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Cytokines in experimental herpes simplex virus infection
Veijo Hukkanen1, Eeva Broberg, Aimo Salmi
1Department of Virology, University of Turku, Kiinamyllynkatu 13, FIN-20520 Turku, Finland. veijo.hukkanen@utu.fi
International Reviews of Immunology
|December 19, 2002
Summary
This review examines how Th1 and Th2 cytokines influence herpes simplex virus (HSV) infections. Understanding these cytokine roles is crucial for developing new gene therapies targeting HSV.
Area of Science:
- Immunology
- Virology
- Molecular Biology
Background:
- Herpes simplex virus (HSV) establishes both productive and latent infections in hosts.
- Immune responses involving macrophages, T lymphocytes (CD4+, CD8+), and B lymphocytes are activated during HSV infection and reactivation.
- Cytokine production, particularly proinflammatory and Th1-type cytokines, is a hallmark of acute and recurrent HSV phases, with Th2 cytokines also detected.
Purpose of the Study:
- To review the roles of specific Th1 and Th2 cytokines during various phases of experimental HSV infections.
- To explore how virus-encoded cytokine transgenes in gene therapy vectors might modulate host immune responses to HSV.
Main Methods:
- Literature review focusing on experimental studies of HSV infections.
- Analysis of cytokine expression patterns during different stages of HSV infection (acute, latent, recurrent).
- Examination of immune cell involvement and cytokine profiles in response to HSV.
Main Results:
- HSV infection elicits a strong immune response characterized by significant cytokine activity.
- Proinflammatory and Th1 cytokines dominate the response, but Th2 cytokines like interleukin-4 are also expressed.
- Cytokine expression is detectable even during the latent phase of HSV infection in sensory ganglia.
Conclusions:
- Cytokines play multifaceted roles throughout the course of HSV infection, influencing both acute and latent phases.
- Further research into cytokine modulation is essential for advancing HSV gene therapy strategies.
- Understanding the interplay between HSV and host cytokines is key to controlling viral pathogenesis and developing effective treatments.