The team showed that a cluster of miRNAs bind to a certain location on the viral RNA, which in turn, blocks the creation of important proteins, and HIV replication. Resting CD4 T cells, they found, are “enriched” with more than the normal amount of these miRNAs compared to the activated T cells. When the researchers used antisense technology to block miRNA-caused viral inhibition, they found that the HIV again was active and able to replicate – proving miRNA’s critical role in maintaining latency.
MicroRNAs may be key to HIV's ability to hide, evade drugs, Jefferson scientists find
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