HIV exhausts the body’s immune system by overactivating it, despite effective antiviral treatment. But there is an existing medication that restores immune cell function.
This is according to a study –HIV-1 derived oligonucleotides induce a type I IFN/STING dependent immune suppression reversible by targeting IFNARI by Cecilia Svanberg, Ravi Prasad Mukku, Sabri O. Besler, Francis R. Hopkins, Christopher Sjöwall, Sofia Nyström, Esaki M. Shankar and Marie Larsson – that was published in the PLOS Pathogens.
For people living with HIV, antiviral treatment is effective in limiting the amount of virus in the blood and slowing the progression of AIDS. But the virus can stay hidden in the body for many years and contribute to premature ageing of the immune system. Despite effective treatment, the immune system is commonly impaired in people with HIV.
For the researchers from Linköping University, there’s a need to investigate how the virus causes dysregulation of the immune system.
In healthy people infected with a virus, a protein called type I interferon is activated that plays a very important role in the body’s immune system. Type I interferon is the first protection against viral infections and also ensures that other parts of the immune system kick in. Once the infection is combated, the amount of type I interferon falls back to a very low level.
In this study, the researchers showed how HIV exploits the body’s type I interferon signaling to drive chronic immune activation, also when the virus is under control due to medication.
“In the case of an HIV infection, type I interferon provides protection in the first stage when the body gets infected. But if the interferon is chronically activated, an overactivation of the immune system will instead facilitate the spread of HIV in the body,” said Svanberg, lead author of the study.
A chronically activated immune system eventually leads to several different types of cells in the immune system becoming exhausted and less effective. Two important cell types affected are dendritic cells and T cells.
The researchers’ experiments on human cells showed that the chronic activation of interferon occurs precisely when dendritic cells and T cells are in contact with each other. This opens up an opportunity to restore immune cell function.
“When we treated the cells with a medication currently used to treat another disease, this perfectly restored the function of the immune cells. It looks just like when HIV is not present,” said Svanberg.
The medication, anifrolumab, blocks type 1 interferon and is used to treat systemic lupus erythematosus, SLE, an autoimmune disease. Other research groups have conducted studies on animals with HIV-like infections, treating them with either anifrolumab or other substances with the same function. The amount of HIV virus in the blood has decreased and the animals’ health has improved.
“Using this interferon blocker together with existing antiviral treatment could possibly improve the health of people living with HIV. We think it would be worth investigating further,” said co-author Larsson.
