Varicella zoster virus immunity: A primer.
Christopher J A Duncan1, Sophie Hambleton2
1Primary Immunodeficiency Group, Institute of Cellular Medicine, 4th Floor Catherine Cookson Building, Newcastle University, Medical School, Newcastle Upon Tyne, NE2 4HH, UK; Department of Infection & Tropical Medicine, Royal Victoria Infirmary, Newcastle Upon Tyne, NE1 4LP, UK.
The Journal of Infection
|April 29, 2015
Summary
Varicella zoster virus (VZV) causes chickenpox and shingles. Innate and cellular immunity, not just antibodies, are key to limiting VZV infection severity and duration, guiding future prevention strategies.
Area of Science:
- Virology
- Immunology
- Epidemiology
Background:
- Varicella zoster virus (VZV) causes widespread human infections, including varicella (chickenpox) and shingles.
- VZV is the only herpesvirus with widely implemented vaccines, impacting its epidemiology.
- The immunological basis of protection against VZV remains unclear.
Purpose of the Study:
- To review evidence defining immunologic risk factors for severe VZV disease.
- To identify key elements of VZV immunity for prevention and treatment strategies.
Main Methods:
- Overview of evidence from animal models.
- Analysis of observational studies on VZV infection.
Main Results:
- Circulating VZV-specific antibodies can prevent primary infection.
- Innate and cellular immune responses are crucial for limiting VZV infection severity and duration.
- Understanding these factors can inform better VZV management.
Conclusions:
- Immune responses beyond antibodies are critical for controlling VZV.
- Targeting innate and cellular immunity may improve VZV prevention and treatment.
- Further research into VZV immunological correlates is warranted.
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