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Brian Wigdahl
Researcher at Drexel University
Publications - 229
Citations - 6653
Brian Wigdahl is an academic researcher from Drexel University. The author has contributed to research in topics: Virus & Long terminal repeat. The author has an hindex of 41, co-authored 215 publications receiving 5987 citations. Previous affiliations of Brian Wigdahl include Thomas Jefferson University & Pennsylvania State University.
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Journal ArticleDOI
Specific interactions between the viral coreceptor CXCR4 and the biguanide-based compound NB325 mediate inhibition of human immunodeficiency virus type 1 infection
Nina Thakkar,Vanessa Pirrone,Shendra Passic,Wei Zhu,Vladyslav Kholodovych,William J. Welsh,Robert F. Rando,Mohamed E. Labib,Brian Wigdahl,Fred C. Krebs +9 more
TL;DR: It is demonstrated that the biguanide-based compound NB325 inhibits HIV-1 infection by specifically interacting with the HIV- 1 coreceptor CXCR4.
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Extracellular human immunodeficiency virus type 1 viral protein R causes reductions in astrocytic ATP and glutathione levels compromising the antioxidant reservoir.
TL;DR: A role of extracellular HIV-1 Vpr in impairing astrocytic levels of intracellular ATP and GSH metabolites is confirmed and studies are underway to better understand the intricate correlation between reductions in ATP andGSH metabolites and how they affect neuronal survival in end-stage disease.
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Use of human antigen presenting cell gene array profiling to examine the effect of human T-cell leukemia virus type 1 Tax on primary human dendritic cells.
TL;DR: In this study, a pathway-specific antigen presenting cell gene array was used to study transcriptional changes induced by exposure of monocyte-derived DCs to extracellular HTLV-1 Tax protein, which suggested that Tax-mediated DC gene regulation might play a critical role in cellular activation and the mechanisms resulting in HTLV
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Region-specific distribution of human immunodeficiency virus type 1 long terminal repeats containing specific configurations of CCAAT/enhancer-binding protein site II in brains derived from demented and nondemented patients.
TL;DR: Different LTR populations with specific C/EBP site II configurations were found in different neuroanatomical regions of the brain, potentially due to differences in the molecular architecture of the LTR, viral entry pathways, and/or brain microenvironments.
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Specific sequence configurations of HIV-1 LTR G/C box array result in altered recruitment of Sp isoforms and correlate with disease progression.
TL;DR: Analysis of LTR Sp binding site sequence variants revealed a C-to-T change at position 5 within Sp site III that increased in frequency and a 5T mutation within Sp sites II, which decreased in frequency during the course of HIV disease.