More Effective Way To Treat HIV Identified

By Staff

Scientists have discovered a more effective way to treat people suffering from HIV whose bodies have built a resistance to drug 'cocktails' currently used to keep them healthy. Researchers from University of South Carolina (USC) in the US identified a novel human protein variant that can be targeted to prevent the human immunodeficiency virus from harming HIV-positive individuals.


"Most HIV drugs target the virus but the virus is not stable, it always mutates - problematic because the virus can become resistant to effective drugs," said I-Chueh Huang, assistant professor at USC. The new study focused on HIV-1, the most widespread version worldwide. HIV can be classified into R5 and X4 viruses. R5 viruses are exclusively associated with primary infection, and X4 viruses emerge in later stages of HIV diseases in half of HIV carriers.

Detection of X4 is an indication that the patient's HIV infection has progressed to a very toxic state. Researchers identified a novel variant within the previously identified family of proteins. They nicknamed it "Delta 20," an immune system protein that suppresses the most damaging HIV strains, X4, by preventing the virus from infecting cells.

This method differs from the more traditional method of targeting viruses that may eventually become resistant to specific medical therapies, researchers said. "Much more research needs to be done, but we may have identified a new approach to treating acute HIV infection," Huang said. "Our finding will not help develop a vaccine because the focus is on innate immunity rather than the virus," Huang said. "Perhaps one day scientists will create medicine that, like 'HIV cocktails,' have to be taken indefinitely.

But the new treatment may be more effective because it is harder for viruses to escape the body's defences," Huang added. The study was published in the journal Proceedings of the National Academy of Sciences.

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    Read more about: hiv treatment
    Story first published: Thursday, August 24, 2017, 21:00 [IST]
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