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Article ; Online: Regulation of HIV-1 transcription in cells of the monocyte-macrophage lineage.

Kilareski, Evelyn M / Shah, Sonia / Nonnemacher, Michael R / Wigdahl, Brian

Retrovirology

2009 Volume 6, Page(s) 118

Abstract: Human immunodeficiency virus type 1 (HIV-1) has been shown to replicate productively in cells of the monocyte-macrophage lineage, although replication occurs to a lesser extent than in infected T cells. As cells of the monocyte-macrophage lineage become ... ...

Abstract	Human immunodeficiency virus type 1 (HIV-1) has been shown to replicate productively in cells of the monocyte-macrophage lineage, although replication occurs to a lesser extent than in infected T cells. As cells of the monocyte-macrophage lineage become differentiated and activated and subsequently travel to a variety of end organs, they become a source of infectious virus and secreted viral proteins and cellular products that likely initiate pathological consequences in a number of organ systems. During this process, alterations in a number of signaling pathways, including the level and functional properties of many cellular transcription factors, alter the course of HIV-1 long terminal repeat (LTR)-directed gene expression. This process ultimately results in events that contribute to the pathogenesis of HIV-1 infection. First, increased transcription leads to the upregulation of infectious virus production, and the increased production of viral proteins (gp120, Tat, Nef, and Vpr), which have additional activities as extracellular proteins. Increased viral production and the presence of toxic proteins lead to enhanced deregulation of cellular functions increasing the production of toxic cellular proteins and metabolites and the resulting organ-specific pathologic consequences such as neuroAIDS. This article reviews the structural and functional features of the cis-acting elements upstream and downstream of the transcriptional start site in the retroviral LTR. It also includes a discussion of the regulation of the retroviral LTR in the monocyte-macrophage lineage during virus infection of the bone marrow, the peripheral blood, the lymphoid tissues, and end organs such as the brain. The impact of genetic variation on LTR-directed transcription during the course of retrovirus disease is also reviewed.
MeSH term(s)	Gene Expression Regulation, Viral ; HIV Infections/metabolism ; HIV Infections/virology ; HIV-1/pathogenicity ; HIV-1/physiology ; Host-Pathogen Interactions ; Humans ; Macrophages/metabolism ; Macrophages/virology ; Monocytes/metabolism ; Monocytes/virology ; Signal Transduction ; Transcription, Genetic ; Virulence ; Virus Replication
Language	English
Publishing date	2009-12-23
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ISSN	1742-4690
ISSN (online)	1742-4690
DOI	10.1186/1742-4690-6-118
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Regulation of HIV-1 transcription in cells of the monocyte-macrophage lineage

Shah Sonia / Kilareski Evelyn M / Nonnemacher Michael R / Wigdahl Brian

Retrovirology, Vol 6, Iss 1, p

2009 Volume 118

Abstract: Abstract Human immunodeficiency virus type 1 (HIV-1) has been shown to replicate productively in cells of the monocyte-macrophage lineage, although replication occurs to a lesser extent than in infected T cells. As cells of the monocyte-macrophage ... ...

Abstract	Abstract Human immunodeficiency virus type 1 (HIV-1) has been shown to replicate productively in cells of the monocyte-macrophage lineage, although replication occurs to a lesser extent than in infected T cells. As cells of the monocyte-macrophage lineage become differentiated and activated and subsequently travel to a variety of end organs, they become a source of infectious virus and secreted viral proteins and cellular products that likely initiate pathological consequences in a number of organ systems. During this process, alterations in a number of signaling pathways, including the level and functional properties of many cellular transcription factors, alter the course of HIV-1 long terminal repeat (LTR)-directed gene expression. This process ultimately results in events that contribute to the pathogenesis of HIV-1 infection. First, increased transcription leads to the upregulation of infectious virus production, and the increased production of viral proteins (gp120, Tat, Nef, and Vpr), which have additional activities as extracellular proteins. Increased viral production and the presence of toxic proteins lead to enhanced deregulation of cellular functions increasing the production of toxic cellular proteins and metabolites and the resulting organ-specific pathologic consequences such as neuroAIDS. This article reviews the structural and functional features of the cis-acting elements upstream and downstream of the transcriptional start site in the retroviral LTR. It also includes a discussion of the regulation of the retroviral LTR in the monocyte-macrophage lineage during virus infection of the bone marrow, the peripheral blood, the lymphoid tissues, and end organs such as the brain. The impact of genetic variation on LTR-directed transcription during the course of retrovirus disease is also reviewed.
Keywords	Medicine (General) ; R5-920 ; Medicine ; R ; DOAJ:Medicine (General) ; DOAJ:Health Sciences ; Immunologic diseases. Allergy ; RC581-607
Subject code	570
Language	English
Publishing date	2009-12-01T00:00:00Z
Publisher	BioMed Central
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: HIV-1 Promoter Single Nucleotide Polymorphisms Are Associated with Clinical Disease Severity.

Nonnemacher, Michael R / Pirrone, Vanessa / Feng, Rui / Moldover, Brian / Passic, Shendra / Aiamkitsumrit, Benjamas / Dampier, Will / Wojno, Adam / Kilareski, Evelyn / Blakey, Brandon / Ku, Tse-Sheun Jade / Shah, Sonia / Sullivan, Neil T / Jacobson, Jeffrey M / Wigdahl, Brian

PloS one

2016 Volume 11, Issue 4, Page(s) e0150835

Abstract: The large majority of human immunodeficiency virus type 1 (HIV-1) markers of disease progression/severity previously identified have been associated with alterations in host genetic and immune responses, with few studies focused on viral genetic markers ... ...

Abstract	The large majority of human immunodeficiency virus type 1 (HIV-1) markers of disease progression/severity previously identified have been associated with alterations in host genetic and immune responses, with few studies focused on viral genetic markers correlate with changes in disease severity. This study presents a cross-sectional/longitudinal study of HIV-1 single nucleotide polymorphisms (SNPs) contained within the viral promoter or long terminal repeat (LTR) in patients within the Drexel Medicine CNS AIDS Research and Eradication Study (CARES) Cohort. HIV-1 LTR SNPs were found to associate with the classical clinical disease parameters CD4+ T-cell count and log viral load. They were found in both defined and undefined transcription factor binding sites of the LTR. A novel SNP identified at position 108 in a known COUP (chicken ovalbumin upstream promoter)/AP1 transcription factor binding site was significantly correlated with binding phenotypes that are potentially the underlying cause of the associated clinical outcome (increase in viral load and decrease in CD4+ T-cell count).
MeSH term(s)	Binding Sites/genetics ; CD4-Positive T-Lymphocytes/metabolism ; CD4-Positive T-Lymphocytes/virology ; Cross-Sectional Studies ; Female ; Genetic Association Studies/methods ; HIV Infections/metabolism ; HIV Infections/pathology ; HIV Infections/virology ; HIV Long Terminal Repeat/genetics ; HIV-1/genetics ; Humans ; Longitudinal Studies ; Male ; Middle Aged ; Polymorphism, Single Nucleotide/genetics ; Promoter Regions, Genetic/genetics ; Severity of Illness Index ; Transcription Factors/genetics ; Viral Load/genetics
Chemical Substances	Transcription Factors
Language	English
Publishing date	2016-04-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0150835
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Article ; Online: HIV-1 Promoter Single Nucleotide Polymorphisms Are Associated with Clinical Disease Severity.

Michael R Nonnemacher / Vanessa Pirrone / Rui Feng / Brian Moldover / Shendra Passic / Benjamas Aiamkitsumrit / Will Dampier / Adam Wojno / Evelyn Kilareski / Brandon Blakey / Tse-Sheun Jade Ku / Sonia Shah / Neil T Sullivan / Jeffrey M Jacobson / Brian Wigdahl

PLoS ONE, Vol 11, Iss 4, p e

2016 Volume 0150835

Abstract	The large majority of human immunodeficiency virus type 1 (HIV-1) markers of disease progression/severity previously identified have been associated with alterations in host genetic and immune responses, with few studies focused on viral genetic markers correlate with changes in disease severity. This study presents a cross-sectional/longitudinal study of HIV-1 single nucleotide polymorphisms (SNPs) contained within the viral promoter or long terminal repeat (LTR) in patients within the Drexel Medicine CNS AIDS Research and Eradication Study (CARES) Cohort. HIV-1 LTR SNPs were found to associate with the classical clinical disease parameters CD4+ T-cell count and log viral load. They were found in both defined and undefined transcription factor binding sites of the LTR. A novel SNP identified at position 108 in a known COUP (chicken ovalbumin upstream promoter)/AP1 transcription factor binding site was significantly correlated with binding phenotypes that are potentially the underlying cause of the associated clinical outcome (increase in viral load and decrease in CD4+ T-cell count).
Keywords	Medicine ; R ; Science ; Q
Language	English
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Defining differential genetic signatures in CXCR4- and the CCR5-utilizing HIV-1 co-linear sequences.

PloS one

2014 Volume 9, Issue 9, Page(s) e107389

Abstract: The adaptation of human immunodeficiency virus type-1 (HIV-1) to an array of physiologic niches is advantaged by the plasticity of the viral genome, encoded proteins, and promoter. CXCR4-utilizing (X4) viruses preferentially, but not universally, infect ... ...

Abstract	The adaptation of human immunodeficiency virus type-1 (HIV-1) to an array of physiologic niches is advantaged by the plasticity of the viral genome, encoded proteins, and promoter. CXCR4-utilizing (X4) viruses preferentially, but not universally, infect CD4+ T cells, generating high levels of virus within activated HIV-1-infected T cells that can be detected in regional lymph nodes and peripheral blood. By comparison, the CCR5-utilizing (R5) viruses have a greater preference for cells of the monocyte-macrophage lineage; however, while R5 viruses also display a propensity to enter and replicate in T cells, they infect a smaller percentage of CD4+ T cells in comparison to X4 viruses. Additionally, R5 viruses have been associated with viral transmission and CNS disease and are also more prevalent during HIV-1 disease. Specific adaptive changes associated with X4 and R5 viruses were identified in co-linear viral sequences beyond the Env-V3. The in silico position-specific scoring matrix (PSSM) algorithm was used to define distinct groups of X4 and R5 sequences based solely on sequences in Env-V3. Bioinformatic tools were used to identify genetic signatures involving specific protein domains or long terminal repeat (LTR) transcription factor sites within co-linear viral protein R (Vpr), trans-activator of transcription (Tat), or LTR sequences that were preferentially associated with X4 or R5 Env-V3 sequences. A number of differential amino acid and nucleotide changes were identified across the co-linear Vpr, Tat, and LTR sequences, suggesting the presence of specific genetic signatures that preferentially associate with X4 or R5 viruses. Investigation of the genetic relatedness between X4 and R5 viruses utilizing phylogenetic analyses of complete sequences could not be used to definitively and uniquely identify groups of R5 or X4 sequences; in contrast, differences in the genetic diversities between X4 and R5 were readily identified within these co-linear sequences in HIV-1-infected patients.
MeSH term(s)	Algorithms ; Cell Line ; Genes, Viral ; HIV-1/genetics ; HIV-1/metabolism ; Humans ; Receptors, CCR5/metabolism ; Receptors, CXCR4/metabolism
Chemical Substances	CCR5 protein, human ; CXCR4 protein, human ; Receptors, CCR5 ; Receptors, CXCR4
Language	English
Publishing date	2014-09-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0107389
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Article ; Online: Defining differential genetic signatures in CXCR4- and the CCR5-utilizing HIV-1 co-linear sequences.

PLoS ONE, Vol 9, Iss 9, p e

2014 Volume 107389

Abstract	The adaptation of human immunodeficiency virus type-1 (HIV-1) to an array of physiologic niches is advantaged by the plasticity of the viral genome, encoded proteins, and promoter. CXCR4-utilizing (X4) viruses preferentially, but not universally, infect CD4+ T cells, generating high levels of virus within activated HIV-1-infected T cells that can be detected in regional lymph nodes and peripheral blood. By comparison, the CCR5-utilizing (R5) viruses have a greater preference for cells of the monocyte-macrophage lineage; however, while R5 viruses also display a propensity to enter and replicate in T cells, they infect a smaller percentage of CD4+ T cells in comparison to X4 viruses. Additionally, R5 viruses have been associated with viral transmission and CNS disease and are also more prevalent during HIV-1 disease. Specific adaptive changes associated with X4 and R5 viruses were identified in co-linear viral sequences beyond the Env-V3. The in silico position-specific scoring matrix (PSSM) algorithm was used to define distinct groups of X4 and R5 sequences based solely on sequences in Env-V3. Bioinformatic tools were used to identify genetic signatures involving specific protein domains or long terminal repeat (LTR) transcription factor sites within co-linear viral protein R (Vpr), trans-activator of transcription (Tat), or LTR sequences that were preferentially associated with X4 or R5 Env-V3 sequences. A number of differential amino acid and nucleotide changes were identified across the co-linear Vpr, Tat, and LTR sequences, suggesting the presence of specific genetic signatures that preferentially associate with X4 or R5 viruses. Investigation of the genetic relatedness between X4 and R5 viruses utilizing phylogenetic analyses of complete sequences could not be used to definitively and uniquely identify groups of R5 or X4 sequences; in contrast, differences in the genetic diversities between X4 and R5 were readily identified within these co-linear sequences in HIV-1-infected patients.
Keywords	Medicine ; R ; Science ; Q
Subject code	572
Language	English
Publishing date	2014-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Development of co-selected single nucleotide polymorphisms in the viral promoter precedes the onset of human immunodeficiency virus type 1-associated neurocognitive impairment.

Journal of neurovirology

2011 Volume 17, Issue 1, Page(s) 92–109

Abstract: The long terminal repeat (LTR) regulates gene expression of HIV-1 by interacting with multiple host and viral factors. Cross-sectional studies in the pre-HAART era demonstrated that single nucleotide polymorphisms (SNPs) in peripheral blood-derived LTRs ( ...

Abstract	The long terminal repeat (LTR) regulates gene expression of HIV-1 by interacting with multiple host and viral factors. Cross-sectional studies in the pre-HAART era demonstrated that single nucleotide polymorphisms (SNPs) in peripheral blood-derived LTRs (a C-to-T change at position 3 of C/EBP site I (3T) and at position 5 of Sp site III (5T)) increased in frequency as disease severity increased. Additionally, the 3T variant correlated with HIV-1-associated dementia. LTR sequences derived by longitudinal sampling of peripheral blood from a single patient in the DrexelMed HIV/AIDS Genetic Analysis Cohort resulted in the detection of the 3T and 5T co-selected SNPs before the onset of neurologic impairment, demonstrating that these SNPs may be useful in predicting HIV-associated neurological complications. The relative fitness of the LTRs containing the 3T and/or 5T co-selected SNPs as they evolve in their native patient-derived LTR backbone structure demonstrated a spectrum of basal and Tat-mediated transcriptional activities using the IIIB-derived Tat and colinear Tat derived from the same molecular clone containing the 3T/5T LTR SNP. In silico predictions utilizing colinear envelope sequence suggested that the patient's virus evolved from an X4 to an R5 swarm prior to the development of neurological complications and more advanced HIV disease. These results suggest that the HIV-1 genomic swarm may evolve during the course of disease in response to selective pressures that lead to changes in prevalence of specific polymorphisms in the LTR, env, and/or tat that could predict the onset of neurological disease and result in alterations in viral function.
MeSH term(s)	AIDS Dementia Complex/virology ; Adult ; Amino Acid Sequence ; Base Sequence ; Cell Line ; Gene Expression Regulation, Viral ; Genotype ; HIV Infections/virology ; HIV Long Terminal Repeat ; HIV-1/genetics ; HIV-1/pathogenicity ; HIV-1/physiology ; Humans ; Longitudinal Studies ; Middle Aged ; Molecular Sequence Data ; Polymorphism, Single Nucleotide ; Promoter Regions, Genetic ; Transcriptional Activation ; Virus Replication ; env Gene Products, Human Immunodeficiency Virus/genetics ; env Gene Products, Human Immunodeficiency Virus/metabolism ; tat Gene Products, Human Immunodeficiency Virus/genetics ; tat Gene Products, Human Immunodeficiency Virus/metabolism
Chemical Substances	env Gene Products, Human Immunodeficiency Virus ; tat Gene Products, Human Immunodeficiency Virus
Language	English
Publishing date	2011-01-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1283265-0
ISSN	1538-2443 ; 1355-0284
ISSN (online)	1538-2443
ISSN	1355-0284
DOI	10.1007/s13365-010-0014-1
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Article: PMA-induced differentiation of a bone marrow progenitor cell line activates HIV-1 LTR-driven transcription.

Alexaki, Aikaterini / Quiterio, Shane J / Liu, Yujie / Irish, Bryan / Kilareski, Evelyn / Nonnemacher, Michael R / Wigdahl, Brian

DNA and cell biology

2007 Volume 26, Issue 6, Page(s) 387–394

Abstract: ... of differentiation and activation markers. Herein we demonstrate that HIV-1 long terminal repeats (LTRs) from T-, M ...

Abstract	Cells of the monocyte-macrophage lineage play an important role in human immunodeficiency virus type 1 (HIV-1)-associated disease. Infected myeloid precursor cells of the bone marrow are thought to be a viral reservoir that may repopulate the peripheral blood, central nervous system (CNS), and other organ systems throughout the course of disease. To model select aspects of HIV-1 infection of the bone marrow compartment in vitro, the erythro-myeloid precursor cell line, TF-1, was used. Phorbol 12-myristate 13-acetate (PMA) was found to induce the TF-1 cell line to differentiate through the myeloid lineage and become activated, as demonstrated by cellular morphologic changes and surface expression of differentiation and activation markers. Herein we demonstrate that HIV-1 long terminal repeats (LTRs) from T-, M-, and dual-tropic molecular clones have similar basal LTR activity in TF-1 cells and that differentiation of these cells by PMA resulted in increased LTR activity. Examination of specific cis-acting elements involved in basal and PMA-induced LTR activity demonstrated that the transcription factor families nuclear factor-kappa B (NF-kappaB) and specificity protein (Sp) contributed to the LTR activity of TF-1 cells, the Sp family being the most critical. These studies elucidate the impact of infected bone marrow monocytic cell differentiation on LTR activity and its potential impact on HIV-1-associated disease.
MeSH term(s)	Antigens, CD/metabolism ; Base Sequence ; CCAAT-Enhancer-Binding Proteins/metabolism ; Cell Differentiation/drug effects ; Cell Line ; DNA, Viral/genetics ; HIV Long Terminal Repeat ; HIV-1/genetics ; Humans ; In Vitro Techniques ; Mutagenesis, Site-Directed ; Myeloid Progenitor Cells/cytology ; Myeloid Progenitor Cells/drug effects ; Myeloid Progenitor Cells/metabolism ; Myeloid Progenitor Cells/virology ; NF-kappa B/metabolism ; Sp Transcription Factors/metabolism ; Tetradecanoylphorbol Acetate/pharmacology ; Transcription, Genetic/drug effects
Chemical Substances	Antigens, CD ; CCAAT-Enhancer-Binding Proteins ; DNA, Viral ; NF-kappa B ; Sp Transcription Factors ; Tetradecanoylphorbol Acetate (NI40JAQ945)
Language	English
Publishing date	2007-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1024454-2
ISSN	1557-7430 ; 1044-5498 ; 0198-0238
ISSN (online)	1557-7430
ISSN	1044-5498 ; 0198-0238
DOI	10.1089/dna.2006.0542
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