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Use of In vivo Imaging to Monitor the Progression of Experimental Mouse Cytomegalovirus Infection in Neonates
Published on: July 6, 2013
Neuropathogenesis in cytomegalovirus infection: indication of the mechanisms using mouse models
Yoshihiro Tsutsui1, Isao Kosugi, Hideya Kawasaki
1Department of Pathology, Hamamatsu University School of Medicine, 1-20-1 Handayama, Hamamatsu 431-3192, Japan. ytsutsui@hama-med.ac.jp
Abstract:
Cytomegalovirus (CMV) is the most frequent infectious cause of developmental brain disorders and also causes brain damage in immunocompromised individuals. Although the brain is one of the main targets of CMV infection, little is known about the neuropathogenesis of the brain disorders caused by CMV in humans because of the limitations in studying human subjects. Murine CMV (MCMV) is similar to human CMV (HCMV) in terms of genome structure, pattern of gene expressions, cell tropism and infectious dynamics. In mouse models, it has been shown that neural stem/progenitor cells are the most susceptible to CMV infection in developing brains. During brain development, lytic infection tends to occur in immature glial cells, presumably causing structural disorders of the brain. In the prolonged phase of infection, CMV preferentially infects neuronal cells. Infection of neurons may tend to become persistent by evasion of immune reactions, anti-apoptotic effects and neuron-specific activation of the e1-promoter, presumably causing functional neuronal disorders. It has also been shown that CMV infection in developing brains may become latent in neural immature cells. Brain disorders may occur long after infection by reactivation of the latent infection.
Insights
Cytomegalovirus (CMV) causes developmental brain disorders by infecting neural stem cells and neurons. This infection can lead to structural and functional brain damage, with potential for long-term effects from latent infections.
Area of Science:
- Neuroscience
- Virology
- Developmental Biology
Background:
- Cytomegalovirus (CMV) is a primary cause of congenital brain damage.
- Human CMV (HCMV) neuropathogenesis is poorly understood due to study limitations.
- Murine CMV (MCMV) serves as a relevant model for HCMV infection dynamics.
Purpose of the Study:
- To elucidate the neuropathogenesis of CMV infection in developing brains.
- To understand how CMV infection leads to structural and functional brain disorders.
- To investigate the role of latent CMV infection in long-term neurological consequences.
Main Methods:
- Utilized mouse models (MCMV) to study CMV infection in developing brains.
- Examined susceptibility of neural stem/progenitor cells to CMV.
- Investigated CMV infection patterns in glial and neuronal cells during different infection phases.
Main Results:
- Neural stem/progenitor cells are highly susceptible to CMV in developing brains.
- Lytic CMV infection primarily targets immature glial cells, potentially causing structural brain issues.
- Prolonged infection involves neuronal cell tropism, leading to functional disorders via immune evasion and specific promoter activation.
- CMV can establish latent infections in immature neural cells, with potential for later reactivation and brain disorder development.
Conclusions:
- CMV infection profoundly impacts developing brain structures and functions.
- Both lytic and latent phases of CMV infection contribute to neuropathogenesis.
- Understanding CMV neuropathogenesis is crucial for addressing developmental brain disorders and neurological complications in immunocompromised individuals.
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