In DepthBiomedicine

Tests identify HIV's final redoubt

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Science  22 Mar 2019:
Vol. 363, Issue 6433, pp. 1260-1261
DOI: 10.1126/science.363.6433.1260

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Summary

Antiretroviral (ARV) drugs powerfully suppress HIV and stave off disease, but in some people, treatment still allows easily detectable, low levels of virus to persist in the blood. These people do not have drug-resistant strains of HIV, nor do they appear to be skipping doses of their ARVs. A new study presented last week at an HIV/AIDS meeting in Seattle, Washington, offers an explanation to this long-standing oddity: The virus is coming from clones of infected cells. These so-called repliclones have HIV integrated into their DNA, and when they make copies of themselves, the new cells also are infected. But drugs can't touch the virus during this type of clonal expansion. ARVs prevent these newly produced viruses from infecting new cells, but they do challenge a popular cure strategy known as "kick and kill," which aims to force cells that have latent HIV infections to produce new viruses and thereby self-destruct. These repliclones are spitting out new viruses so they don't need to be kicked, and they're not being destroyed quickly enough during the production process. A second study presented at the meeting suggested a potential, if futuristic, way around the problem: Use the genome editor CRISPR to cut HIV out of infected chromosomes. Researchers showed some success with this idea in a monkey model, but others cautioned that many questions remain about CRISPR's ability to safely excise HIV and to reach enough infected cells for it to make a difference.