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Understanding the pathogenesis of HSV-associated erythema multiforme
L Aurelian1, H Kokuba, J W Burnett
1Virology/Immunology Laboratories, Department of Pharmacology & Experimental Therapeutics, University of Maryland, School of Medicine, Baltimore, Md., USA. Laurelia@umaryland.edu
Dermatology (Basel, Switzerland)
|November 13, 1998
Summary
Herpes simplex virus-associated erythema multiforme (HAEM) may stem from viral protein effects and immune responses to herpes simplex virus (HSV) antigens. This pathogenesis involves viral DNA and proteins triggering an inflammatory cascade in the skin.
Area of Science:
- Dermatology
- Virology
- Immunology
Background:
- Erythema multiforme (EM) is a polymorphic skin eruption frequently linked to infections, particularly herpes simplex virus (HSV).
- Understanding the pathogenesis of HSV-associated EM (HAEM) is crucial for effective patient management.
- Current understanding necessitates a deeper dive into the interplay between viral factors and host immune responses.
Purpose of the Study:
- To elucidate the combined viropathic and immunological mechanisms underlying HSV-associated EM (HAEM).
- To propose a model for HAEM pathogenesis involving HSV proteins and T-cell mediated immune responses.
- To review evidence supporting the proposed pathogenesis and identify factors influencing HAEM recurrence and severity.
Main Methods:
- Review of existing scientific literature and evidence.
- Analysis of proposed mechanisms involving viral proteins (e.g., DNA polymerase) and immune cells (macrophages, T cells).
- Identification of host and viral factors potentially modulating HAEM presentation.
Main Results:
- HAEM is hypothesized to result from HSV DNA polymerase (Pol) effects combined with an immune reaction to HSV antigens.
- Viral DNA and proteins are processed by macrophages and presented to T cells, leading to T-cell activation and recruitment to HSV-expressing skin sites.
- An inflammatory cascade is generated, potentially influenced by specific HSV genes, capillary dynamics, and environmental factors.
Conclusions:
- The pathogenesis of HAEM likely involves a dual mechanism of viropathic effects and immune responses to HSV.
- Factors such as HSV gene identity, cutaneous microvasculature, and temperature may influence HAEM's clinical presentation and recurrence.
- Further research into these mechanisms can guide improved management strategies for HAEM.