Infection of humans with Epstein-Barr virus (EBV) may cause infectious mononucleosis (IM). Analysis of single EBV-infected cells from tonsils of IM patients for rearranged immunoglobulin genes revealed two strategies of EBV for rapid and massive spread in the B cell compartment: the direct infection of many naive as well as memory and/or germinal center B cells and the expansion of the latter cells to large clones. In IM, the generation of virus-harboring memory B cells from naive B cells passing through a germinal center reaction likely plays no role. Members of clones can show distinct morphologies and likely also EBV gene expression patterns, and this ability implies a mechanism by which EBV-harboring cells can evade immune surveillance and establish a pool of persisting EBV-infected B cells.

Myoepithelial and luminal cells of human exocrine glands can be positively identified with two different monoclonal antibodies. Myoepithelial cells including those of the salivary gland, mammary gland and sweat gland are positively identified by an antibody CKB1. This antibody does not stain luminal cells, but stains the basal cell layer of certain human stratified epithelia and a few basal cells in simple epithelia. Thus myoepithelial cells and basal cells have certain common features. Luminal cells can be positively stained with the CK5 monoclonal keratin antibody specific for keratin polypeptide 18; this antibody does not stain myoepithelial cells. Of interest is that CKB1 also appears to stain basal and suprabasal cells in certain hyperplastic conditions.

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We report three adenomatous middle-ear tumours, an adenoma, an adenocarcinoma and a semimalignant adenomatous tumour, with special attention to CT and MRI findings. In all cases we found small intratympanic masses in which the ossicles were embedded. All showed contrast enhancement and similar signal intensity as brain tissue on T1- and T2-weighted images. The biological nature of the tumours was not reflected by the imaging or operative findings.