In a major breakthrough, new research has identified how HIV infection causes mass suicide of immune cells and how an existing anti-inflammatory drug can block cellular self-destruction.
Further, they have identified an existing anti-inflammatory drug that in laboratory tests blocks the death of these cells -- and now are planning a Phase II clinical trial to determine if this drug or a similar drug can prevent HIV-infected people from developing AIDS and related conditions.
Scientists at the Gladstone Institute figured out how, during an HIV infection, a protein known as IFI16, senses fragments of HIV DNA in abortively infected immune cells.
This triggers the activation of the human enzyme caspase-1 and leads to pyroptosis, a fiery and highly inflammatory form of cell death. This mass death of immune cells causes AIDS.
In lab tests, the scientists found that an existing anti-inflammatory inhibits caspase-1, thereby preventing pyroptosis and breaking the cycle of cell death and inflammation.
"This discovery ables us to identify a potential new therapy for blocking the disease's progression and improving on current antiretroviral medications for HIV-infected people," said Robert F. Siliciano, professor of medicine at Johns Hopkins University
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HIV infected an additional 2.3 million people last year, according to UNAIDS, bringing the global total of HIV-positive people to 35.3 million. Antiretroviral medications (ARVs) can prevent HIV infections from causing AIDS, but they do not cure AIDS. Also, nearly 16 million people who carry the virus do not have access to ARVs, according to World Health Organisation (WHO).
"This has been an absolutely fascinating voyage of discovery," said team-member Warner Greene, a molecular virologist at the Gladstone Institute of Virology and Immunology in San Francisco, California.
The researchers are now planning a Phase II clinical trial to determine if this drug or a similar drug can prevent HIV-infected people from developing AIDS and related conditions.
The findings of the study have been published in the journal Nature.