Method aims to 'outfox' HIV virus

Scientists working in the laboratory were able to block HIV infection by inactivating a key human protein.

Most drugs used against HIV target the virus's own proteins. But HIV mutates at such a high rate, modifying its genes, that drug resistant strains emerge quickly.

Strategies designed to outmanoeuvre the virus such as switching medications and prescribing multiple drugs can increase the risk of side effects and make life more difficult for the patient.

The new approach targets a protein produced by human cells rather than HIV, and is therefore impervious to the virus's mutations. Researchers in the US found that inactivating the protein, known as ITK, suppressed HIV's ability to infect key human immune cells.

ITK is a signalling molecule that activates T cells, part of the body's immune system.

When HIV enters the body it enters T cells and takes them over. Instead of defending the body against invaders, the T cells now devote themselves to helping the HIV virus replicate. But without active ITK, the virus cannot take advantage of the signalling pathways within T cells it needs to make this happen.

Dr Pamela Schwartzberg, from Boston University, Massachusetts, one of the study's senior investigators, said: "We were pleased and excited to realise the outcome of our approach. Suppression of the ITK protein caused many of the pathways that HIV uses to be less active, thereby inhibiting or slowing HIV replication."

The scientists studied the effects of ITK inactivation on cell cultures exposed to HIV. Suppressing ITK reduced the ability of the virus to enter T cells and have its genetic material transcribed. However, ITK inactivation did not significantly affect the survival of T cells. Mice deficient in ITK were still able to ward off various types of viral infection, although their immune responses were delayed.

The findings were reported in the online edition of the journal Proceedings of the National Academy of Sciences.