VZV: molecular basis of persistence (latency and reactivation)
- PMID: 21348068
- Bookshelf ID: NBK47371
VZV: molecular basis of persistence (latency and reactivation)
Excerpt
Primary infection with varicella-zoster virus (VZV) causes varicella manifested by fever and a vesicular rash. During primary infection the virus disseminates in lymphocytes to the skin and other organs, and replicates in and establishes a latent infection in the nervous system (Croen et al., 1988). Early studies demonstrated viral DNA in human trigeminal and dorsal root ganglia by in situ hybridization and Southern blotting (Gilden et al., , ; Hyman et al., 1983). More recent studies, using PCR, have demonstrated latent VZV in multiple cranial nerve, dorsal root, and autonomic ganglia (Furuta et al., , ; Gilden et al., ; Mahalingham et al., 1990). The virus can reactivate from these sites to cause herpes zoster.
Copyright © Cambridge University Press 2007.
Sections
- Site of VZV latency
- Quantification of VZV DNA load during latency
- Animal models for VZV latency
- VZV transcripts expressed during latency
- VZV proteins expressed during latency
- Function of VZV latency-associated proteins
- VZV genes required for establishment of latent infection
- In vitro models for VZV latency
- Reactivation of VZV
- Comparison of VZV latency with that of other alphaherpesviruses
- Is the large number of transcripts in VZV latency due to reactivation?
- Models for VZV latency
- VZV proteins localize to the cytoplasm, instead of the nucleus of neurons and thus are unable to carry out their activities
- VZV proteins have different activities in neurons than in permissive cells due to differences in cellular proteins
- Future directions
- References
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