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Host Proteins Ku and HMGA1 As Participants of HIV-1 Transcription.

Shadrina OA, Knyazhanskaya ES, Korolev SP, Gottikh MB - Acta Naturae (2016 Jan-Mar)

Bottom Line: The latency maintenance is also a problematic question.We also describe the differential influence of the HMGA1 protein on the induced and basal transcription of HIV-1.Finally, we offer possible mechanisms for Ku and HMGA1 proteins in the proviral transcription regulation.

View Article: PubMed Central - PubMed

Affiliation: Faculty of Bioengineering and Bioinformatics, Lomonosov Moscow State University, Leninskie Gory, Moscow, 119991, Russia.

ABSTRACT
Human immunodeficiency virus type 1 is known to use the transcriptional machinery of the host cell for viral gene transcription, and the only viral protein that partakes in this process is Tat, the viral trans-activator of transcription. During acute infection, the binding of Tat to the hairpin at the beginning of the transcribed viral RNA recruits the PTEFb complex, which in turn hyperphosphorylates RNA-polymerase II and stimulates transcription elongation. Along with acute infection, HIV-1 can also lead to latent infection that is characterized by a low level of viral transcription. During the maintenance and reversal of latency, there are no detectable amounts of Tat protein in the cell and the mechanism of transcription activation in the absence of Tat protein remains unclear. The latency maintenance is also a problematic question. It seems evident that cellular proteins with a yet unknown nature or role regulate both transcriptional repression in the latent phase and its activation during transition into the lytic phase. The present review discusses the role of cellular proteins Ku and HMGA1 in the initiation of transcription elongation of the HIV-1 provirus. The review presents data regarding Ku-mediated HIV-1 transcription and its dependence on the promoter structure and the shape of viral DNA. We also describe the differential influence of the HMGA1 protein on the induced and basal transcription of HIV-1. Finally, we offer possible mechanisms for Ku and HMGA1 proteins in the proviral transcription regulation.

No MeSH data available.


Related in: MedlinePlus

Binding sites of transcription factors in HIV-1 5’-LTR. Schematicrepresentation of HIV-1 provirus and the major binding sites of transcriptionfactors. Positions of the 5’-LTR regions are specified: U3 (nucleotides1–455), R (456–552), and U5 (553–634). The transcriptioninitiation site is shown with an arrow and corresponds to the border betweenthe U3 and R regions [13].
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Figure 1: Binding sites of transcription factors in HIV-1 5’-LTR. Schematicrepresentation of HIV-1 provirus and the major binding sites of transcriptionfactors. Positions of the 5’-LTR regions are specified: U3 (nucleotides1–455), R (456–552), and U5 (553–634). The transcriptioninitiation site is shown with an arrow and corresponds to the border betweenthe U3 and R regions [13].

Mentions: Viral DNA integrated into the cellular genome carries long terminal repeats(LTRs) at its ends. Each of them consists of U3, R, and U5 regions(Fig. 1).Transcription starts at the border between the U3and R regions in the 5’-LTR, since the viral promoter recognized by RNApolymerase II (RNAP II) and some other regulatory elements are located in theU3 region. 5’-LTR contains four functional regions partaking in theregulation of the HIV-1 genome transcription: the modulatory region, theenhancer, the promoter, and the leader regions(Fig. 1)[13]. They contain many binding sites for thecellular transcription factors, including the ones that play a crucial role inthe transcriptional regulation: NF-κB, NFAT, Sp1, and AP-1(Fig. 1).These factors are involved in the initiation of transcription[1, 13].


Host Proteins Ku and HMGA1 As Participants of HIV-1 Transcription.

Shadrina OA, Knyazhanskaya ES, Korolev SP, Gottikh MB - Acta Naturae (2016 Jan-Mar)

Binding sites of transcription factors in HIV-1 5’-LTR. Schematicrepresentation of HIV-1 provirus and the major binding sites of transcriptionfactors. Positions of the 5’-LTR regions are specified: U3 (nucleotides1–455), R (456–552), and U5 (553–634). The transcriptioninitiation site is shown with an arrow and corresponds to the border betweenthe U3 and R regions [13].
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4837570&req=5

Figure 1: Binding sites of transcription factors in HIV-1 5’-LTR. Schematicrepresentation of HIV-1 provirus and the major binding sites of transcriptionfactors. Positions of the 5’-LTR regions are specified: U3 (nucleotides1–455), R (456–552), and U5 (553–634). The transcriptioninitiation site is shown with an arrow and corresponds to the border betweenthe U3 and R regions [13].
Mentions: Viral DNA integrated into the cellular genome carries long terminal repeats(LTRs) at its ends. Each of them consists of U3, R, and U5 regions(Fig. 1).Transcription starts at the border between the U3and R regions in the 5’-LTR, since the viral promoter recognized by RNApolymerase II (RNAP II) and some other regulatory elements are located in theU3 region. 5’-LTR contains four functional regions partaking in theregulation of the HIV-1 genome transcription: the modulatory region, theenhancer, the promoter, and the leader regions(Fig. 1)[13]. They contain many binding sites for thecellular transcription factors, including the ones that play a crucial role inthe transcriptional regulation: NF-κB, NFAT, Sp1, and AP-1(Fig. 1).These factors are involved in the initiation of transcription[1, 13].

Bottom Line: The latency maintenance is also a problematic question.We also describe the differential influence of the HMGA1 protein on the induced and basal transcription of HIV-1.Finally, we offer possible mechanisms for Ku and HMGA1 proteins in the proviral transcription regulation.

View Article: PubMed Central - PubMed

Affiliation: Faculty of Bioengineering and Bioinformatics, Lomonosov Moscow State University, Leninskie Gory, Moscow, 119991, Russia.

ABSTRACT
Human immunodeficiency virus type 1 is known to use the transcriptional machinery of the host cell for viral gene transcription, and the only viral protein that partakes in this process is Tat, the viral trans-activator of transcription. During acute infection, the binding of Tat to the hairpin at the beginning of the transcribed viral RNA recruits the PTEFb complex, which in turn hyperphosphorylates RNA-polymerase II and stimulates transcription elongation. Along with acute infection, HIV-1 can also lead to latent infection that is characterized by a low level of viral transcription. During the maintenance and reversal of latency, there are no detectable amounts of Tat protein in the cell and the mechanism of transcription activation in the absence of Tat protein remains unclear. The latency maintenance is also a problematic question. It seems evident that cellular proteins with a yet unknown nature or role regulate both transcriptional repression in the latent phase and its activation during transition into the lytic phase. The present review discusses the role of cellular proteins Ku and HMGA1 in the initiation of transcription elongation of the HIV-1 provirus. The review presents data regarding Ku-mediated HIV-1 transcription and its dependence on the promoter structure and the shape of viral DNA. We also describe the differential influence of the HMGA1 protein on the induced and basal transcription of HIV-1. Finally, we offer possible mechanisms for Ku and HMGA1 proteins in the proviral transcription regulation.

No MeSH data available.


Related in: MedlinePlus