Scientists have announced a novel method of attacking the human immunodeficiency virus, HIV, the cause of AIDS.  The study, a collaboration between Boston University and the National Human Genome Research Institute (NHGRI), investigated the targeting of a protein located on human immune cells.  Once targeted, the virus was unable to infect these cells.  Eric Green, the director of the NHGRI said that “This new insight represents an important contribution to HIV research,” and spoke of the discovery as “an exciting model for deriving potential new HIV therapies.”

The human immune system is made up of white blood cells, a large proportion of which are known as T cells.  It is these cells of the human body that the HIV virus infects.  The researchers interfered with a signalling protein on the surface of these cells called interleukin-2-inducible T cell kinase, known as ITK.  The protein is responsible for the activation of T-cells, required for the body to mount an efficient immune response.  Schwartzberg, one of the lead researchers, explained how “suppression of the ITK protein caused many of the pathways that HIV uses to be less active, thereby inhibiting or slowing HIV replication.”

Drugs in the past have targeted proteins present on the virus itself.  This is problematic due to drug-resistant strains appearing as a result of the proteins rapidly altering in composition, a process called genetic mutation.  The human cells have a much lower mutation rate thereby making them an optimal target.

The inactivation of ITK was carried out using a chemical and a genetic inhibitor.  The T cells were then exposed to the virus and its effects studied during different stages of the virus’s replication cycle.  It was not only shown that the ability of the virus to enter cells was reduced but interference did not affect the cell’s ability to survive.

The study was published earlier this month in the online edition of the prestigious journal; Proceedings of the National Academy of Sciences.



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