New protein helps to eliminate dormant HIV viruses from body
Protein developed in laboratory marks cells infected by the virus, easing its localization and destruction by the immune system
14/12/2015
Eliminating hidden HIV-infected cells would limit the dependence on antiretroviral drugs
Eliminating HIV from the human body is one of sciences current obsessions. Among the approaches towards this goal is the attempt to annihilate the dormant infected cells, which are invisible to the immune system and antiviral drugs. In addition, a study in this course seems to be close to success.
Researchers at the National Institute of Health, USA have created, in laboratory, a protein – called VRC07-?CD3 – able to mark cells infected by the virus, easing its localization and destruction by the immune system.
The finding could assist in a problem that affects patients treated with antiretrovirals, since the prolonged use of these drugs increases the risk of developing, for example, heart diseases. The method cannot be interrupted since there is a risk the dormant virus could again attack healthy cells.
Eliminating occult HIV-infected cells would limit the dependence on antiretroviral drugs, explained the researchs authors. Other studies with animals and humans, however, are necessary to determine the viability of the approach with the new protein.
How it works
The researchers discovered that the VRC07-?CD3 protein activated and killed auxiliary HIV-infected T cells that were dormant. These cells, retrieved from people under antiretroviral therapy, were incubated in laboratory with assassin T cells from the same patients.
Each one of the two ends of the VRC07-?CD3 has different functions. The first activates the T lymphocyte through a bond to a surface molecule called CD3 receptor. The other end, based on an antibody called VRC07, bonds to over 90% of the existing HIV types. At all, the protein eases the death of latent HIV-infected cells in three steps.
First, the CD3 bond end connects to the HIV-infected auxiliary T-cells, activating these cells in a way it triggers HIV production, displaying pieces of the virus in its surface. Next, the proteins part that bonds to the HIV attaches to these virus pieces, while the CD3 bonding extremity connects to one of the assassin T-cells, activating and approaching it from the auxiliary T-cell. Finally, the activated assassin T-cells destroy the HIV-infected auxiliary T-cell.
The authors of the study, published in an article on Nature Communications also found an adapted version of this protein for monkeys infected with the simian form of the HIV – called SIV – and that are under antiretroviral therapy. The researchers are now studying the effectiveness of VRC07-?CD3 addapted to these animals.
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