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Unraveling the links between neurodegeneration and Epstein-Barr virus-mediated cell cycle dysregulation.
Tiwari, Deeksha; Mittal, Nitish; Jha, Hem Chandra.
Afiliación
  • Tiwari D; Department of Biosciences and Biomedical Engineering, Indian Institute of Technology Indore, India.
  • Mittal N; Computational and Systems Biology, Biozentrum, University of Basel, Klingelbergstrasse 50-70, 4056, Basel, Switzerland.
  • Jha HC; Department of Biosciences and Biomedical Engineering, Indian Institute of Technology Indore, India.
Curr Res Neurobiol ; 3: 100046, 2022.
Article en En | MEDLINE | ID: mdl-36685766
ABSTRACT
The Epstein-Barr virus is a well-known cell cycle modulator. To establish successful infection in the host, EBV alters the cell cycle at multiple steps via antigens such as EBNAs, LMPs, and certain other EBV-encoded transcripts. Interestingly, several recent studies have indicated the possibility of EBV's neurotrophic potential. However, the effects and outcomes of EBV infection in the CNS are under-explored. Additionally, more and more epidemiological evidence implicates the cell-cycle dysregulation in neurodegeneration. Numerous hypotheses which describe the triggers that force post-mitotic neurons to re-enter the cell cycle are prevalent. Apart from the known genetic and epigenetic factors responsible, several reports have shown the association of microbial infections with neurodegenerative pathology. Although, studies implicating the herpesvirus family members in neurodegeneration exist, the involvement of Epstein-Barr virus (EBV), in particular, is under-evaluated. Interestingly, a few clinical studies have reported patients of AD or PD to be seropositive for EBV. Based on the findings mentioned above, in this review, we propose that EBV infection in neurons could drive it towards neurodegeneration through dysregulation of cell-cycle events and induction of apoptosis.
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Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Idioma: En Revista: Curr Res Neurobiol Año: 2022 Tipo del documento: Article País de afiliación: India

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Idioma: En Revista: Curr Res Neurobiol Año: 2022 Tipo del documento: Article País de afiliación: India