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Nov 29, 2013 01:22 PM EST

Scientists from Spanish universities and research centers designed small synthetic molecules that could stop the replication of the AIDS virus.

The molecules created are capable of joining the genetic material of AIDS and block its replication, an achievement that has been obtained for the first time in the world, according to a press release.

The group of researchers, led by José Gallego from Universidad Católica de Valencia "San Vicente Mártir" created a synthetic molecule that inhibits the output of genetic material of the virus from the infected cell nucleus to the cytoplasm. This results in the blocking of the virus replication and saving other cells from being infected by the virus.

The new virus inhibitors, called terphenyls, developed by this group of scientists, were designed by computer to reproduce the interactions of one of the proteins encoded by the virus, the viral protein Rev.

The genetic material of the AIDS virus, or HIV-1, is formed by ribonucleic acid (RNA), and encodes several proteins that allow it to penetrate the human cells and reproduce within them.

The terphenyls join Rev's receptor in the viral RNA, preventing the interaction between the protein and its RNA receptor.

"This interaction is necessary for the virus genetic material to leave the infected cell nucleus and, thus, it is essential for the survival of HIV-1," according to a statement in the press release. "The fact that the terphenyls block the virus genetic material output of the cell prevents the infection of other cells."

Traditionally, pharmaceutical companies have focused on the development of medicines that act on target proteins, as the approach to the receptors made out of RNA is considerably complex.

HIV infects 34 million people worldwide in 2010, according to the World Health Organization. According to a press release, the emergence of resistance to the current antiretroviral therapies and the lack of an effective vaccine highlight the necessity of identifying the new medicines that act on other virus targets. 

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