Washington: Researchers have discovered a molecular invisibility cloak that enables HIV, the virus that causes AIDS, to hide inside cells of the body without triggering the body's natural defence systems.
The new study shows how 'uncloaking' the virus using an experimental drug triggers an immune response that stops the virus from replicating in cells grown in the laboratory. The findings could lead to new treatments and help to improve existing therapies for HIV infection.
The innate immune system is the body's first line of defence against infection and incorporates an alarm system present in all cells of the body that detects the presence of 'foreign' material from invading bacteria and viruses.
When the alarm is tripped, the infected cell begins an anti-viral programme and sends out warning signals to alert other cells that a virus is around. HIV infects vital cells of the immune system so its ability to replicate undetected without triggering this alarm system has puzzled scientists since the discovery of the virus.
The team identified two molecules inside host cells that are recruited by HIV after infection that stop the virus from reproducing its genetic material too early. The effect is to shield the virus from the alarm system and stop the innate immune system from kicking into action.
In the absence of these molecules, either by depletion from infected cells or blocking their recruitment using an experimental drug, HIV is exposed to the alarm system and an anti-virus immune response is triggered. Targeting the cloaking molecules and not the virus itself makes it much more difficult for the virus to mutate and become resistant to this treatment approach, a significant problem with standard HIV therapies.
"The hope is that one day we may be able develop a treatment that helps the body to clear the virus before the infection is able to take hold," professor Greg Towers , a Wellcome Trust Senior Research Fellow at UCL and lead author of the study
The experimental drug used in the study is based on Cyclosporine, a drug that is widely used to prevent organ rejection in transplant patients because of its ability to dampen the immune response.
The study is published in the journal Nature.