New Delhi, March 16: Indian biologists have uncovered a trick played by the human immunodeficiency virus to fool and evade the immune system, fuelling hopes for a novel strategy to fight HIV.

The scientists in New Delhi and Bangalore have deciphered the mechanism of a devious “handshake” between a protein of HIV and molecules in human cells that allows the virus to escape destruction early during the infection.

“We’ve caught a glimpse of how HIV hijacks biological machinery in human cells to ensure its own survival,” said Shahid Jameel, head of virology at the International Centre for Genetic Engineering and Biotechnology, New Delhi, a team member.

The human immune system is a complex network of proteins and cells that work in harmony to detect, trap and destroy invading microbes. When a virus enters a cell, a number of proteins migrate to the surface of the cell, tagging it as infected, and alerting killer cells from other arms of the immune system to mount an attack and destroy the infected cell.

The Indian study, published in the journal Cell Host and Microbe on Wednesday, has shown that an HIV protein called Nef latches itself to the tails of two such molecules — CD80 and CD86 — that play a crucial role in stimulating immune killer cells. The Nef protein binds to CD80 and CD86 found on the surface of infected cells and drags them into the interior of the cells.

“By pulling CD80 and CD86 inside the cells, Nef protein blocks stimulation of killer cells, and HIV evades immune destruction very early in the infection,” said Satyajit Rath, a scientist at the National Institute of Immunology, New Delhi.

The scientists from the two Delhi institutes along with Bangalore’s National Centre for Biological Sciences have cautioned that their study was based on HIV in human cells in the laboratory and the mechanism is yet to be verified in animals.

The findings have fuelled hope among researchers that it may be possible to disrupt Nef interaction with CD80 and CD86 with small molecules and allow the immune system’s killer cells to multiply and mount an attack on HIV-infected cells.

“This gives us a different target to look at for future treatment strategies,” Jameel said. However, researchers point out that the study addresses an early stage of the infection when the virus is lurking in a class of cells called macrophages. “We have no technology today to detect HIV infection at such an early stage,” said Vineeta Bal, a team member at NII.

Rath said the findings are encouraging enough to think about screening chemicals to find molecules that may block the Nef action on CD80 and CD86 molecules. “But we can’t predict whether such an approach will work. We don’t know whether HIV has backup strategies,” he said. Biologists have known for long that HIV uses several tricks to escape the human immune system.

The department of biotechnology and the Indian Council of Medical Research have approved a project to verify the Nef’s “handshake” with CD80 and CD86 in mice. Ideally, such results should be verified in non-human primates — monkeys infected with a cousin of HIV named SIV — but India lacks the rigorous laboratory facilities required to infect monkeys with HIV.

“We’re hoping others will pick this up and investigate the mechanism in non-human primates, but India must work towards developing the infrastructure needed for monkey models,” Jameel said.