scholarly journals Enhanced Expression and HIV-1 Inhibition of Chimeric tRNALys3-Ribozymes under Dual U6 snRNA and tRNA Promoters

2002 ◽  
Vol 6 (4) ◽  
pp. 481-489 ◽  
Author(s):  
Zongli Chang ◽  
Shawn Westaway ◽  
Shirley Li ◽  
John A. Zaia ◽  
John J. Rossi ◽  
...  
Keyword(s):  
U6 Snrna ◽  
Enhanced Expression ◽  
Hiv 1

Enhanced Expression, Secretion, and Large-Scale Purification of Recombinant HIV-1 gp120 in Insect Cells Using the Baculovirus egt and p67 Signal Peptides

1993 ◽  
Vol 4 (5) ◽  
pp. 349-357 ◽  
Author(s):  
C.I. Murphy ◽  
J.R. Mcintire ◽  
D.V. Davis ◽  
H. Hodgdon ◽  
J.R. Seals ◽  
...  
Keyword(s):  
Large Scale ◽  
Insect Cells ◽  
Signal Peptides ◽  
Enhanced Expression ◽  
Hiv 1

Enhanced expression of fractalkine in HIV-1 associated dementia

2001 ◽  
Vol 115 (1-2) ◽  
pp. 168-175 ◽  
Author(s):  
C.F. Pereira ◽  
J. Middel ◽  
G. Jansen ◽  
J. Verhoef ◽  
H.S.L.M. Nottet
Keyword(s):  
Enhanced Expression ◽  
Hiv 1

scholarly journals Dual regulation of L-selectin (CD62L) by HIV-1: Enhanced expression by Vpr in contrast with cell-surface down-modulation by Nef and Vpu

Virology ◽  
2018 ◽  
Vol 523 ◽  
pp. 121-128 ◽  
Author(s):  
Erica Giuliani ◽  
Lia Vassena ◽  
Silvia Galardi ◽  
Alessandro Michienzi ◽  
Maria Giovanna Desimio ◽  
...  
Keyword(s):  
Cell Surface ◽  
Enhanced Expression ◽  
Hiv 1

scholarly journals STAT1 signaling modulates HIV-1–induced inflammatory responses and leukocyte transmigration across the blood-brain barrier

Blood ◽  
2008 ◽  
Vol 111 (4) ◽  
pp. 2062-2072 ◽  
Author(s):  
Anathbandhu Chaudhuri ◽  
Bo Yang ◽  
Howard E. Gendelman ◽  
Yuri Persidsky ◽  
Georgette D. Kanmogne
Keyword(s):  
Blood Brain Barrier ◽  
Inflammatory Responses ◽  
Janus Kinase ◽  
Brain Barrier ◽  
Signal Transducers ◽  
Monocyte Migration ◽  
Blood Brain ◽  
Integral Role ◽  
Enhanced Expression ◽  
Hiv 1

The relationship among neuroinflammation, blood-brain barrier (BBB) dysfunction, and progressive HIV-1 infection as they affect the onset and development of neuroAIDS is incompletely understood. One possible link is signal transducers and activators of transcription (STATs) pathways. These respond to proinflammatory and regulatory factors and could affect neuroinflammatory responses induced from infected cells and disease-affected brain tissue. Our previous works demonstrated that HIV-1 activates pro-inflammatory and interferon-alpha–inducible genes in human brain microvascular endothelial cells (HBMECs) and that these genes are linked to the Janus kinase (JAK)/STAT pathway. We now demonstrate that HIV-1 activates STAT1, induces IL-6 expression, and diminishes expression of claudin-5, ZO-1, and ZO-2 in HBMECs. The STAT1 inhibitor, fludarabine, blocked HIV-1–induced IL-6, diminished HIV-1–induced claudin-5 and ZO-1 down-regulation, and blocked HIV-1– and IL-6–induced monocyte migration across a BBB model. Enhanced expression and activation of STAT1 and decreased claudin-5 were observed in microvessels from autopsied brains of patients with HIV-1–associated dementia. These data support the notion that STAT1 plays an integral role in HIV-1–induced BBB damage and is relevant to viral neuropathogenesis. Inhibition of STAT1 activation could provide a unique therapeutic strategy to attenuate HIV-1–induced BBB compromise and as such improve clinical outcomes.

Enhanced expression of the CXCR4 co-receptor in HIV-1-infected individuals correlates with the emergence of syncytia-inducing strains

2000 ◽  
Vol 6 (1) ◽  
pp. 19-24 ◽  
Author(s):  
Roberto Manetti ◽  
Lorenzo Cosmi ◽  
Grazia Galli ◽  
Francesco Annunziato ◽  
Marcello Mazzetti ◽  
...  
Keyword(s):  
Enhanced Expression ◽  
Hiv 1

HIV-1 gp120-Induced Apoptosis in the Rat Neocortex Involves Enhanced Expression of Cyclo-oxygenase Type 2 (COX-2)

1998 ◽  
Vol 244 (3) ◽  
pp. 819-824 ◽  
Author(s):  
G. Bagetta ◽  
M.T. Corasaniti ◽  
A.M. Paoletti ◽  
L. Berliocchi ◽  
R. Nisticò ◽  
...  
Keyword(s):  
Rat Neocortex ◽  
Enhanced Expression ◽  
Cox 2 ◽  
Induced Apoptosis ◽  
Hiv 1

scholarly journals Cocaine augments neuro-inflammation via modulating extracellular vesicle release in HIV-1 infected immune cells

Retrovirology ◽  
2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Manojkumar Narayanan ◽  
Rutuja Kulkarni ◽  
Shuxian Jiang ◽  
Fatah Kashanchi ◽  
Anil Prasad
Keyword(s):  
T Cells ◽  
Immune Cells ◽  
Molecular Mechanisms ◽  
Extracellular Vesicle ◽  
Triggered Release ◽  
Sigma 1 Receptor ◽  
Enhanced Expression ◽  
Infected Cells ◽  
Novel Therapeutic Strategies ◽  
Hiv 1

Abstract Background Extracellular Vesicles (EV) recently have been implicated in the pathogenesis of HIV-1 syndromes, including neuroinflammation and HIV-1 associated neurological disorder (HAND). Cocaine, an illicit stimulant drug used worldwide is known to exacerbate these HIV-1 associated neurological syndromes. However, the effects of cocaine on EV biogenesis and roles of EVs in enhancing HIV-1 pathogenesis are not yet well defined. Results Here, we investigated the effects of cocaine on EV biogenesis and release in HIV-1 infected immune cells and explored their roles in elicitation of neuroinflammation. We found that cocaine significantly augmented the release of EVs from uninfected and HIV-1 infected T-cells, DCs and macrophages. Further analysis of the molecular components of EVs revealed enhanced expression of adhesion molecules integrin β1 and LFA-1 in those EVs derived from cocaine treated cells. Intriguingly, in EVs derived from HIV-1 infected cells, cocaine treatment significantly increased the levels of viral genes in EVs released from macrophages and DCs, but not in T-cells. Exploring the molecular mechanism to account for this, we found that DCs and macrophages showed enhanced expression of the cocaine receptor Sigma 1-Receptor compared to T-cells. In addition, we found that cocaine significantly altered the integrity of the RNA-induced silencing complex (RISC) in HIV-1 infected macrophages and DCs compared to untreated HIV-1 infected cells. Characterizing further the molecular mechanisms involved in how cocaine increased EV release, we found that cocaine decreased the expression of the interferon-inducible protein BST-2; this resulted in altered trafficking of intracellular virus containing vesicles and EV biogenesis and release. We also observed EVs released from cocaine treated HIV-1 infected macrophages and DCs enhanced HIV-1 trans-infection to T-cells compared to those from untreated and HIV-1 infected cells. These EVs triggered release of proinflammatory cytokines in human brain microvascular endothelial cells (HBMECs) and altered monolayer integrity. Conclusions Taken together, our results provide a novel mechanism which helps to elucidate the enhanced prevalence of neurological disorders in cocaine using HIV-1 infected individuals and offers insights into developing novel therapeutic strategies against HAND in these hosts.

scholarly journals HIV-1 Transactivator of Transcription (Tat) Co-operates With AP-1 Factors to Enhance c-MYC Transcription

2021 ◽  
Vol 9 ◽  
Author(s):  
Leonardo Alves de Souza Rios ◽  
Lungile Mapekula ◽  
Nontlantla Mdletshe ◽  
Dharshnee Chetty ◽  
Shaheen Mowla
Keyword(s):  
Gene Promoter ◽  
Population Group ◽  
Active Role ◽  
Luciferase Reporter ◽  
Non Hodgkin Lymphoma ◽  
Enhanced Expression ◽  
Reporter Assays ◽  
Patient Prognosis ◽  
Hiv 1

HIV-1 infection often leads to the development of co-morbidities including cancer. Burkitt lymphoma (BL) is one of the most over-represented non-Hodgkin lymphoma among HIV-infected individuals, and displays a highly aggressive phenotype in this population group, with comparatively poorer outcomes, despite these patients being on anti-retroviral therapy. Accumulating evidence indicates that the molecular pathogenesis of HIV-associated malignancies is unique, with components of the virus playing an active role in driving oncogenesis, and in order to improve patient prognosis and treatment, a better understanding of disease pathobiology and progression is needed. In this study, we found HIV-1 Tat to be localized within the tumor cells of BL patients, and enhanced expression of oncogenic c-MYC in these cells. Using luciferase reporter assays we show that HIV-1 Tat enhances the c-MYC gene promoter activity and that this is partially mediated via two AP-1 binding elements located at positions -1128 and -1375 bp, as revealed by mutagenesis experiments. We further demonstrate, using pull-down assays, that Tat can exist within a protein complex with the AP-1 factor JunB, and that this complex can bind these AP-1 sites within the c-MYC promoter, as shown by in vivo chromatin immunoprecipitation assays. Therefore, these findings show that in HIV-infected individuals, Tat infiltrates B-cells, where it can enhance the expression of oncogenic factors, which contributes toward the more aggressive disease phenotype observed in these patients.

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