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Article ; Online: Sustained type I interferon signaling after human immunodeficiency virus type 1 infection of human iPSC derived microglia and cerebral organoids.

Boreland, Andrew J / Stillitano, Alessandro C / Lin, Hsin-Ching / Abbo, Yara / Hart, Ronald P / Jiang, Peng / Pang, Zhiping P / Rabson, Arnold B

iScience

2024 Volume 27, Issue 5, Page(s) 109628

Abstract: Human immunodeficiency virus type-1 (HIV-1)-associated neurocognitive disorder (HAND) affects up to half of people living with HIV-1 and causes long term neurological consequences. The pathophysiology of HIV-1-induced glial and neuronal functional ... ...

Abstract	Human immunodeficiency virus type-1 (HIV-1)-associated neurocognitive disorder (HAND) affects up to half of people living with HIV-1 and causes long term neurological consequences. The pathophysiology of HIV-1-induced glial and neuronal functional deficits in humans remains enigmatic. To bridge this gap, we established a model simulating HIV-1 infection in the central nervous system using human induced pluripotent stem cell (iPSC)-derived microglia combined with sliced neocortical organoids. Incubation of microglia with two replication-competent macrophage-tropic HIV-1 strains (JRFL and YU2) elicited productive infection and inflammatory activation. RNA sequencing revealed significant and sustained activation of type I interferon signaling pathways. Incorporating microglia into sliced neocortical organoids extended the effects of aberrant type I interferon signaling in a human neural context. Collectively, our results illuminate a role for persistent type I interferon signaling in HIV-1-infected microglia in a human neural model, suggesting its potential significance in the pathogenesis of HAND.
Language	English
Publishing date	2024-03-28
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2024.109628
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Article: Dysregulated neuroimmune interactions and sustained type I interferon signaling after human immunodeficiency virus type 1 infection of human iPSC derived microglia and cerebral organoids.

Boreland, Andrew J / Stillitano, Alessandro C / Lin, Hsin-Ching / Abbo, Yara / Hart, Ronald P / Jiang, Peng / Pang, Zhiping P / Rabson, Arnold B

bioRxiv : the preprint server for biology

2023

Abstract: Human immunodeficiency virus type-1 (HIV-1) associated neurocognitive disorder (HAND) affects up to half of HIV-1 positive patients with long term neurological consequences, including dementia. There are no effective therapeutics for HAND because the ... ...

Abstract	Human immunodeficiency virus type-1 (HIV-1) associated neurocognitive disorder (HAND) affects up to half of HIV-1 positive patients with long term neurological consequences, including dementia. There are no effective therapeutics for HAND because the pathophysiology of HIV-1 induced glial and neuronal functional deficits in humans remains enigmatic. To bridge this knowledge gap, we established a model simulating HIV-1 infection in the central nervous system using human induced pluripotent stem cell (iPSC) derived microglia combined with sliced neocortical organoids. Upon incubation with two replication-competent macrophage-tropic HIV-1 strains (JRFL and YU2), we observed that microglia not only became productively infected but also exhibited inflammatory activation. RNA sequencing revealed a significant and sustained activation of type I interferon signaling pathways. Incorporating microglia into sliced neocortical organoids extended the effects of aberrant type I interferon signaling in a human neural context. Collectively, our results illuminate the role of persistent type I interferon signaling in HIV-1 infected microglial in a human neural model, suggesting its potential significance in the pathogenesis of HAND.
Language	English
Publishing date	2023-10-30
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.10.25.563950
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Article ; Online: Zbtb20 identifies and controls a thymus-derived population of regulatory T cells that play a role in intestinal homeostasis.

Krzyzanowska, Agata K / Haynes Ii, Rashade A H / Kovalovsky, Damian / Lin, Hsin-Ching / Osorio, Louis / Edelblum, Karen L / Corcoran, Lynn M / Rabson, Arnold B / Denzin, Lisa K / Sant'Angelo, Derek B

Science immunology

2022 Volume 7, Issue 71, Page(s) eabf3717

Abstract: The expression of BTB-ZF transcription factors such as ThPOK in ... ...

Abstract	The expression of BTB-ZF transcription factors such as ThPOK in CD4
MeSH term(s)	Animals ; Colitis/chemically induced ; Homeostasis ; Intestines ; Mice ; Mice, Knockout ; T-Lymphocytes, Regulatory/metabolism ; Transcription Factors/genetics
Chemical Substances	Transcription Factors ; Zbtb20 protein, mouse
Language	English
Publishing date	2022-05-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ISSN	2470-9468
ISSN (online)	2470-9468
DOI	10.1126/sciimmunol.abf3717
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Article ; Online: BCCIP is required for nucleolar recruitment of eIF6 and 12S pre-rRNA production during 60S ribosome biogenesis.

Ye, Caiyong / Liu, Bochao / Lu, Huimei / Liu, Jingmei / Rabson, Arnold B / Jacinto, Estela / Pestov, Dimitri G / Shen, Zhiyuan

Nucleic acids research

2021 Volume 48, Issue 22, Page(s) 12817–12832

Abstract: Ribosome biogenesis is a fundamental process required for cell proliferation. Although evolutionally conserved, the mammalian ribosome assembly system is more complex than in yeasts. BCCIP was originally identified as a BRCA2 and p21 interacting protein. ...

Abstract	Ribosome biogenesis is a fundamental process required for cell proliferation. Although evolutionally conserved, the mammalian ribosome assembly system is more complex than in yeasts. BCCIP was originally identified as a BRCA2 and p21 interacting protein. A partial loss of BCCIP function was sufficient to trigger genomic instability and tumorigenesis. However, a complete deletion of BCCIP arrested cell growth and was lethal in mice. Here, we report that a fraction of mammalian BCCIP localizes in the nucleolus and regulates 60S ribosome biogenesis. Both abrogation of BCCIP nucleolar localization and impaired BCCIP-eIF6 interaction can compromise eIF6 recruitment to the nucleolus and 60S ribosome biogenesis. BCCIP is vital for a pre-rRNA processing step that produces 12S pre-rRNA, a precursor to the 5.8S rRNA. However, a heterozygous Bccip loss was insufficient to impair 60S biogenesis in mouse embryo fibroblasts, but a profound reduction of BCCIP was required to abrogate its function in 60S biogenesis. These results suggest that BCCIP is a critical factor for mammalian pre-rRNA processing and 60S generation and offer an explanation as to why a subtle dysfunction of BCCIP can be tumorigenic but a complete depletion of BCCIP is lethal.
MeSH term(s)	Animals ; BRCA2 Protein/genetics ; Carcinogenesis/genetics ; Cell Cycle Proteins/genetics ; Cell Proliferation/genetics ; Cyclin-Dependent Kinase Inhibitor p21/genetics ; Eukaryotic Initiation Factors/genetics ; Fibroblasts ; Genomic Instability/genetics ; Humans ; Mice ; NIH 3T3 Cells ; Protein Interaction Maps/genetics ; RNA, Ribosomal/genetics ; RNA, Ribosomal, 5.8S/genetics ; Ribosome Subunits, Large, Eukaryotic/genetics ; Ribosomes/genetics
Chemical Substances	BCCIP protein, mouse ; BRCA2 Protein ; BRCA2 protein, human ; CDKN1A protein, human ; Cell Cycle Proteins ; Cyclin-Dependent Kinase Inhibitor p21 ; EIF6 protein, human ; Eukaryotic Initiation Factors ; RNA, Ribosomal ; RNA, Ribosomal, 5.8S ; RNA, ribosomal, 12S
Language	English
Publishing date	2021-01-03
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	186809-3
ISSN	1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
ISSN (online)	1362-4962 ; 1362-4954
ISSN	0301-5610 ; 0305-1048
DOI	10.1093/nar/gkaa1114
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Zs.A 1067: Show issues

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Article: Human T-cell Leukemia Virus Type 1 and

Dykie, Adam / Wijesinghe, Tharaka / Rabson, Arnold B / Madugula, Kiran / Farinas, Christian / Wilson, Sydney / Abraham, David / Jain, Pooja

Pathogens (Basel, Switzerland)

2020 Volume 9, Issue 11

Abstract: Infection with human T-cell leukemia/lymphoma virus type 1 (HTLV-1) has been associated with various clinical syndromes including co-infection ... ...

Abstract	Infection with human T-cell leukemia/lymphoma virus type 1 (HTLV-1) has been associated with various clinical syndromes including co-infection with
Language	English
Publishing date	2020-10-29
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2695572-6
ISSN	2076-0817
ISSN	2076-0817
DOI	10.3390/pathogens9110904
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Article ; Online: Requirement of Bccip for the Regeneration of Intestinal Progenitors.

Lu, Huimei / Ye, Caiyong / Liu, Jingmei / Rabson, Arnold B / Verzi, Michael / De, Subhajyoti / Shen, Zhiyuan

The American journal of pathology

2020 Volume 191, Issue 1, Page(s) 66–78

Abstract: BCCIP was originally identified as a BRCA2 and CDKN1A/p21 interaction protein. Although a partial loss of BCCIP function is sufficient to trigger genomic instability and tumorigenesis, complete deletion of BCCIP is lethal to cells. Using Rosa26-CreERT2 ... ...

Abstract	BCCIP was originally identified as a BRCA2 and CDKN1A/p21 interaction protein. Although a partial loss of BCCIP function is sufficient to trigger genomic instability and tumorigenesis, complete deletion of BCCIP is lethal to cells. Using Rosa26-CreERT2 mouse models, we found that induced Bccip deletion in adult mice caused an acute intestinal epithelial denudation that cannot be relieved by co-deletion of Trp53. The critical role of Bccip in intestine epithelial renewal was verified with a Villin-CreERT2 mouse model. The epithelium degeneration was associated with a rapid loss of the proliferative capability of the crypt progenitor cells in vivo, lack of crypt base columnar stem cell markers, and a failure of in vitro crypt organoid growth. RNA-Seq analysis of freshly isolated intestinal crypt cells showed that Bccip deletion caused an overwhelming down-regulation of genes involved in mitotic cell division but an up-regulation of genes involved in apoptosis and stress response to microbiomes. Our data not only indicate that intestinal epithelium is the most sensitive tissue to whole-body deletion of Bccip but also point to Bccip as a novel and critical factor for the proliferation of the intestinal progenitors. These findings have significant implications for understanding why a hypomorphic loss of BCCIP functions is more relevant to tumorigenesis.
MeSH term(s)	Animals ; Cell Cycle Proteins/metabolism ; Cell Proliferation/physiology ; Intestinal Mucosa/metabolism ; Mice ; Regeneration/physiology ; Stem Cells/metabolism
Chemical Substances	BCCIP protein, mouse ; Cell Cycle Proteins
Language	English
Publishing date	2020-10-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2943-9
ISSN	1525-2191 ; 0002-9440
ISSN (online)	1525-2191
ISSN	0002-9440
DOI	10.1016/j.ajpath.2020.09.009
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Ud II Zs.76: Show issues

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Article ; Online: Strongyloides stercoralis and HTLV-1 coinfection in CD34+ cord blood stem cell humanized mice: Alteration of cytokine responses and enhancement of larval growth.

Springer, Lauren E / Patton, John B / Zhan, Tingting / Rabson, Arnold B / Lin, Hsin-Ching / Manser, Tim / Lok, James B / Hess, Jessica A / Abraham, David

PLoS neglected tropical diseases

2021 Volume 15, Issue 7, Page(s) e0009559

Abstract: Viral and parasitic coinfections are known to lead to both enhanced disease progression and altered disease states. HTLV-1 and Strongyloides stercoralis are co-endemic throughout much of their worldwide ranges resulting in a significant incidence of ... ...

Abstract	Viral and parasitic coinfections are known to lead to both enhanced disease progression and altered disease states. HTLV-1 and Strongyloides stercoralis are co-endemic throughout much of their worldwide ranges resulting in a significant incidence of coinfection. Independently, HTLV-1 induces a Th1 response and S. stercoralis infection induces a Th2 response. However, coinfection with the two pathogens has been associated with the development of S. stercoralis hyperinfection and an alteration of the Th1/Th2 balance. In this study, a model of HTLV-1 and S. stercoralis coinfection in CD34+ umbilical cord blood hematopoietic stem cell engrafted humanized mice was established. An increased level of mortality was observed in the HTLV-1 and coinfected animals when compared to the S. stercoralis infected group. The mortality was not correlated with proviral loads or total viral RNA. Analysis of cytokine profiles showed a distinct shift towards Th1 responses in HTLV-1 infected animals, a shift towards Th2 cytokines in S. stercoralis infected animals and elevated TNF-α responses in coinfected animals. HTLV-1 infected and coinfection groups showed a significant, yet non-clonal expansion of the CD4+CD25+ T-cell population. Numbers of worms in the coinfection group did not differ from those of the S. stercoralis infected group and no autoinfective larvae were found. However, infective larvae recovered from the coinfection group showed an enhancement in growth, as was seen in mice with S. stercoralis hyperinfection caused by treatment with steroids. Humanized mice coinfected with S. stercoralis and HTLV-1 demonstrate features associated with human infection with these pathogens and provide a unique opportunity to study the interaction between these two infections in vivo in the context of human immune cells.
MeSH term(s)	Animals ; Antigens, CD34/blood ; Cell Line ; Coinfection ; Cytokines/genetics ; Cytokines/metabolism ; Fetal Blood ; HTLV-I Infections/complications ; HTLV-I Infections/immunology ; Hematopoietic Stem Cells/metabolism ; Human T-lymphotropic virus 1 ; Larva/growth & development ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Strongyloides stercoralis/growth & development ; Strongyloidiasis/complications ; Strongyloidiasis/immunology
Chemical Substances	Antigens, CD34 ; Cytokines
Language	English
Publishing date	2021-07-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2429704-5
ISSN	1935-2735 ; 1935-2735
ISSN (online)	1935-2735
ISSN	1935-2735
DOI	10.1371/journal.pntd.0009559
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Article: Fratricidal retroviruses: a new twist in gene therapy.

Rabson, Arnold B

Cancer biology & therapy

2003 Volume 2, Issue 1, Page(s) 100–102

MeSH term(s)	Animals ; Antiviral Agents/pharmacology ; Cells, Cultured ; Gene Expression Regulation, Viral ; Genetic Therapy ; Genetic Vectors ; Humans ; Leukemia Virus, Feline/physiology ; Prodrugs ; Retroviridae Infections/genetics ; Retroviridae Infections/therapy ; Retroviridae Proteins, Oncogenic/genetics ; Retroviridae Proteins, Oncogenic/metabolism ; Transgenes ; Tumor Virus Infections/genetics ; Tumor Virus Infections/therapy ; Viral Envelope Proteins/genetics ; Viral Envelope Proteins/metabolism ; Virus Diseases/therapy ; Virus Replication
Chemical Substances	Antiviral Agents ; Prodrugs ; Retroviridae Proteins, Oncogenic ; Viral Envelope Proteins ; glycoprotein gp70, Feline leukemia virus
Language	English
Publishing date	2003-04-02
Publishing country	United States
Document type	Comment ; Editorial
ZDB-ID	2146305-0
ISSN	1538-4047
ISSN	1538-4047
DOI	10.4161/cbt.250
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Zs.A 5887: Show issues

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Article ; Online: Effects of participation in a U.S. trial of newborn genomic sequencing on parents at risk for depression.

Schwartz, Talia S / Christensen, Kurt D / Uveges, Melissa K / Waisbren, Susan E / McGuire, Amy L / Pereira, Stacey / Robinson, Jill O / Beggs, Alan H / Green, Robert C / Bachmann, Gloria A / Rabson, Arnold B / Holm, Ingrid A

Journal of genetic counseling

2021 Volume 31, Issue 1, Page(s) 218–229

Abstract: Much emphasis has been placed on participant's psychological safety within genomic research studies; however, few studies have addressed parental psychological health effects associated with their child's participation in genomic studies, particularly ... ...

Abstract	Much emphasis has been placed on participant's psychological safety within genomic research studies; however, few studies have addressed parental psychological health effects associated with their child's participation in genomic studies, particularly when parents meet the threshold for clinical concern for depression. We aimed to determine if parents' depressive symptoms were associated with their child's participation in a randomized-controlled trial of newborn exome sequencing. Parents completed the Edinburgh Postnatal Depression Scale (EPDS) at baseline, immediately post-disclosure, and 3 months post-disclosure. Mothers and fathers scoring at or above thresholds for clinical concern on the EPDS, 12 and 10, respectively, indicating possible Major Depressive Disorder with Peripartum Onset, were contacted by study staff for mental health screening. Parental concerns identified in follow-up conversations were coded for themes. Forty-five parents had EPDS scores above the clinical threshold at baseline, which decreased by an average of 2.9 points immediately post-disclosure and another 1.1 points 3 months post-disclosure (both p ≤ .014). For 28 parents, EPDS scores were below the threshold for clinical concern at baseline, increased by an average of 4.7 points into the elevated range immediately post-disclosure, and decreased by 3.8 points at 3 months post-disclosure (both p < .001). Nine parents scored above thresholds only at 3 months post-disclosure after increasing an average of 5.7 points from immediately post-disclosure (p < .001). Of the 82 parents who scored above the threshold at any time point, 43 (52.4%) were reached and 30 (69.7%) of these 43 parents attributed their elevated scores to parenting stress, balancing work and family responsibilities, and/or child health concerns. Only three parents (7.0%) raised concerns about their participation in the trial, particularly their randomization to the control arm. Elevated scores on the EPDS were typically transient and parents attributed their symptomatology to life stressors in the postpartum period rather than participation in a trial of newborn exome sequencing.
MeSH term(s)	Child ; Depression ; Depression, Postpartum/diagnosis ; Depression, Postpartum/prevention & control ; Depression, Postpartum/psychology ; Depressive Disorder, Major ; Female ; Genomics ; Humans ; Infant, Newborn ; Mothers/psychology ; Parents/psychology
Language	English
Publishing date	2021-07-26
Publishing country	United States
Document type	Journal Article ; Randomized Controlled Trial ; Research Support, N.I.H., Extramural
ZDB-ID	1117799-8
ISSN	1573-3599 ; 1059-7700
ISSN (online)	1573-3599
ISSN	1059-7700
DOI	10.1002/jgc4.1475
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Zs.A 4263: Show issues

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Article ; Online: Human T-cell Leukemia Virus Type 1 and Strongyloides stercoralis

Adam Dykie / Tharaka Wijesinghe / Arnold B. Rabson / Kiran Madugula / Christian Farinas / Sydney Wilson / David Abraham / Pooja Jain

Pathogens, Vol 9, Iss 904, p

Partners in Pathogenesis

2020 Volume 904

Abstract: Infection with human T-cell leukemia/lymphoma virus type 1 (HTLV-1) has been associated with various clinical syndromes including co-infection with Strongyloides stercoralis , which is an intestinal parasitic nematode and the leading cause of ... ...

Abstract	Infection with human T-cell leukemia/lymphoma virus type 1 (HTLV-1) has been associated with various clinical syndromes including co-infection with Strongyloides stercoralis , which is an intestinal parasitic nematode and the leading cause of strongyloidiasis in humans. Interestingly, HTLV-1 endemic areas coincide with regions citing high prevalence of S. stercoralis infection, making these communities optimal for elucidating the pathogenesis of co-infection and its clinical significance. HTLV-1 co-infection with S. stercoralis has been observed for decades in a number of published patient cases and case series; however, the implications of this co-infection remain elusive. Thus far, data suggest that S. stercoralis increases proviral load in patients co-infected with HTLV-1 compared to HTLV-1 infection alone. Furthermore, co-infection with HTLV-1 has been associated with shifting the immune response from Th2 to Th1, affecting the ability of the immune system to address the helminth infection. Thus, despite this well-known association, further research is required to fully elucidate the impact of each pathogen on disease manifestations in co-infected patients. This review provides an analytical view of studies that have evaluated the variation within HTLV-1 patients in susceptibility to S. stercoralis infection, as well as the effects of strongyloidiasis on HTLV-1 pathogenesis. Further, it provides a compilation of available clinical reports on the epidemiology and pathology of HTLV-1 with parasitic co-infection as well as data from mechanistic studies suggesting possible immunopathogenic mechanisms. Furthermore, specific areas of potential future research have been highlighted to facilitate advancing understanding of the complex interactions between these two pathogens.
Keywords	HTLV-1 ; ATLL ; HAM/TSP ; strongyloidiasis ; co-infection ; Medicine ; R
Subject code	616
Language	English
Publishing date	2020-10-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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