Dora Y. Ho

ORCID: 0000-0003-0709-2414
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About
Contact & Profiles
Research Areas
  • Herpesvirus Infections and Treatments
  • Antifungal resistance and susceptibility
  • Cytomegalovirus and herpesvirus research
  • Virus-based gene therapy research
  • Fungal Infections and Studies
  • RNA regulation and disease
  • Neuroscience and Neuropharmacology Research
  • Infectious Diseases and Mycology
  • Immunodeficiency and Autoimmune Disorders
  • Neutropenia and Cancer Infections
  • Mycobacterium research and diagnosis
  • Mosquito-borne diseases and control
  • Viral gastroenteritis research and epidemiology
  • Heat shock proteins research
  • Neuroinflammation and Neurodegeneration Mechanisms
  • RNA Interference and Gene Delivery
  • Poxvirus research and outbreaks
  • Polyomavirus and related diseases
  • Biochemical effects in animals
  • Viral-associated cancers and disorders
  • Healthcare and Venom Research
  • Viral Infections and Immunology Research
  • Autoimmune and Inflammatory Disorders Research
  • Plant Pathogens and Fungal Diseases
  • Influenza Virus Research Studies

Stanford University
2015-2025

Stanford Medicine
2008-2024

Cancer Institute (WIA)
2024

Stanford Cancer Institute
2024

Palo Alto University
2022

Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico
2020

The University of Texas MD Anderson Cancer Center
2020

Fukuoka University
2020

University of Alabama at Birmingham
2019

Stanford Health Care
2016

Abstract Brain areas damaged by stroke and seizures express high levels of the 27‐kd heat shock protein (HSP72). Whether HSP72 represents merely a marker stress or plays role in improving neuron survival these cases has been debated. Some induced tolerance experiments have provided correlative evidence for neuroprotective effect, others documented neuroprotection absence synthesis. We report that gene transfer therapy with defective herpes simplex virus vectors overexpressing hsp 72 improves...

10.1002/ana.410440403 article EN Annals of Neurology 1998-10-01

During latent infection by herpes simplex virus (HSV), an abundant latency-associated transcript (LAT) that is antisense to a predominant viral alpha gene (ICP0) found localized in the nucleus of sensory neurons. We disrupted both copies LAT HSV-1 genome insertion Escherichia coli lacZ under promoter control. The resulting recombinant virus, RH142, does not express any detectable either latently or productively infected cells, although beta-galactosidase expression readily neurons mice....

10.1073/pnas.86.19.7596 article EN Proceedings of the National Academy of Sciences 1989-10-01

There is an increased risk of infection in patients with cancer that results higher morbidity and mortality. Several factors can predispose these to infectious complications. Some such include immunocompromised states like neutropenia, allogeneic hematopoietic cell transplantation, graft-versus-host disease, while others immunosuppressive agents corticosteroids, purine analogs, monoclonal antibodies, other emerging therapeutics CAR T-cell therapy. The NCCN Guidelines for the Prevention...

10.6004/jnccn.2024.0056 article EN Journal of the National Comprehensive Cancer Network 2024-11-01

species and Mucorales agents are the primary etiologies of invasive fungal disease (IFD). Biomarkers that predict outcomes needed to improve care. Patients diagnosed with aspergillosis mucormycosis using plasma cell-free DNA (cfDNA) PCR were retested weekly for 4 weeks. The outcome included all-cause mortality at 6 weeks months based on baseline cycle threshold (CT) values results follow-up cfDNA testing. Forty-five patients

10.1128/jcm.00394-24 article EN Journal of Clinical Microbiology 2024-04-11

Because of their postmitotic nature, neurons are difficult subjects for gene transfer. To circumvent this, we have used a defective herpes simplex virus vector to overexpress the rat brain glucose transporter (GT) under control human cytomegalovirus ie1 promoter. This vector, designated vIE1GT, was propagated using type 1 temperature-sensitive mutant, ts756. GT expressed from vIE1GT readily immunoprecipitated membrane fractions vIE1GT-infected Vero cells. By indirect double...

10.1073/pnas.90.8.3655 article EN Proceedings of the National Academy of Sciences 1993-04-15

Considerable interest has focused on the possibility of using viral vectors to deliver genes central nervous system for purpose decreasing necrotic neuronal injury. To that end, we have previously shown a herpes simplex virus (HSV) vector expressing Bcl-2 could protect neurons from ischemia. In study, was delivered before However, such gene therapy be clinical use, must protective even if after onset insult. present show an HSV protects striatal when focal Rats were exposed middle cerebral...

10.1097/00004647-199707000-00003 article EN Journal of Cerebral Blood Flow & Metabolism 1997-07-01

Mold plasma cell-free DNA (cfDNA) PCR is a promising non-invasive diagnostic modality for early diagnosis of invasive mold disease (IMD) in immunocompromised patients. Although cfDNA has been shown to be highly accurate, the value procedures collect specimens conventional fungal diagnostics following testing remains unclear. This retrospective single-center cohort study included patients with performed 7 days before or 2 after specimen collection. detected Aspergillus species, Mucorales...

10.1093/cid/ciaf021 article EN Clinical Infectious Diseases 2025-01-17

Abstract: Recently, preinduction of the heat shock response has been shown to protect CNS neurons undergoing various stressful insults, e.g., heat, ischemia, or exposure excitotoxins. However, it is not known which proteins induced by mediate protective effects. Previous correlative evidence points a role for highly stress‐induced 72‐kDa protein (hsp72). whether hsp72 expression alone can against range acute neuronal insults. We constructed herpes simplex virus‐1 vector carrying rat brain...

10.1046/j.1471-4159.1997.68030961.x article EN Journal of Neurochemistry 1997-03-01

Background and Purpose —Increased intracellular calcium accumulation is known to potentiate ischemic injury. Whether endogenous calcium-binding proteins can attenuate this injury has not been clearly established, existing data are conflicting. Calbindin D28K (CaBP) one such buffer. We investigated whether CaBP overexpression neuroprotective against transient focal cerebral ischemia. Methods —Bipromoter, replication-incompetent herpes simplex virus vectors that encoded the genes for cabp and,...

10.1161/01.str.32.4.1028 article EN Stroke 2001-04-01

We have generated herpes simplex virus (HSV) vectors vIE1GT and v alpha 4GT bearing the GLUT-1 isoform of rat brain glucose transporter (GT) under control human cytomegalovirus ie1 HSV 4 promoters, respectively. previously reported that such enhance uptake in hippocampal cultures hippocampus. In this study we demonstrate can maintain neuronal metabolism reduce extent neuron loss after a period hypoglycemia. Microinfusion GT into hippocampus also reduces kainic acid-induced seizure damage CA3...

10.1073/pnas.92.16.7247 article EN Proceedings of the National Academy of Sciences 1995-08-01

Herpes simplex virus vectors bearing a glucose transporter (GT) gene and marker were found to protect neurons against 1-h focal ischemic insult. Rats receiving the GT vector vα22βgalα4GT exhibited 67.4 ± 35.3% survival of virally targeted in hemisphere compared with contralateral control (n = 7), whereas rats only 32.8 17.9% 9). This significant improvement (105%, p 0.022) suggests that energy failure is an important contributor neuropathology damage striatum, it can be alleviated by...

10.1097/00004647-199603000-00001 article EN Journal of Cerebral Blood Flow & Metabolism 1996-03-01

Abstract : Increases in cytoplasmic Ca 2+ concentration ([Ca ] i ) can lead to neuron death. Preventing a rise [Ca by removing from the extracellular space or adding chelators cytosol of target cells ameliorates neurotoxicity associated with increases. Another potential route decreasing neurotoxic impact is overexpress one large number constitutive calcium‐binding proteins. Previous studies this laboratory demonstrated that overexpression gene for protein calbindin D 28K , via herpes simplex...

10.1046/j.1471-4159.1999.0731200.x article EN Journal of Neurochemistry 1999-09-01

To describe and discuss the utility potential pitfalls of ribosomal RNA locus sequencing for direct identification invasive fungi from fresh formalin-fixed, paraffin-embedded specimens.DNA was extracted tissue subjected to real-time polymerase chain reaction (PCR) targeting ITS2 D2 regions fungal locus. Cycle performed on PCR products, identity sequences determined using a public database.Four clinical cases infection are presented illustrate DNA determining etiology when microbiological...

10.1309/ajcpnsu2sdzd9wpw article EN American Journal of Clinical Pathology 2013-07-29

Invasive fungal infection (IFI) is a growing cause of morbidity and mortality in oncology transplant patients. Diagnosis IFI often delayed due to need for invasive biopsy low sensitivity conventional diagnostic methods. Fungal cell-free DNA (cfDNA) detection plasma novel testing modality the noninvasive diagnosis IFI.A bioinformatic pipeline was created interrogate genomes identify multicopy sequences cfDNA polymerase chain reaction (PCR) targeting. A real-time PCR panel developed 12 genera...

10.1093/cid/ciab158 article EN Clinical Infectious Diseases 2021-02-15

Herpes simplex virus-based amplicon vectors have been used for gene transfer into cultured neurons and the adult CNS. Since constitutive expression of a foreign or overexpression an endogenous may deleterious effects, ability to control temporal would be advantageous. To achieve inducible expression, we incorporated tetracycline-responsive promoter system showed, both in vitro vivo, that can modulated by tetracycline. Using firefly luciferase as reporter gene, maximal repression tetracycline...

10.1016/0169-328x(96)00097-6 article EN cc-by-nc-nd Molecular Brain Research 1996-09-01

Abstract: Disruption of Ca 2+ homeostasis often leads to neuron death. Recently, the function calcium‐binding proteins as neuronal buffers has been debated. We tested whether calbindin D 28k functions an intracellular buffer by constructing bicistronic herpes simplex virus vectors deliver rat cDNA hippocampal neurons in vitro. Neurons were infected with delivering or a negative control mock‐infected. After 12 24 h hypoglycemia, cells made aglycemic during fura‐2 calcium ratiometric imaging....

10.1046/j.1471-4159.1997.69031039.x article EN Journal of Neurochemistry 1997-09-01

Abstract: Because neurons are postmitotic, they irreplaceable once succumb to necrotic insults such as hypoglycemia, ischemia, and seizure. A paucity of energy can exacerbate the toxicities these insults; thus, a plausible route protect from injury would be enhance their glucose uptake capability. We have demonstrated previously that defective herpes simplex virus (HSV) vectors overexpressing rat brain transporter (GT) gene ( gt ) in adult hippocampus hippocampal cultures. Furthermore, we...

10.1046/j.1471-4159.1995.65020842.x article EN Journal of Neurochemistry 1995-08-01

With its natural propensity to infect and establish life-long latency in neurons, herpes simplex virus type 1 (HSV-1) has been successfully employed by various laboratories as vectors for gene transfer into neurons. However, analysis of cytopathic effects vivo vitro limited. In this study, we examined the 2 HSV-1 α4 mutants (ts756 d120) on adult rat hippocampus striatum d120 hippocampal neurons culture. We assessed damage stringent counting surviving after infection demonstrated that while...

10.1016/0165-0270(94)00150-f article EN cc-by-nc-nd Journal of Neuroscience Methods 1995-04-01
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