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Ancient immune defense mechanism is no match for HIV-1

Researchers have discovered that mammalian cells infected with HIV-1 engage a primitive defense mechanism that was previously observed only in plants and invertebrates. The research also reveals exactly how HIV-1 successfully thwarts this rare form of immunity in vertebrate cells. However, elucidation of the mechanism HIV-1 uses to protect itself provides some critical insight into a potential vulnerability within the HIV-1 molecule. Identification of what might be a long sought after weakness in the virus may have application for rational design of future anti-HIV-1 therapies. The study is published in the May issue of Immunity.

RNA silencing is a type of natural immune defense in which sequence-specific RNA degradation follows the recognition of double-stranded RNA (dsRNA). The dsRNA is processed by a protein called Dicer, which chops the long strands of RNA into smaller pieces, resulting in the production of an RNA-induced silencing complex (RISC). RISC can specifically identify and degrade complementary target RNA. This process is known as RNA interference (RNAi) and can silence the ability of a virus to successfully reproduce itself. Although this mechanism has been artificially manipulated to selectively inhibit specific genes in mammalian cells, it was not known whether mammalian viruses naturally elicit this type of immunity in vertebrate cells.

Drs. Yamina Bennasser and Kuan-Teh Jeang from the Molecular Virology Section at the National Institute of Allergy and Infectious Disease and colleagues found that infection with HIV-1 induces RNAi in human cells. However, the researchers discovered that HIV-1 has an intriguing strategy to combat this cellular defense. The HIV-1 protein Tat, well known as a transcriptional activator, also can function as a suppressor of RNA silencing (SRS). Tat helps HIV-1 to elude the cell's natural RNAi defense by interfering with the ability of Dicer to process dsRNAs.

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Source:Cell Press


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