Breakthrough Process Could Prevent Transmission of HIV

Researchers have developed a way to crack open cells of the human immunodeficiency virus (HIV), making the disease vulnerable to the immune system. According to researchers, the breakthrough opens up the possibility of new vaccines that could prevent the transmission of HIV.

The new study is based upon the results of a previous study conducted by the same researchers, in which it was shown that HIV-1 infected cells were more likely to be eliminated by the immune system when Nef and Vpu—2 proteins within the virus—were deactivated due to gene mutation.
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For the new study, researchers placed molecules called JP-III-48 onto the surfaces of cells that were infected with HIV. These molecules imitate the protein CD4, which is located on T lymphocytes and causes the immune system to be vulnerable to HIV infection.

“The virus has to get rid of the CD4 proteins to protect itself. Adding the small molecule forces the viral envelop to open, like a flower. The antibodies that are naturally present after the infection can then target the infected cells so they are killed by the immune system,” explained Jonathan Richard, PhD, lead author of the study and a postdoctoral researcher at the CRCHUM.

The discovery could lead to the development of a vaccine to protect against HIV infection. The investigators also hope to use the molecule as part of a “shock and kill” treatment method to eliminate HIV reservoirs within patients already infected with the virus.

The complete study is published in the May issue of Proceedings of the National Academy of Sciences of the United States of America.

-Michelle Canales Butcher

References:

1. University of Montreal. Researchers “un-can” the HIV virus. May 4, 2015. www.nouvelles.umontreal.ca/udem-news/news/20150504-researchers-un-can-the-hiv-virus.html. Accessed May 5, 2015.

2. Richard J, Veillette M, Brassard N, et al. CD4 mimetics sensitize HIV-1 infected cells to ADCC. PNAS. 2015 May [epub ahead of print] doi: 10.o73/pnas.1506755112.