security Agent. HIV-1, shown here on a cell, can be stopped at the entrance to the cell so small RNAs are used to disable a key receiver.
short stretches of RNA, called small RNAs, can interfere with gene function and are thought to protect the genome against DNA or harmful viruses. A new study now shows that these bits of RNA can be used to make cells resistant to one of the most deadly viruses, HIV.
HIV enters cells through receptors studding the surface of the soldiers of the immune system called T-helper cells. To do this, the HIV binds to a protein called CD4 and is assisted by another protein called CCR5. Because people who have a mutation in their CCR5 gene, which produces the co-receptor, are resistant to infection by HIV, scientists have long suspected that disrupt the production of CCR5 could be a way to "immunize" the cells against HIV.
virologist David Baltimore of the California Institute of Technology in Pasadena, Irvin Chen virologist with the University of California, Los Angeles, and colleagues decided to see if they could use small interfering RNAs (siRNA), class of small RNAs to inhibit CCR5 gene. The team created a gene therapy by packaging the molecules within a vector - a virus called a lentivirus, which was derived from the virus itself. According postdoctoral researcher Xiao-Feng Qin, first author of the study, once inside the cell copies DNA siRNA integrate into the chromosomes of the cell, allowing the progeny of that cell inherit a largely inactive gene CCR5 . SiRNA blocked CCR5 expression up to ten times in daughter cells with cells expressing normal CCR5. Caused by HIV-1, control cells showed levels of three to seven times higher infection that cells with reduced expression of CCR5, the team reports in the online issue December 23 procedure National Academy of Sciences .
"This is a beautiful, well-controlled, and obviously CCR5 is a target of interest in anti-HIV gene therapy," says molecular biologist John Rossi of City of Hope Cancer Center near Los Angeles but he said that this strategy will be more effective when combined with additional viral targets -.. something that the group is already working to Baltimore others agree that more work is needed "There is one. important first step, but, like all genetic therapies, access to clinical path is still a ways off, "says virologist Judy Lieberman of Harvard Medical School's Center for Blood Research in Boston.
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