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Updated: May 21, 2026

Ex Vivo Infection of Murine Epidermis with Herpes Simplex Virus Type 1
Published on: August 24, 2015
Herpes simplex virus and varicella zoster virus, the house guests who never leave
Paul R Kinchington1, Anthony J St Leger, Jean-Marc G Guedon
1Department of Ophthalmology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA. Hendricksrr@upmc.edu.
Abstract:
Human alphaherpesviruses including herpes simplex viruses (HSV-1, HSV-2) and varicella zoster virus (VZV) establish persistent latent infection in sensory neurons for the life of the host. All three viruses have the potential to reactivate causing recurrent disease. Regardless of the homology between the different virus strains, the three viruses are characterized by varying pathologies. This review will highlight the differences in infection pattern, immune response, and pathogenesis associated with HSV-1 and VZV.
Insights
Human alphaherpesviruses like herpes simplex virus (HSV-1, HSV-2) and varicella zoster virus (VZV) cause lifelong latent infections. This review contrasts HSV-1 and VZV infection patterns, immune responses, and pathogenesis.
Area of Science:
- Virology
- Immunology
- Neuroscience
Background:
- Human alphaherpesviruses, including herpes simplex viruses (HSV-1, HSV-2) and varicella zoster virus (VZV), establish persistent latent infections in sensory neurons.
- These viruses can reactivate, leading to recurrent diseases with distinct pathologies despite genetic similarities.
- Understanding these differences is crucial for managing viral infections and developing targeted therapies.
Purpose of the Study:
- To review and highlight the key differences in infection patterns between HSV-1 and VZV.
- To compare the host immune responses elicited by HSV-1 and VZV infections.
- To elucidate the distinct pathogenetic mechanisms underlying HSV-1 and VZV diseases.
Main Methods:
- Literature review of existing studies on HSV-1 and VZV.
- Comparative analysis of viral infection dynamics, latency establishment, and reactivation.
- Synthesis of data on cellular and humoral immune responses to each virus.
- Examination of pathobiological mechanisms leading to clinical manifestations.
Main Results:
- HSV-1 and VZV exhibit differential tropism and latency sites within the nervous system.
- Distinct immune evasion strategies and inflammatory responses are associated with HSV-1 and VZV.
- Pathologies arising from HSV-1 and VZV infections vary significantly in clinical presentation and severity.
Conclusions:
- HSV-1 and VZV, while related, display unique characteristics in their interaction with the host.
- Differences in infection patterns, immune responses, and pathogenesis necessitate distinct clinical management approaches.
- Further research into these specific viral attributes can inform the development of novel antiviral strategies.
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