Professor of Neurology, Dana-Farber Cancer Institute
Neurology
Dr. Dana H. Gabuzda, MD
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Dana Gabuzda works in the field of Neurology. She researched medicine at Harvard Medical School. Harvard Medical School is one of the top medical schools in the US. Harvard Medical School has a rank of 1 in research and a 12 in primary care Dr. Dana H. Gabuzda is a published physician. She published 100 publications, including: 'Apoptosis induced by infection of primary brain cultures with diverse human immunodeficiency virus type 1 isolates: evidence for a role of the envelope.'
Publications
- Bioinformatic analysis of neurotropic HIV envelope sequences identifies polymorphisms in the gp120 bridging sheet that increase macrophage-tropism through enhanced int...
- Identification and characterization of a macrophage-tropic SIV envelope glycoprotein variant in blood from early infection in SIVmac251-infected macaques.
- Loss of a conserved N-linked glycosylation site in the SIV envelope glycoprotein V2 region enhances macrophage tropism by increasing CD4-independent cell-to-cell trans...
- Applications and Limitations of Inflammatory Biomarkers for Studies on Neurocognitive Impairment in HIV Infection.
- A Machine Learning Approach for Identifying Amino Acid Signatures in the HIV Env Gene Predictive of Dementia.
- Evolution of the aging brain transcriptome and synaptic regulation.
- Plasma metabolomics identifies lipid abnormalities linked to markers of inflammation, microbial translocation, and hepatic function in HIV patients receiving protease ...
- Identification of membrane anchorage domains of the HIV-1 gp160 envelope glycoprotein precursor.
- Effects of changes in gp120-CD4 binding affinity on human immunodeficiency virus type 1 envelope glycoprotein function and soluble CD4 sensitivity.
- Allelic variation in the effects of the nef gene on replication of human immunodeficiency virus type 1.
- Characterization of a discontinuous human immunodeficiency virus type 1 gp120 epitope recognized by a broadly reactive neutralizing human monoclonal antibody.
- Cellular regulation of visna virus gene expression and its role in pathogenesis.
- Rapid complementation assays measuring replicative potential of human immunodeficiency virus type 1 envelope glycoprotein mutants.
- Changes in the transmembrane region of the human immunodeficiency virus type 1 gp41 envelope glycoprotein affect membrane fusion.
- Biological activity of human immunodeficiency virus type 1 Vif requires membrane targeting by C-terminal basic domains.
- Macrophage tropism of human immunodeficiency virus type 1 isolates from brain and lymphoid tissues predicts neurotropism independent of coreceptor specificity.
- Opposite effects of IL-10 on the ability of dendritic cells and macrophages to replicate primary CXCR4-dependent HIV-1 strains.
- Role of Vif in stability of the human immunodeficiency virus type 1 core.
- Chemokine receptors and mechanisms of cell death in HIV neuropathogenesis.
- Cell-dependent mechanisms restrict the HIV type 1 coreceptor activity of US28, a chemokine receptor homolog encoded by human cytomegalovirus.
- Chemokine receptors and virus entry in the central nervous system.
- Circulating CD2+ monocytes are dendritic cells.
- ERK MAP kinase links cytokine signals to activation of latent HIV-1 infection by stimulating a cooperative interaction of AP-1 and NF-kappaB.
- Regulation of human immunodeficiency virus type 1 infectivity by the ERK mitogen-activated protein kinase signaling pathway.
- The CXC-chemokine, H174: expression in the central nervous system.
- Apoptosis induced by infection of primary brain cultures with diverse human immunodeficiency virus type 1 isolates: evidence for a role of the envelope.
- Mitogen-activated protein kinase phosphorylates and regulates the HIV-1 Vif protein.
- Chemokine receptors in HIV-1 infection of the central nervous system.
- Neuronal apoptosis induced by HIV-1 Tat protein and TNF-alpha: potentiation of neurotoxicity mediated by oxidative stress and implications for HIV-1 dementia.
- Localization of HIV-1 co-receptors CCR5 and CXCR4 in the brain of children with AIDS.
- Human immunodeficiency virus type 1 Vif protein binds to the Pr55Gag precursor.
- Ultrastructure of HIV-1 genomic RNA.
- Astrocyte apoptosis induced by HIV-1 transactivation of the c-kit protooncogene.
- CCR3 and CCR5 are co-receptors for HIV-1 infection of microglia.
- Role of Vif in human immunodeficiency virus type 1 reverse transcription.
- Apoptosis induced by HIV-1 infection of the central nervous system.
- Phosphorylation of Vif and its role in HIV-1 replication.
- Effects of CD4 synthetic peptides on HIV type I envelope glycoprotein function.
- Inhibition of beta-amyloid production by activation of protein kinase C.
- Role of vif during packing of the core of HIV-1.
- Inhibition of energy metabolism alters the processing of amyloid precursor protein and induces a potentially amyloidogenic derivative.
- The intracytoplasmic domain of gp41 mediates polarized budding of human immunodeficiency virus type 1 in MDCK cells.
- A Plasma Biomarker Signature of Immune Activation in HIV Patients on Antiretroviral Therapy.
- Nef-mediated enhancement of cellular activation and human immunodeficiency virus type 1 replication in primary T cells is dependent on association with p21-activated k...
- Plasma sCD14 is a biomarker associated with impaired neurocognitive test performance in attention and learning domains in HIV infection.
- CD4 and MHC class 1 down-modulation activities of nef alleles from brain- and lymphoid tissue-derived primary HIV-1 isolates.
- HIVBrainSeqDB: a database of annotated HIV envelope sequences from brain and other anatomical sites.
- Serological markers for inflammatory bowel disease in AIDS patients with evidence of microbial translocation.
- Evidence for adaptive evolution at the divergence between lymphoid and brain HIV-1 nef genes.
- Transcriptional profiling reveals developmental relationship and distinct biological functions of CD16+ and CD16- monocyte subsets.
- Enhanced macrophage tropism of HIV in brain and lymphoid tissues is associated with sensitivity to the broadly neutralizing CD4 binding site antibody b12.
- Soluble CD4 and CD4-mimetic compounds inhibit HIV-1 infection by induction of a short-lived activated state.
- Tissue-specific sequence alterations in the human immunodeficiency virus type 1 envelope favoring CCR5 usage contribute to persistence of dual-tropic virus in the brain.
- Regulation of APOBEC3 proteins by a novel YXXL motif in human immunodeficiency virus type 1 Vif and simian immunodeficiency virus SIVagm Vif.
- Bioinformatic prediction programs underestimate the frequency of CXCR4 usage by R5X4 HIV type 1 in brain and other tissues.
- Microbial translocation is associated with increased monocyte activation and dementia in AIDS patients.
- The HIV-1 Vif protein mediates degradation of Vpr and reduces Vpr-induced cell cycle arrest.
- Asn 362 in gp120 contributes to enhanced fusogenicity by CCR5-restricted HIV-1 envelope glycoprotein variants from patients with AIDS.
- Identification of an APOBEC3G binding site in human immunodeficiency virus type 1 Vif and inhibitors of Vif-APOBEC3G binding.
- Pathogenicity and immunogenicity of attenuated, nef-deleted HIV-1 strains in vivo.
- Phenotype and envelope gene diversity of nef-deleted HIV-1 isolated from long-term survivors infected from a single source.
- Loss of the N-linked glycosylation site at position 386 in the HIV envelope V4 region enhances macrophage tropism and is associated with dementia.
- Viral phenotypes and antibody responses in long-term survivors infected with attenuated human immunodeficiency virus type 1 containing deletions in the nef and long te...
- High frequency of defective vpu compared with tat and rev genes in brain from patients with HIV type 1-associated dementia.
- Changes in the V3 region of gp120 contribute to unusually broad coreceptor usage of an HIV-1 isolate from a CCR5 Delta32 heterozygote.
- Reconstitution of human immunodeficiency virus-induced neurodegeneration using isolated populations of human neurons, astrocytes, and microglia and neuroprotection med...
- Macrophage entry mediated by HIV Envs from brain and lymphoid tissues is determined by the capacity to use low CD4 levels and overall efficiency of fusion.
- CD16+ monocytes produce IL-6, CCL2, and matrix metalloproteinase-9 upon interaction with CX3CL1-expressing endothelial cells.
- The HIV Env variant N283 enhances macrophage tropism and is associated with brain infection and dementia.
- CD4 and MHC-I downregulation are conserved in primary HIV-1 Nef alleles from brain and lymphoid tissues, but Pak2 activation is highly variable.
- Mechanisms of HIV-1 neurotropism.
- Use of laser capture microdissection to detect integrated HIV-1 DNA in macrophages and astrocytes from autopsy brain tissues.
- Elicitation from virus-naive individuals of cytotoxic T lymphocytes directed against conserved HIV-1 epitopes.
- CD16+ monocyte-derived macrophages activate resting T cells for HIV infection by producing CCR3 and CCR4 ligands.
- A zinc-binding region in Vif binds Cul5 and determines cullin selection.
- Genetic and functional analysis of R5X4 human immunodeficiency virus type 1 envelope glycoproteins derived from two individuals homozygous for the CCR5delta32 allele.
- A hydrophobic binding surface on the human immunodeficiency virus type 1 Nef core is critical for association with p21-activated kinase 2.
- CD16+ monocytes exposed to HIV promote highly efficient viral replication upon differentiation into macrophages and interaction with T cells.
- HIV-1 envelope pseudotyped viral vectors and infectious molecular clones expressing the same envelope glycoprotein have a similar neutralization phenotype, but culture...
- Nuclear localization of HIV type 1 Vif isolated from a long-term asymptomatic individual and potential role in virus attenuation.
- Distinct mechanisms of CD4+ and CD8+ T-cell activation and bystander apoptosis induced by human immunodeficiency virus type 1 virions.
- Pathogenesis of macrophage tropic HIV-1.
- Phosphorylation of a novel SOCS-box regulates assembly of the HIV-1 Vif-Cul5 complex that promotes APOBEC3G degradation.
- Transendothelial migration of CD16+ monocytes in response to fractalkine under constitutive and inflammatory conditions.
- Camelized rabbit-derived VH single-domain intrabodies against Vif strongly neutralize HIV-1 infectivity.
- N-linked glycosylation in the CXCR4 N-terminus inhibits binding to HIV-1 envelope glycoproteins.
- Contribution of proteoglycans to human immunodeficiency virus type 1 brain invasion.
- Apoptosis of bystander T cells induced by human immunodeficiency virus type 1 with increased envelope/receptor affinity and coreceptor binding site exposure.
- Vif overcomes the innate antiviral activity of APOBEC3G by promoting its degradation in the ubiquitin-proteasome pathway.
- Genetic and functional analysis of full-length human immunodeficiency virus type 1 env genes derived from brain and blood of patients with AIDS.
- Fractalkine preferentially mediates arrest and migration of CD16+ monocytes.
- CD2 engagement induces dendritic cell activation: implications for immune surveillance and T-cell activation.
- Persistence of dual-tropic HIV-1 in an individual homozygous for the CCR5 Delta 32 allele.
- Functional neutralization of HIV-1 Vif protein by intracellular immunization inhibits reverse transcription and viral replication.
- Increased CCR5 affinity and reduced CCR5/CD4 dependence of a neurovirulent primary human immunodeficiency virus type 1 isolate.
- Human immunodeficiency virus type 1 neutralization measured by flow cytometric quantitation of single-round infection of primary human T cells.
- Regulation of CC chemokine receptor 5 and CD4 expression and human immunodeficiency virus type 1 replication in human macrophages and microglia by T helper type 2 cyto...
- Generation of beta-amyloid in the secretory pathway in neuronal and nonneuronal cells.
- Subcellular localization of the Vif protein of human immunodeficiency virus type 1.
Schools
Harvard Medical School
Doctors Specialties
- Neurology
Accepted Insurances
Education
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Johns Hopkins University -
Massachusetts General Hospital -
Harvard Medical School
Hospital
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Dana-Farber Cancer Institute
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