PubMed · 14036382
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G M HOWARD, H E KAUFMAN. 1962. Herpes simplex keratitis.. https://doi.org/10.1001/archopht.1962.00960020375013
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During the first decade after the discovery of primary effusion lymphoma (PEL), sporadic and serial reports suggested that Kaposi-sarcoma-associated-herpesvirus/human-herpesvirus-8 (KSHV/HHV-8)-associated lymphomas in their liquid and solid presentation are clinically distinct, representing part of the spectrum of PEL. In HIV-seropositive patients with serous effusions, these solid lymphomas were reported before the development of an effusion lymphoma and following resolution of PEL. More recently, solid lymphomas not associated with lymphomatous effusion have been found in HIV-seropositive and HIV-seronegative patients. Despite the diversification in the clinical presentation of KSHV/HHV-8-associated lymphomas, most cases demonstrated a similar morphology, immunophenotype and KSHV/HHV-8 viral status.
BACKGROUND: Accurate numbers of copies of Kaposi sarcoma-associated herpesvirus (KSHV) and numbers of virus-infected cells in lesions caused by KSHV-associated diseases are unknown. METHODS: Quantitative polymerase chain reaction (PCR) and computerized imaging of immunohistochemical analysis were performed on pathologic sections of samples from persons with KSHV-associated diseases. RESULTS: Real-time PCR and semiquantitative PCR-Southern blotting demonstrated that DNA extracted from biopsy samples of KS lesions contained approximately 1-2 viral copies/cell. KSHV-associated lymphoma contained 10-50 viral copies/cell. Computerized-image analysis demonstrated that approximately 49% of cells expressed KSHV-encoded latency-associated nuclear antigen in KS biopsy samples. On the basis of results of real-time PCR and computerized-image analysis, the predicted number of viral copies was 3.2 viral copies/cell in KS lesions. Computerized-image analysis also revealed that the expression of open-reading frame (ORF)-50 protein, an immediate early protein of KSHV, was very rare in KS lesions, which implies that they were mainly composed of proliferating cells latently infected with KSHV. In multicentric Castleman disease lesions, 25% of virus-infected cells expressed ORF50 protein, which suggests the frequent lytic replication of KSHV. CONCLUSIONS: Numbers of viral copies and of virus-positive cells vary among KSHV-associated diseases, which suggests different mechanisms of viral pathogenesis. The combination of real-time PCR and computerized-image analysis provides a useful tool for the assessment of the number of viral copies in KSHV-associated diseases.
The role of viral infection in the etiology of febrile seizures is a relatively neglected field of neurologic research. A National Institutes of Health Consensus Conference (1981) omitted reference to causes of infections and the role of fever in febrile seizures, and emphasized outcome and anticonvulsant treatment. In an earlier review of the world literature (1924-1964), except for roseola infantum, viral infections as a cause of febrile seizures were rarely diagnosed. The present review includes reports of viruses most commonly associated with febrile seizures in the last decade, especially human herpesvirus-6 and influenza. The specificity and neurotropic properties of some viruses in the febrile seizure mechanism, a possible encephalitic or encephalopathic pathology, and the essential role of fever and height of the body temperature as a measure of the febrile seizure threshold are discussed. Cytokine and immune response to infection, and a genetic susceptibility to febrile seizures are additional etiologic factors. Future research should emphasize early detection of causative viruses, the nature of viral neurotropism, and the role of cytokines in fever induction. Trials of antiviral agents and vaccines, with attention to safety concerns, and more effective antipyretics would address the febrile seizure mechanism more specifically than anticonvulsant therapies.