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Article ; Online: Evolving paradigms in the pathogenesis of HIV-1-associated dementia.

Fischer-Smith, Tracy / Rappaport, Jay

Expert reviews in molecular medicine

2005 Volume 7, Issue 27, Page(s) 1–26

Abstract: HIV-1-associated dementia (HIV-D) remains a significant consequence of HIV-1 infection and AIDS. Since the clinical introduction of highly active antiretroviral therapy (HAART), the incidence of HIV-D has decreased, yet the prevalence has increased as ... ...

Abstract	HIV-1-associated dementia (HIV-D) remains a significant consequence of HIV-1 infection and AIDS. Since the clinical introduction of highly active antiretroviral therapy (HAART), the incidence of HIV-D has decreased, yet the prevalence has increased as patients are living longer under treatment. Additionally, a less severe form of HIV-D, minor cognitive motor disorder, has become an increasing issue. Two different models have been proposed for virus entry in the central nervous system (CNS) in HIV-D. In the 'Trojan horse' model, the virus enters the CNS early carried by macrophages and infects resident glia; later in the course of infection, virus replication is activated and additional monocyte/macrophages are recruited into the CNS via cytokine/chemokine networks and endothelial-cell-leukocyte interactions at the blood-brain barrier. In the 'late invasion' model, an inherently invasive activated monocyte subset is expanded from bone marrow as a result of immune dysregulation in the periphery in the setting of AIDS. In this review we discuss these two separate, although not mutually exclusive, means for virus entry and persistence in the CNS. Additionally, we explore mechanisms for neuronal injury and apoptosis, including the role of virus, viral and host proteins, oxidative stress and products of infected or uninfected activated microglia and astrocytes. Potential therapeutic strategies are also briefly discussed.
MeSH term(s)	AIDS Dementia Complex/metabolism ; AIDS Dementia Complex/pathology ; AIDS Dementia Complex/virology ; Central Nervous System/metabolism ; Central Nervous System/pathology ; Central Nervous System/virology ; HIV Infections/metabolism ; HIV Infections/pathology ; HIV Infections/virology ; HIV-1/pathogenicity ; Humans
Language	English
Publishing date	2005-12-02
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ISSN	1462-3994
ISSN (online)	1462-3994
DOI	10.1017/S1462399405010239
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Article: CD163/CD16 coexpression by circulating monocytes/macrophages in HIV: potential biomarkers for HIV infection and AIDS progression.

Fischer-Smith, Tracy / Tedaldi, Ellen M / Rappaport, Jay

AIDS research and human retroviruses

2008 Volume 24, Issue 3, Page(s) 417–421

Abstract: Monocytes and macrophages play a prominent role in the establishment of HIV-1 infection, virus dissemination, and development of viral reservoirs. Like T cells, macrophages display immune polarization that can promote or impair adaptive immunity. We ... ...

Abstract	Monocytes and macrophages play a prominent role in the establishment of HIV-1 infection, virus dissemination, and development of viral reservoirs. Like T cells, macrophages display immune polarization that can promote or impair adaptive immunity. We hypothesize that dysregulation of monocyte/macrophage activation and differentiation may promote immune dysfunction and contribute to AIDS pathogenesis. Using flow cytometry, we analyzed the frequency of monocyte subsets in human immunodeficiency virus type 1 (HIV-1) infection relative to seronegative controls, focusing on the CD163(+)/CD16(+) monocyte as a likely precursor of the "alternatively activated" macrophage. Individuals with detectable HIV-1 infection showed an increase in the frequency of CD163(+)/CD16(+) monocytes (CD14(+)) when compared to seronegative or HIV-1-infected persons with undetectable viral loads. A positive correlation between increased CD163(+)/CD16(+) monocyte frequency and viral load was revealed that was not seen between viral load and the number of CD4(+) T cells or frequency of CD16(+) monocytes (without CD163 subtyping). We also found a strong inverse correlations between CD16(+) monocytes (r = -0.71, r(2) = 0.5041, p = 0.0097) or CD163(+)/CD16(+) monocytes (r = -0.86, r(2) = 0.7396, p = 0.0003) and number of CD4(+) T cells below 450 cells/microl. An inverse relationship between CD163(+)/CD16(+) and CD163(+)/CD16() monocytes suggests the expanded CD163(+)/CD16(+) population is derived exclusively from within the "alternatively activated" (MPhi-2) subset. These data suggest a potential role for CD163(+)/CD16(+) monocytes in virus production and disease progression. CD163(+)/CD16(+) monocytes may be a useful biomarker for HIV-1 infection and AIDS progression and a possible target for therapeutic intervention.
MeSH term(s)	Antigens, CD/analysis ; Antigens, Differentiation, Myelomonocytic/analysis ; Biomarkers ; CD4 Lymphocyte Count ; Disease Progression ; Flow Cytometry ; HIV Infections/diagnosis ; HIV Infections/immunology ; Humans ; Lipopolysaccharide Receptors/analysis ; Macrophages/chemistry ; Monocytes/chemistry ; Receptors, Cell Surface/analysis ; Receptors, IgG/analysis ; Viral Load
Chemical Substances	Antigens, CD ; Antigens, Differentiation, Myelomonocytic ; Biomarkers ; CD163 antigen ; Lipopolysaccharide Receptors ; Receptors, Cell Surface ; Receptors, IgG
Language	English
Publishing date	2008-03-31
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	639130-8
ISSN	1931-8405 ; 0889-2229
ISSN (online)	1931-8405
ISSN	0889-2229
DOI	10.1089/aid.2007.0193
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Article ; Online: CSF-1R up-regulation is associated with response to pharmacotherapy targeting tyrosine kinase activity in AML cell lines.

Kogan, Michael / Fischer-Smith, Tracy / Kaminsky, Rafal / Lehmicke, Gabrielle / Rappaport, Jay

Anticancer research

2012 Volume 32, Issue 3, Page(s) 893–899

Abstract: Background: The oncogenic potential of colony stimulating factor 1 receptor (CSF-1R) has been well described, while its relevance for human acute myelogenous leukemia (AML) is still undetermined. In a recent clinical trial for AML, sunitinib was found ... ...

Abstract	Background: The oncogenic potential of colony stimulating factor 1 receptor (CSF-1R) has been well described, while its relevance for human acute myelogenous leukemia (AML) is still undetermined. In a recent clinical trial for AML, sunitinib was found to hold potential therapeutic benefit, however, the mechanism for this remains unknown. Materials and methods: In this study, we treated three myeloid cell lines, Mono-Mac 1, THP-1, and U937, with sunitinib, and a small-molecule CSF-1R inhibitor (cFMS-I) to test the anticancer effect of such treatment. Results: Mono-Mac 1 cells had inhibited proliferation and extracellular-signal regulated kinase activity as a result of CSF-1R inhibition and a dose-dependent increase in CSF-1R expression with both sunitinib and cFMS-I. Conclusion: Our results suggest potential for CSF-1R as an important target of sunitinib or other similar drugs. Future study of CSF-1R may produce more targeted therapeutic approaches and aid in the development of personalized medicine for AML.
MeSH term(s)	Antineoplastic Agents/therapeutic use ; Cell Line, Tumor ; Humans ; Leukemia, Myeloid, Acute/drug therapy ; Leukemia, Myeloid, Acute/enzymology ; Leukemia, Myeloid, Acute/metabolism ; Leukemia, Myeloid, Acute/pathology ; Protein-Tyrosine Kinases/antagonists & inhibitors ; Receptor, Macrophage Colony-Stimulating Factor/metabolism ; Signal Transduction ; Up-Regulation
Chemical Substances	Antineoplastic Agents ; Protein-Tyrosine Kinases (EC 2.7.10.1) ; Receptor, Macrophage Colony-Stimulating Factor (EC 2.7.10.1)
Language	English
Publishing date	2012-03-07
Publishing country	Greece
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	604549-2
ISSN	1791-7530 ; 0250-7005
ISSN (online)	1791-7530
ISSN	0250-7005
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Article ; Online: Macrophage colony-stimulating factor in the pathogenesis of HIV infection: potential target for therapeutic intervention.

Haine, Valerie / Fischer-Smith, Tracy / Rappaport, Jay

Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology

2006 Volume 1, Issue 1, Page(s) 32–40

Abstract: Macrophage colony stimulating factor (M-CSF) appears to play a major role in promoting and maintaining reservoirs of human immunodeficiency virus type 1 (HIV-1) in infected individuals. HIV-1 infection induces production of M-CSF by macrophages, which in ...

Abstract	Macrophage colony stimulating factor (M-CSF) appears to play a major role in promoting and maintaining reservoirs of human immunodeficiency virus type 1 (HIV-1) in infected individuals. HIV-1 infection induces production of M-CSF by macrophages, which in turn promotes further infection of macrophages via increases in CD4 and CCR5 receptors, as well as increases in virus gene expression. M-CSF promotes the ontogeny and survival of macrophages, contributing to both the number and longevity of these infected cells. M-CSF dysregulation promotes the differentiation of monocytes toward macrophages and osteoclasts and at the same time may inhibit differentiation toward dendritic cells, resulting in immune impairment. The potential role of M-CSF in HIV-associated end organ diseases including HIV-associated dementia, HIV-associated nephropathy, and osteoporosis is discussed. This review emphasizes the need for developing M-CSF antagonists for treatment of HIV-1-infected patients.
MeSH term(s)	Animals ; Cell Differentiation/immunology ; HIV Infections/immunology ; HIV Infections/metabolism ; HIV-1/immunology ; Humans ; Macrophage Colony-Stimulating Factor/immunology ; Macrophage Colony-Stimulating Factor/metabolism ; Macrophage Colony-Stimulating Factor/therapeutic use ; Macrophages/cytology ; Macrophages/metabolism ; Macrophages/virology
Chemical Substances	Macrophage Colony-Stimulating Factor (81627-83-0)
Language	English
Publishing date	2006-04-13
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2227405-4
ISSN	1557-1904 ; 1557-1890
ISSN (online)	1557-1904
ISSN	1557-1890
DOI	10.1007/s11481-005-9003-1
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Article ; Online: Macrophage colony stimulating factor regulation by nuclear factor kappa B: a relevant pathway in human immunodeficiency virus type 1 infected macrophages.

Kogan, Michael / Haine, Valerie / Ke, Yuxong / Wigdahl, Brian / Fischer-Smith, Tracy / Rappaport, Jay

DNA and cell biology

2011 Volume 31, Issue 3, Page(s) 280–289

Abstract: Macrophage colony stimulating factor (M-CSF) is a cytokine that promotes monocyte differentiation and survival. When overexpressed, M-CSF contributes to pathology in a wide variety of diseases, including osteoporosis, obesity, certain human cancers, and ... ...

Abstract	Macrophage colony stimulating factor (M-CSF) is a cytokine that promotes monocyte differentiation and survival. When overexpressed, M-CSF contributes to pathology in a wide variety of diseases, including osteoporosis, obesity, certain human cancers, and in human immunodeficiency virus type 1 (HIV-1) infection, particularly with respect to monocyte/macrophage infection and the development of HIV-1 associated central nervous system disorders. In this study, our aim was to expand the current knowledge of M-CSF regulation, focusing on nuclear factor kappa B (NF-κB), a transcription factor playing a prominent role during inflammation and HIV-1 infection. Our results suggest that tumor necrosis factor alpha (TNF-α) promotes M-CSF secretion in primary macrophages and activates the -1310/+48 bp M-CSF promoter in Mono-Mac 1 cells. Inhibitors of the NF-κB pathway diminish this response. We identified four putative NF-κB and four CCAAT-enhancer-binding protein beta binding sites within the M-CSF promoter. Our findings, using promoter constructs mutated at individual NF-κB sites within the M-CSF promoter region, suggest that these sites are redundant with respect to NF-κB regulation. TNF-α treatment promoted NF-κB p65 binding to the M-CSF promoter in phorbol 12-myristate 13-acetate (PMA) treated U937 cells chronically infected with HIV-1 (U1 cells), but not in PMA treated uninfected U937 cells, suggesting that the presence of HIV-1 increases the NF-κB response. In conclusion, our findings demonstrate that NF-κB induces M-CSF expression on a promoter level via multiple functional NF-κB binding sites and that this pathway is likely relevant in HIV-1 infection of macrophages.
MeSH term(s)	Cells, Cultured ; Gene Expression Regulation ; HIV-1 ; Humans ; Macrophage Colony-Stimulating Factor/genetics ; Macrophages/metabolism ; Macrophages/virology ; NF-kappa B/metabolism ; Promoter Regions, Genetic
Chemical Substances	NF-kappa B ; Macrophage Colony-Stimulating Factor (81627-83-0)
Language	English
Publishing date	2011-09-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1024454-2
ISSN	1557-7430 ; 0198-0238 ; 1044-5498
ISSN (online)	1557-7430
ISSN	0198-0238 ; 1044-5498
DOI	10.1089/dna.2011.1357
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Article ; Online: Monocyte/macrophage trafficking in acquired immunodeficiency syndrome encephalitis: lessons from human and nonhuman primate studies.

Fischer-Smith, Tracy / Bell, Christie / Croul, Sidney / Lewis, Mark / Rappaport, Jay

Journal of neurovirology

2008 Volume 14, Issue 4, Page(s) 318–326

Abstract: Here the authors discuss evidence in human and animal models supporting two opposing views regarding the pathogenesis of human immunodeficiency virus (HIV) in the central nervous system (CNS): (1) HIV infection in the CNS is a compartmentalized infection, ...

Abstract	Here the authors discuss evidence in human and animal models supporting two opposing views regarding the pathogenesis of human immunodeficiency virus (HIV) in the central nervous system (CNS): (1) HIV infection in the CNS is a compartmentalized infection, with the virus-infected macrophages entering the CNS early, infecting resident microglia and astrocytes, and achieving a state of latency with evolution toward a fulminant CNS infection late in the course of disease; or alternatively, (2) events in the periphery lead to altered monocyte/macrophage (MPhi) homeostasis, with increased CNS invasion of infected and/or uninfected MPhis. Here the authors have reevaluated evidence presented in the favor of the latter model, with a discussion of phenotypic characteristics distinguishing normal resident microglia with those accumulating in HIV encephalitis (HIVE). CD163 is normally expressed by perivascular MPhi s but not resident microglia in normal CNS of humans and rhesus macaques. In agreement with other studies, the authors demonstrate expression of CD163 by brain MPhi s in HIVE and simian immunodeficiency virus encephalitis (SIVE). CNS tissues from HIV-sero positive individuals with HIVE or HIV-associated progressive multifocal leukoencephalopathy (PML) were also examined. In HIVE, the authors further demonstrate colocalization of CD163 and CD16 (Fcgamma III recptor) gene expression, the latter marker associated with HIV infection of monocyte in vivo and permissivity of infection. Indeed, CD163(+) MPhis and microglia are often productively infected in HIVE CNS. In SIV infected rhesus macaques, CD163(+) cells accumulate perivascularly, within nodular lesions and the parenchyma in animals with encephalitis. Likewise, parenchymal microglia and perivascular MPhi s are CD163(+) in HIVE. In contrast to HIVE, CD163(+)perivascular and parenchymal MPhi s in HIV-associated PML were only associated with areas of demyelinating lesions. Interestingly, SIV-infected rhesus macaques whose viral burden was predominantly at 1 x 10(6) copies/ml or greater developed encephalitis. To further investigate the relationship between CD163(+)/CD16(+) MPhis/microglia in the CNS and altered homeostasis in the periphery, the authors performed flow-cytometric analyses of peripheral blood mononuclear cells (PBMCs) from SIV-infected rhesus macaques. The results demonstrate an increase in the percent frequency of CD163(+)/CD16(+) monocytes in animals with detectable virus that correlated significantly with increased viral burden and CD4(+) T-cell decline. These results suggest the importance of this monocyte subset in HIV/SIV CNS disease, and also in the immune pathogenesis of lentiviral infection. The authors further discuss the potential role of CD163(+)/CD16(+) monocyte/MPhi subset expansion, altered myeloid homeostasis, and potential consequences for immune polarization and suppression. The results and discussion here suggest new avenues for the development of acquired immunodeficiency syndrome (AIDS) therapeutics and vaccine design.
MeSH term(s)	Acquired Immunodeficiency Syndrome/complications ; Acquired Immunodeficiency Syndrome/physiopathology ; Animals ; Central Nervous System/physiopathology ; Central Nervous System/virology ; Encephalitis, Viral/etiology ; Encephalitis, Viral/physiopathology ; HIV/physiology ; Humans ; Macaca mulatta ; Macrophages/metabolism ; Macrophages/virology ; Monocytes/metabolism ; Monocytes/pathology ; Simian Acquired Immunodeficiency Syndrome/complications ; Simian Acquired Immunodeficiency Syndrome/physiopathology ; Simian Acquired Immunodeficiency Syndrome/virology ; Simian Immunodeficiency Virus/physiology
Language	English
Publishing date	2008-09-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1283265-0
ISSN	1538-2443 ; 1355-0284
ISSN (online)	1538-2443
ISSN	1355-0284
DOI	10.1080/13550280802132857
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Article ; Online: Neuronal ferritin heavy chain and drug abuse affect HIV-associated cognitive dysfunction.

Pitcher, Jonathan / Abt, Anna / Myers, Jaclyn / Han, Rachel / Snyder, Melissa / Graziano, Alessandro / Festa, Lindsay / Kutzler, Michele / Garcia, Fernando / Gao, Wen-Jun / Fischer-Smith, Tracy / Rappaport, Jay / Meucci, Olimpia

The Journal of clinical investigation

2014 Volume 124, Issue 2, Page(s) 656–669

Abstract: Interaction of the chemokine CXCL12 with its receptor CXCR4 promotes neuronal function and survival during embryonic development and throughout adulthood. Previous studies indicated that μ-opioid agonists specifically elevate neuronal levels of the ... ...

Abstract	Interaction of the chemokine CXCL12 with its receptor CXCR4 promotes neuronal function and survival during embryonic development and throughout adulthood. Previous studies indicated that μ-opioid agonists specifically elevate neuronal levels of the protein ferritin heavy chain (FHC), which negatively regulates CXCR4 signaling and affects the neuroprotective function of the CXCL12/CXCR4 axis. Here, we determined that CXCL12/CXCR4 activity increased dendritic spine density, and also examined FHC expression and CXCR4 status in opiate abusers and patients with HIV-associated neurocognitive disorders (HAND), which is typically exacerbated by illicit drug use. Drug abusers and HIV patients with HAND had increased levels of FHC, which correlated with reduced CXCR4 activation, within cortical neurons. We confirmed these findings in a nonhuman primate model of SIV infection with morphine administration. Transfection of a CXCR4-expressing human cell line with an iron-deficient FHC mutant confirmed that increased FHC expression deregulated CXCR4 signaling and that this function of FHC was independent of iron binding. Furthermore, examination of morphine-treated rodents and isolated neurons expressing FHC shRNA revealed that FHC contributed to morphine-induced dendritic spine loss. Together, these data implicate FHC-dependent deregulation of CXCL12/CXCR4 as a contributing factor to cognitive dysfunction in neuroAIDS.
MeSH term(s)	AIDS Dementia Complex/complications ; AIDS Dementia Complex/physiopathology ; Adult ; Aged ; Animals ; Apoferritins/chemistry ; Brain/drug effects ; Cell Line ; Chemokine CXCL12/metabolism ; Dendritic Spines/drug effects ; Female ; Humans ; Iron/chemistry ; Macaca ; Male ; Middle Aged ; Morphine/chemistry ; Neurons/drug effects ; Neurons/metabolism ; Patch-Clamp Techniques ; Phosphorylation ; RNA, Small Interfering/metabolism ; Rats ; Receptors, CXCR4/metabolism ; Substance-Related Disorders/complications ; Substance-Related Disorders/physiopathology
Chemical Substances	CXCL12 protein, human ; CXCR4 protein, human ; Chemokine CXCL12 ; RNA, Small Interfering ; Receptors, CXCR4 ; Morphine (76I7G6D29C) ; Apoferritins (9013-31-4) ; Iron (E1UOL152H7)
Language	English
Publishing date	2014-01-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI70090
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Article: Macrophage/microglial accumulation and proliferating cell nuclear antigen expression in the central nervous system in human immunodeficiency virus encephalopathy.

Fischer-Smith, Tracy / Croul, Sidney / Adeniyi, Aderonke / Rybicka, Katarzyna / Morgello, Susan / Khalili, Kamel / Rappaport, Jay

The American journal of pathology

2004 Volume 164, Issue 6, Page(s) 2089–2099

Abstract: This study was performed to quantitate and characterize the mononuclear phagocytes (MPs) in human immunodeficiency virus encephalopathy (HIVE) by immunohistochemistry in an effort to gain insights into potential mechanisms of central nervous system (CNS) ...

Abstract	This study was performed to quantitate and characterize the mononuclear phagocytes (MPs) in human immunodeficiency virus encephalopathy (HIVE) by immunohistochemistry in an effort to gain insights into potential mechanisms of central nervous system (CNS) accumulation. Single- and double-labeled studies using antibodies against CD14, CD16, CD68, proliferating cell nuclear antigen (PCNA), Ki-67, von Willebrand factor, and HIV-1 p24 were performed using brain tissue from patients with HIVE, HIV-1 infection without encephalitis, and seronegative controls. A substantial increase in MPs was observed in CNS tissue from patients with HIVE, relative to seronegative controls and patients with acquired immune deficiency syndrome but without encephalitis, as determined by CD68 and CD16 immunohistochemistry. A large proportion of CD16+ MPs in HIVE CNS tissue were PCNA+, but do not appear to be proliferating, based on limited Ki-67 positivity. Although virtually all cells positive for HIV-1 p24 were PCNA+, there were many PCNA+ cells where HIV-1 p24 expression was not detected. PCNA positivity was also observed in some endothelial cells and ependymal cells in HIVE CNS. Our results would support a role for HIV-1-induced alterations in MP trafficking and homeostasis in the pathogenesis of HIVE.
MeSH term(s)	AIDS Dementia Complex/genetics ; AIDS Dementia Complex/pathology ; Antigens, CD/analysis ; Brain/pathology ; Brain/virology ; Central Nervous System/pathology ; Central Nervous System/virology ; Gene Expression Regulation ; HIV Core Protein p24/analysis ; HIV-1 ; Humans ; Immunohistochemistry ; Macrophages/pathology ; Macrophages/virology ; Microglia/pathology ; Microglia/virology ; Proliferating Cell Nuclear Antigen/analysis ; Receptors, IgG/analysis
Chemical Substances	Antigens, CD ; HIV Core Protein p24 ; Proliferating Cell Nuclear Antigen ; Receptors, IgG
Language	English
Publishing date	2004-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	2943-9
ISSN	1525-2191 ; 0002-9440
ISSN (online)	1525-2191
ISSN	0002-9440
DOI	10.1016/S0002-9440(10)63767-4
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Article ; Online: A globally synthesised and flagged bee occurrence dataset and cleaning workflow.

Dorey, James B / Fischer, Erica E / Chesshire, Paige R / Nava-Bolaños, Angela / O'Reilly, Robert L / Bossert, Silas / Collins, Shannon M / Lichtenberg, Elinor M / Tucker, Erika M / Smith-Pardo, Allan / Falcon-Brindis, Armando / Guevara, Diego A / Ribeiro, Bruno / de Pedro, Diego / Pickering, John / Hung, Keng-Lou James / Parys, Katherine A / McCabe, Lindsie M / Rogan, Matthew S /

Minckley, Robert L / Velazco, Santiago J E / Griswold, Terry / Zarrillo, Tracy A / Jetz, Walter / Sica, Yanina V / Orr, Michael C / Guzman, Laura Melissa / Ascher, John S / Hughes, Alice C / Cobb, Neil S

Scientific data

2023 Volume 10, Issue 1, Page(s) 747

Abstract: Species occurrence data are foundational for research, conservation, and science communication, but the limited availability and accessibility of reliable data represents a major obstacle, particularly for insects, which face mounting pressures. We ... ...

Abstract	Species occurrence data are foundational for research, conservation, and science communication, but the limited availability and accessibility of reliable data represents a major obstacle, particularly for insects, which face mounting pressures. We present BeeBDC, a new R package, and a global bee occurrence dataset to address this issue. We combined >18.3 million bee occurrence records from multiple public repositories (GBIF, SCAN, iDigBio, USGS, ALA) and smaller datasets, then standardised, flagged, deduplicated, and cleaned the data using the reproducible BeeBDC R-workflow. Specifically, we harmonised species names (following established global taxonomy), country names, and collection dates and, we added record-level flags for a series of potential quality issues. These data are provided in two formats, "cleaned" and "flagged-but-uncleaned". The BeeBDC package with online documentation provides end users the ability to modify filtering parameters to address their research questions. By publishing reproducible R workflows and globally cleaned datasets, we can increase the accessibility and reliability of downstream analyses. This workflow can be implemented for other taxa to support research and conservation.
MeSH term(s)	Animals ; Bees ; Publishing ; Workflow
Language	English
Publishing date	2023-11-02
Publishing country	England
Document type	Dataset ; Journal Article
ZDB-ID	2775191-0
ISSN	2052-4463 ; 2052-4463
ISSN (online)	2052-4463
ISSN	2052-4463
DOI	10.1038/s41597-023-02626-w
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Article: Early establishment and antigen dependence of simian immunodeficiency virus-specific CD8+ T-cell defects.

Mueller, Yvonne M / Petrovas, Constantinos / Do, Duc H / Altork, Susan R / Fischer-Smith, Tracy / Rappaport, Jay / Altman, John D / Lewis, Mark G / Katsikis, Peter D

Journal of virology

2007 Volume 81, Issue 20, Page(s) 10861–10868

Abstract: Differentiation and survival defects of human immunodeficiency virus (HIV)-specific CD8(+) T cells may contribute to the failure of HIV-specific CD8(+) T cells to control HIV replication. It is not known, however, whether simian immunodeficiency virus ( ... ...

Abstract	Differentiation and survival defects of human immunodeficiency virus (HIV)-specific CD8(+) T cells may contribute to the failure of HIV-specific CD8(+) T cells to control HIV replication. It is not known, however, whether simian immunodeficiency virus (SIV)-infected rhesus macaques show comparable defects in these virus-specific CD8(+) T cells or when such defects are established during infection. Peripheral blood cells from acutely and chronically infected rhesus macaques were stained ex vivo for memory subpopulations and examined by in vitro assays for apoptosis sensitivity. We show here that SIV-specific CD8(+) T cells from chronically SIV infected rhesus macaques show defects comparable to those observed in HIV infection, namely, a skewed CD45RA(-) CD62L(-) effector memory phenotype, reduced Bcl-2 levels, and increased levels of spontaneous and CD95-induced apoptosis of SIV-specific CD8(+) T cells. Longitudinal studies showed that the survival defects and phenotype are established early in the first few weeks of SIV infection. Most importantly, they appear to be antigen driven, since most probably the loss of epitope recognition due to viral escape results in the reversal of the phenotype and reduced apoptosis sensitivity, something we observed also for animals treated with antiretroviral therapy. These findings further support the use of SIV-infected rhesus macaques to investigate the phenotypic changes and apoptotic defects of HIV-specific CD8(+) T cells and indicate that such defects of HIV-specific CD8(+) T cells are the result of chronic antigen stimulation.
MeSH term(s)	Animals ; Antigen Presentation ; Antigens, Viral/immunology ; Apoptosis ; CD8-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/pathology ; CD8-Positive T-Lymphocytes/virology ; Chronic Disease ; Immunologic Memory ; Immunophenotyping ; Longitudinal Studies ; Macaca mulatta ; Simian Acquired Immunodeficiency Syndrome/immunology ; Simian Immunodeficiency Virus/immunology
Chemical Substances	Antigens, Viral
Language	English
Publishing date	2007-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80174-4
ISSN	1098-5514 ; 0022-538X
ISSN (online)	1098-5514
ISSN	0022-538X
DOI	10.1128/JVI.00813-07
Database	MEDical Literature Analysis and Retrieval System OnLINE

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