Varicella zoster virus infection.
Anne A Gershon1, Judith Breuer2, Jeffrey I Cohen3
1Columbia University College of Physicians and Surgeons, 630 West 168th Street, New York, New York 10032, USA.
Nature Reviews. Disease Primers
|May 19, 2016
Summary
Varicella zoster virus (VZV) causes chickenpox and shingles. While immunity develops after infection or vaccination, it doesn't prevent reactivation, necessitating distinct vaccines for chickenpox and shingles prevention.
Area of Science:
- Virology
- Immunology
- Neurology
Background:
- Varicella zoster virus (VZV) causes chickenpox (varicella) and shingles (zoster).
- VZV establishes latency after primary infection, with potential for reactivation causing severe complications like postherpetic neuralgia.
- Complications of VZV reactivation include myelitis, meningitis, stroke, and various organ-specific infections.
Purpose of the Study:
- To review the pathogenesis, diagnosis, treatment, and prevention of VZV infections.
- To emphasize the molecular mechanisms underlying VZV-related diseases.
- To discuss the limitations of current immunity in preventing VZV reactivation.
Main Methods:
- Literature review and synthesis of current knowledge on VZV.
- Analysis of molecular events regulating VZV pathogenesis and latency.
- Discussion of diagnostic and therapeutic strategies for VZV infections.
Main Results:
- VZV latency is established post-primary infection, but immunity does not prevent reactivation.
- Reactivation leads to zoster and potentially severe neurological and systemic complications.
- Two distinct vaccines exist: one for varicella prevention and another for zoster prevention.
Conclusions:
- Understanding VZV molecular pathogenesis is crucial for managing its diverse clinical manifestations.
- Current vaccines effectively prevent varicella but not reactivation; zoster vaccines target reactivation.
- Further research into VZV pathogenesis may improve treatment and prevention strategies for VZV-related diseases.
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