New insights into how HIV becomes latent in host cells could lead the way to improved retroviral therapy, according to a report in the August issue of linkurl:__Cell Host and Microbe.__;http://www.cellhostandmicrobe.com/content/article/abstract?uid=PIIS1931312808001881 Once HIV infection occurs, the virus can integrate into actively transcribed host genes, where it becomes latent. These reservoirs of latent HIV can reactivate and continue to spread the disease after linkurl:retroviral therapy;http://www.the-scientist.com/2007/9/1/40/1/ -- which can only target active virus -- has removed the majority of the viral load. Now, researchers led by B. Matija Peterlin and colleagues at the Rosalind Russell Medical Research Center at the University of California, San Francisco have found two mechanisms that, at least experimentally, trigger transcription of latent HIV. While there are many mechanisms by which a virus can become latent, Peterlin's group focused on transcriptional interference, in which a virus silences itself by integrating into a commonly used gene. The cell's own...
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