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. 2013 Sep 24;2013(4):41-47.
doi: 10.4137/VRT.S12147.

T Cell Transcription Factors and Their Impact on HIV Expression

Katarzyna Kaczmarek  1 , Ayana Morales  2 , Andrew J Henderson  3
Affiliations

T Cell Transcription Factors and Their Impact on HIV Expression

Katarzyna Kaczmarek et al. Virology (Auckl). .

Abstract

By targeting CD4+ effector T cells, HIV has a dramatic impact on the depletion, expansion and function of the different polarized T cell subsets. The maturation of T cell lineages is in part driven by intrinsic transcription factors that potentially influence how efficiently HIV replicates. In this review, we explore whether transcription factors that are required for polarizing T cells influence HIV replication. In particular, we examine provirus transcription as well as the establishment and maintenance of HIV latency. Furthermore, it is suggested these factors may provide novel cell-specific therapeutic strategies for targeting the HIV latent reservoir.

Keywords: CD4+ T cells; HIV; latency; transcription.

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Figures

Figure 1
Figure 1
Model of Sequential CD4+ T Cell Differentiation. Upon activation by antigen presenting cell (APC), naïve T cell (TH0) undergoes differentiation into effector or memory populations. The different effector populations have capacity to mature into effector memory T cells (TEM). Stem cell memory T cells (TSCM), follicular helper T cells (TFH) and regulatory T cells (Treg) mature into central memory T cells (TCM), which then can become transitional memory T cells (TTM) and further convert into TEM.
Figure 2
Figure 2
Model for HIV Transcriptional Regulation. During initiation of HIV transcription RNAP II is recruited to the HIV LTR and transcribes nascent TAR RNA. However, methyltransferases, HDACs, and transcriptional repressors bind to the HIV LTR resulting in paused RNAP II. Upon cell stimulation transcriptional activators and enhancers are recruited to HIV LTR, Tat binds to TAR RNA and recruits P-TEFb to activate RNAP II by phosphorylating its CTD. Histone modifying factors remodel and remove methyl groups from Nuc-0 and Nuc-1 making the chromatin more accessible to the transcriptional machinery.
Figure 3
Figure 3
Model for Potential Role of Bcl-6 and Blimp-1 in HIV Transcription. Blimp-1 and Bcl-6 have potential binding sites in the HIV LTR. We hypothesize that Bcl-6 favors the high expression of HIV in TFH cells, while Blimp-1, an antagonist of Bcl-6, contributes to paused RNAP II and thus to the establishment of HIV latency. See text for details.
See this image and copyright information in PMC

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