Scientists discover protein that may help halt the spread of HIV
Scientists have discovered an HIV Aids treatment that may help sufferers avoid the problem of drug resistance.
Scientists have found that the virus can be significantly weakened by inactivating a key human protein called ITK.
Current treatments target the proteins in the HIV virus. This approach weakens the virus but in time it will mutate and resist the drugs that the sufferer is taking.
To combat this doctors will change the combination of the drugs but in time the virus will become resistant to those too. In addition to this, the changing of combinations can bring on serious side effects.
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.
The HIV virus uses the bodies T cells to spread the virus, but by inactivating the ITK protein the virus looses can no longer use T cells.
ITK is a signalling molecule that activates T cells, part of the body’s immune system.
Scientists studied the effects of ITK inactivation on cell cultures exposed to HIV and found that suppressing ITK reduced the ability of the virus to enter T cells and have its genetic material transcribed.
Scientists tested the treatment on mice and found that they although they were able to fight other infections, their response to infection was delayed.
The treatment will be welcomed by poorer countries as the treatment would significantly reduce the amount of drugs that a patient would need to take to stay alive.
Anti-retroviral drugs are expensive and the majority of the world’s infected individuals do not have access to medications and treatments for HIV Aids.
Other research to improve current treatments includes decreasing side effects of current drugs, further simplifying drug regimens to improve adherence, and determining the best sequence of regimens to manage drug resistance.
