to keep replicating in a certain cell.
Jennifer Donovan | EurekAlert!
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