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Chapter 7 : Viral Proteins Determining Biologic Features of HIV

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Viral Proteins Determining Biologic Features of HIV, Page 1 of 2

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Abstract:

Initial molecular studies of the HIV genome defined in general the relative importance of various viral genes for infection and replication. The influence of the viral envelope on cell tropism and cytotoxicity was appreciated. These approaches led to the recognition of several regulatory genes affecting virus production. Subsequent studies have emphasized how these genetic regions in the virus, interacting with intracellular factors, can be responsible for various biologic and serologic properties. The findings on the viral proteins associated with many of these features of both HIV-1 and HIV-2 infection are summarized in this chapter. Several reports initially demonstrated that the envelope region contains the primary genetic sequences responsible for cell tropism (i.e., T-cell-line and macrophage tropism), cytopathology, CD4 protein modulation, and virus neutralization. The HIV genes that encode accessory or regulatory proteins that help in HIV replication are considered in the chapter. Besides defining the role of Env in cell tropism, observations with interviral recombinants have identified, to some extent, the specific regions in the viral envelope that can determine induction of cell death, downmodulation of CD4 expression on cells, and sensitivity of HIV to sCD4 inactivation. The genetic regions influencing these biologic properties are described in this chapter. The genetic regions are cytopathicity, CD4 protein modulation, and soluble CD4 neutralization. New information has been obtained on the function of the accessory genes of HIV-1. The findings have been valuable for understanding the steps involved in HIV infection and providing insights into normal cell function (e.g., Tat and Rev).

Citation: Levy J. 2007. Viral Proteins Determining Biologic Features of HIV, p 149-164. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch07

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Small Interfering RNA
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Memory B Cell
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Simian virus 40
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Figures

Image of Figure 7.1
Figure 7.1

Comparison of the amino acid sequence of the V3 regions of the HIV-1 and HIV-2 strains. The complete V3 sequence of a molecular clone of HIV-1 is shown, and the five amino acid residues that differ in HIV-1 are designated. The positions of amino acid residues are relative to the HIV-1 genome referenced in the Los Alamos AIDS and Human Retroviruses database. Reprinted from reference 4112 with permission.

Citation: Levy J. 2007. Viral Proteins Determining Biologic Features of HIV, p 149-164. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch07
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Image of Figure 7.2
Figure 7.2

Major features of the HIV-1 LTR in viral DNA. The LTR contains -acting sequences that function in either integration or transcription of the provirus, and is divided into three regions (U3, R, and U5), which are generated from the single-stranded viral RNA genome by the reverse transcription process. The convention uses +1 to identify the 5’ ends of viral transcripts, which are capped at initiation of viral RNA synthesis. The 5’ LTR of HIV-1 contains the single promoter for transcription of all viral genes and is divided into four functional regions: the modulatory region (—454 to —104), the enhancer region (—105 to —79), the core or basal promoter (—78 to —1), and the transactivation response element (TAR) (+1 to +60). Deletions in a portion of the U3 region augment initiation of viral transcription; accordingly, this region has been designated the negative regulatory element (NRE) (—340 to —184). This figure identifies the sites for binding of selected cellular transcription factors, labeled in italics, that provide for positive regulation of viral transcription: GATA-2,3 (—441 to —373, —343 to —338), c-MYB (—304 to —299), NF-IL6 (—258 to —238), RBF-1 (—151 to —141), ETS-1 (—160 to —140), RBF-2 (—131 to —121), ETS-2 (—104 to —95), RBF-1 (—104 to —80), (—104 to —95, —91 to —81), SP1 (three sites, —78 to —46), TBP (TATA box at —27 to —23), LBP-1 (—39 to —16), LEF-1 (+17 to +32), USF (+35 to +60), and AP-1 (+92 to +102, +160 to +167). The dotted circle shows the location of a nucleosome (nuc-1), which is remodeled in chromatin during transcriptional activation of the 5’ LTR. Host factors, such as YY1, recruit histone deacetylases to maintain nuc-1 in a hypoacetylated state and thereby inhibit transcription. A hexamer site for addition of poly-(A) tails to viral transcripts is located at +73 to +78; this site, although contained in both LTRs, is functional in the 3’ LTR. The transcription factor binding sites mediate combinatorial DNA:protein and protein: protein interactions and thereby produce a complex regulatory network to regulate HIV transcription in various cell types in response to different extracellular stimuli. This figure is based on a more comprehensive list of transcription factors that interact with the HIV-1 LTR. For references and further discussion, see reference 3469a. Figure provided by P. Luciw.

Citation: Levy J. 2007. Viral Proteins Determining Biologic Features of HIV, p 149-164. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch07
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Download as Powerpoint

References

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Tables

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Table 7.1

Cellular host range of HIV-2 and HIV-1SF mutant viruses

Citation: Levy J. 2007. Viral Proteins Determining Biologic Features of HIV, p 149-164. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch07
Generic image for table
Table 7.2

HIV properties reflecting envelope conformation

Citation: Levy J. 2007. Viral Proteins Determining Biologic Features of HIV, p 149-164. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch07
Generic image for table
Table 7.3

Potential functions of Tat in HIV infection

Citation: Levy J. 2007. Viral Proteins Determining Biologic Features of HIV, p 149-164. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch07
Generic image for table
Table 7.4

Potential functions of Nef in HIV infection

Citation: Levy J. 2007. Viral Proteins Determining Biologic Features of HIV, p 149-164. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch07
Generic image for table
Table 7.5

Potential functions of Vpr in HIV infection

Citation: Levy J. 2007. Viral Proteins Determining Biologic Features of HIV, p 149-164. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch07
Generic image for table
Table 7.6

Potential functions of Vpu in HIV infection

Citation: Levy J. 2007. Viral Proteins Determining Biologic Features of HIV, p 149-164. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch07

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