ArticleThe American journal of pathology2003
Neuron-specific activation of murine cytomegalovirus early gene e1 promoter in transgenic mice.
Article in The American journal of pathology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 24 citations in OpenAlex.
- Unravelling the Viral Hypothesis of Schizophrenia: A Comprehensive Review of Mechanisms and Evidence.International journal of molecular sciences · 2025Review
- Review
- Prolonged activation of cytomegalovirus early gene e1-promoter exclusively in neurons during infection of the developing cerebrum.Acta neuropathologica communications · 2021Article
- Article
- Inhibition of Human Cytomegalovirus Entry into Host Cells Through a Pleiotropic Small Molecule.International journal of molecular sciences · 2020Article
- The 6-Aminoquinolone WC5 inhibits different functions of the immediate-early 2 (IE2) protein of human cytomegalovirus that are essential for viral replication.Antimicrobial agents and chemotherapy · 2014Article
- Aberrant fetal macrophage/microglial reactions to cytomegalovirus infection.Annals of clinical and translational neurology · 2014Article
- A short cis-acting motif in the M112-113 promoter region is essential for IE3 to activate M112-113 gene expression and is important for murine cytomegalovirus replication.Journal of virology · 2013Article
- Effects of rat cytomegalovirus on the nervous system of the early rat embryo.Virologica Sinica · 2012Article
- Persistent humoral immune responses in the CNS limit recovery of reactivated murine cytomegalovirus.PloS one · 2012Article
- Temporal profiling of the coding and noncoding murine cytomegalovirus transcriptomes.Journal of virology · 2011Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The brain is the main target in congenital cytomegalovirus (CMV) infection and immunocompromised patients. No definite evidence that a CMV has special affinity for the central nervous system (CNS) has been published. Here, we generated transgenic mice with an e1 promoter/enhancer region connected to the reporter gene lacZ. Surprisingly, expression of the transgene was completely restricted to the CNS in all lines of transgenic mice. The transgene was expressed in subpopulation of neurons in the cerebral cortex, hippocampus, diencephalon, brainstem, cerebellum, and spinal cord in all of the lines. Non-neuronal cells in the CNS were negative for transgene expression. Activation of the transgene was first observed in neurons of mesencephalon in late gestation, and then the number of positive neurons increased in various parts of the brain as development proceeded. Upon infection of the transgenic mouse brains with MCMV, the location of the activated neurons became more extensive, and the number of such neurons increased. These results suggest that there are host factor(s) that directly activate the MCMV early gene promoter in neurons. This neuron-specific activation may be associated with persistent infection in the brain and may be responsible for the neuronal dysfunction and neuronal cell loss caused by CMV infection.
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