Scientists from the University of Cambridge in the UK have discovered a mutant form of an immune protein is able to block infection and spread of the human immunodeficiency virus (HIV) in immune cells. Their findings could lead to new ways to fight HIV by offering a new target for drug developers.
A report on the study appears in the latest online issue of the journal Retrovirology.
Senior author Professor Chris Rudd, of the University’s Department of Pathology, says:
“One exciting aspect about this new target for HIV intervention is that we should be able to fight HIV without compromising the immune system’s ability to battle infections.”
The World Health Organisation (WHO) estimates there are over 35 million people living with HIV today. In the last 30 years, the virus has killed over 25 million people.
And although there has been dramatic progress in fighting the virus, with new infections dropping by a third in 2012 compared with 2001, HIV remains a major global public health problem.
HIV attacks T cells, a type of white blood cell that plays a major role in the immune system.
The virus enters T cells by binding to one of their surface receptors, CD4. Once inside, HIV hijacks cell resources and uses them to rapidly replicate itself and release the copies to infect other T cells.
The spread occurs when an infected T cell is attached to an uninfected cell.
In this study, the researchers investigated an immune cell protein called adhesion and degranulation-promoting adaptor protein (ADAP) because it is already known that ADAP is involved in regulating T cell adhesion and proliferation.
But they note despite this knowledge, little has been uncovered about any links between ADAP and infection by HIV.
Their study is the first to show that ADAP regulates infection by HIV-1 via two distinct mechanisms: virus replication within T cells and virus spread due to contact between infected and uninfected T cells.
And they also discovered that a particular mutant form of ADAP is able to interfere with HIV-1 infection by blocking these two mechanisms.
Prof. Rudd says:
“The ADAP mutant is potent in its interference of HIV-1 transmission because it targets simultaneously two critical events, viral replication and the spread of the virus from one T cell to another.”
He suggests one treatment possibility could be to give HIV-infected individuals T cells expressing the mutant protein.
In another remarkable study published recently, an international team revealed how they eradicated HIV in cells with an antifungal drug.