Cytomegalovirus (CMV) is a ubiquitous herpes virus that develops lifelong latency following primary infection and can be reactivated following immune suppression. CMV encephalopathy has been described in few reports after hematopoietic stem cell transplantation and in patients with acquired immunodeficiency syndrome. To the best of our knowledge, CMV encephalopathy following CAR-T cells infusion had not been previously reported. Initial CMV viral load and monitoring are crucial in patients with CAR-T cells to allow early intervention with aggressive antiviral treatment without delay if needed.
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Susceptibility of Mouse Brain to MCMV Infection and Neuroinflammation During Ontogeny.
Pathogens
December 2024
Center for Proteomics, Faculty of Medicine, University of Rijeka, 51000 Rijeka, Croatia.
Human cytomegalovirus (HCMV) rarely infects the brain following infection of adult individuals. However, the virus readily infects the brain during congenital HCMV (cHCMV) infection, frequently causing severe neurodevelopmental and neurological sequelae. Interestingly, although the incidence of cHCMV infection is 0.
View Article and Find Full Text PDFA vaccine against cytomegalovirus: how close are we?
J Clin Invest
January 2025
Department of Pediatrics, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
The pursuit of a vaccine against the human cytomegalovirus (HCMV) has been ongoing for more than 50 years. HCMV is the leading infectious cause of birth defects, including damage to the brain, and is a common cause of complications in organ transplantation. The complex biology of HCMV has made vaccine development difficult, but a recent meeting sponsored by the National Institute of Allergy and Infectious Diseases in September of 2023 brought together experts from academia, industry, and federal agencies to discuss progress in the field.
View Article and Find Full Text PDFIn vivo self-assembled siRNAs within small extracellular vesicles attenuate LRRK2-induced neurodegeneration in Parkinson's disease models.
J Control Release
December 2024
Nanjing Drum Tower Hospital Center of Molecular Diagnostic and Therapy, State Key Laboratory of Pharmaceutical Biotechnology, Jiangsu Engineering Research Center for MicroRNA Biology and Biotechnology, NJU Advanced Institute of Life Sciences (NAILS), School of Life Sciences, Nanjing University, Nanjing, Jiangsu 210023, China; The Second People's Hospital of Changzhou, The Third Affiliated Hospital of Nanjing Medical University, Changzhou Medical Center, Nanjing Medical University, Changzhou, Jiangsu 213003, China. Electronic address:
Rationale: Mutations in the leucine-rich repeat kinase 2 (LRRK2) gene play an important role in Parkinson's disease (PD) pathogenesis, and downregulation of LRRK2 has become a promising therapy for PD. Here, we developed a synthetic biology strategy for the self-assembly and delivery of small interfering RNAs (siRNAs) of LRRK2 into the substantia nigra via small extracellular vesicles (sEVs) using a genetic circuit (in the form of naked DNA plasmid) to attenuate PD-like phenotypes in mouse model.
Methods: We generated the genetic circuit encoding both a neuron-targeting rabies virus glycoprotein (RVG) tag and a LRRK2 siRNA under the control of a cytomegalovirus (CMV) promoter, and assessed its therapeutic effects using LRRK2 mouse models of PD.
Optimization of antiviral dosing in Herpesviridae encephalitis: a promising approach to improve outcome?
Clin Microbiol Infect
December 2024
Institute of Medical Microbiology and Virology, University Medical Center, Göttingen, Germany.
Background: Despite established antiviral therapy for herpes simplex virus, varicella zoster and cytomegalovirus encephalitis, the outcome remains poor.
Objectives: To assess pharmacokinetic (PK) and pharmacodynamic (PD) data of antiviral drugs in the central nervous system (CNS) to optimize the treatment of Herpesviridae encephalitis.
Sources: PUBMED search 1950 to September 2024, terms (1) "encephalitis" and ("HSV" or "VZV" or "CMV") or (2) cerebrospinal and ("(val)acyclovir" or "(val)ganciclovir" or "foscarnet" or "cidofovir").
TRIM37 exacerbates cerebral ischemic injury by regulating the PPARγ/NF-κB pathway.
Neuroreport
February 2025
Department of Neurosurgery, the First Affiliated Hospital of Hainan Medical University, Haikou.
Ischemic stroke is the primary cause of mortality for individuals with disability worldwide. Tripartite motif 37 (TRIM37) plays multiple regulatory roles in various cellular processes. Our research aimed to investigate the effects of TRIM37 on the progression of ischemic stroke and its related mechanisms.
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