Human immunodeficiency virus, HIV, is a retrovirus that relies on a large number of human host factors for propagation. Tat specific factor 1, Tat-SF1, has been identified as one of those host factors. It is a relatively understudied human protein originally thought to be required for viral transcription. However, recent findings suggest that overall HIV RNA levels remained the same with Tat-SF1 knockdown. Instead, it was the ratios of the three RNA size classes that were affected. This would be consistent with Tat-SF1 playing a role in RNA splicing, export or stability. We hypothesize that if Tat-SF1 levels are knocked down in human cells, then altered stabilization of HIV RNA isoforms will be detected. An HIV-expressing plasmid was transfected into HeLa cells in control and Tat-SF1 knockdown cells. Then, actinomycin D was added to stop transcription before RNA purification. The RNA was reverse transcribed and HIV RNA levels were analyzed by quantitative PCR. Preliminary data shows that unspliced and singly spliced RNA was selectively stabilized while the fully spliced was destabilized in Tat-SF1 knockdown cells compared the control. These results are consistent with Tat-SF1 selectively stabilizing HIV RNAs. Further exploration of this mechanism could be used toward future HIV drug therapies.

Tat-specific factor 1’s role in HIV RNA stability

253rd National Meeting (2017)

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