"Our study provides critical insight on a paramount issue in HIV research: Why is the body unable to mount an efficient immune response to HIV to prevent transmission?" said one of the researchers Sumit Chanda, professor and director of Sanford Burnham Prebys Medical Discovery Institute (SBP) in the US.
The findings showed that a deficiency in NLRX1 -- an intracellular protein -- reduces the replication of the HIV virus.
It also slows down the power of immune system and promotes immunity to infection.
"Importantly, we were able to show that deficiencies in NLRX1 reduce HIV replication, suggesting that the development of small molecules to modulate the innate immune response may inhibit viral transmission and promote immunity to infection," Chanda added, in the paper published in the journal Cell Host and Microbe.
Further, host immune checkpoints that control the immune response to cancer were also discovered.
"This research expands our understanding of the role of host proteins in viral replication and the innate immune response to HIV infection, and can be extended to DNA viruses such as HSV and vaccinia," added another researcher Haitao Guo, postdoctoral research associate at University of North Carolina.
Immune checkpoints are immunological "brakes" that prevent the over-activation of the immune system on healthy cells.
Tumour cells often take advantage of these checkpoints to escape detection of the immune system.
The results have important implications for improving HIV antiviral therapies, creating effective viral vaccines, and advance a new approach to treat cancer, the team concluded.(IANS)