T the level of gene expression act cooperatively to establish and maintain HIV latency. In conclusion, our study reveals that TI represents a key mechanism that antagonizes proviral gene expression to promote the latency of HIV. Furthermore, it demonstrates several means that could be used to counteract TI for reactivating latent HIV. Future mechanistic studies linking TI and other transcriptional
F Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892 USA Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892 USA; Biostatistics Research Branch, Division of Clinical Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892 USAdAIDS cNationaland Cancer Virus Program,
F Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892 USA Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892 USA; Biostatistics Research Branch, Division of Clinical Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892 USAdAIDS cNationaland Cancer Virus Program,
And from cells expressing Tat protein, 48 h after electroporation. qPCR was performed in the presence of SyBr Green (Sigma). Primer sequences and positions are in Table S1. Construction of stably transfected cell lines LMP vectors (Open Biosystems) expressing two microRNA-adapted shRNAs (shRNAmir) against the ER and a control shRNAmir (Table S1) were transfected into Phoenix cells with FuGENE6 rea
Ns dormant. In contrast, we demonstrated that TI could be counteracted by specific inhibition of the upstream transcription or by cooperative activation of transcription initiation and elongation from the 5'LTR by the viral and host TFs. In the latter scenario, we envision that RNAPII initiating from the viral promoter competes successfully with the RNAPII that is elongating through the 5'LTR. Bec
Ns dormant. In contrast, we demonstrated that TI could be counteracted by specific inhibition of the upstream transcription or by cooperative activation of transcription initiation and elongation from the 5'LTR by the viral and host TFs. In the latter scenario, we envision that RNAPII initiating from the viral promoter competes successfully with the RNAPII that is elongating through the 5'LTR. Bec
T the level of gene expression act cooperatively to establish and maintain HIV latency. In conclusion, our study reveals that TI represents a key mechanism that antagonizes proviral gene expression to promote the latency of HIV. Furthermore, it demonstrates several means that could be used to counteract TI for reactivating latent HIV. Future mechanistic studies linking TI and other transcriptional
And from cells expressing Tat protein, 48 h after electroporation. qPCR was performed in the presence of SyBr Green (Sigma). Primer sequences and positions are in Table S1. Construction of stably transfected cell lines LMP vectors (Open Biosystems) expressing two microRNA-adapted shRNAs (shRNAmir) against the ER and a control shRNAmir (Table S1) were transfected into Phoenix cells with FuGENE6 rea