The long term goal of this study is to understand the pathogenesis of the type of erythema multiforme designated EM minor. Since the discovery that the large majority of cases of EM minor are associated with herpes simplex virus [HSV], a novel hypothesis that the skin lesions of EM minor develop as a result of a HSV-specific immune response directed against virus within those sites in the skin has been developed. It was found that HSV nucleic acids may be present in healed skin lesions of EM minor, leading to the possibility of a latent virus state. In this study molecular virology techniques such as amplification of HSV specific nucleic acids by the polymerase chain reaction [PCR] will be used to examine important clinical questions regarding the pathogenesis of EM minor. The study will focus on the state of the virus within EM skin sites and we will attempt to detect latency associated transcripts [LATS] of herpes simplex virus. A model of herpes simplex virus latency in skin cells will be established. Strategies such as DNA fingerprinting by restriction enzyme analysis of herpes viral isolates and viral typing by PCR of blood and EM skin will be employed. Long-term viral co-culture strategies will be employed to obtain replicating virus from EM skin and from blood samples. These studies are designed to see if EM skin is a site of extraneuronal HSV latency and as a model for study of host-viral interactions.
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