We studied 3231 patients with acute central nervous system (CNS) symptoms of suspected viral origin to elucidate the current etiologic spectrum. In 46% of the cases, a viral finding was observed. Varicella-zoster virus (VZV) was the main agent associated with encephalitis, as well as meningitis and myelitis. VZV comprised 29% of all confirmed or probable etiologic agents. Herpes simplex virus (HSV) and enteroviruses accounted 11% each, and influenza A virus 7%. VZV seems to have achieved a major role in viral infections of CNS. In encephalitis in our population, VZV is clearly more commonly associated with these neurological diseases than HSV. The increase in VZV findings may in part be a pseudophenomenon due to improved diagnostic methods, however, a true increase may have occurred and the pathogenetic mechanisms behind this should be elucidated.

Binding and pinocytosis of polyvalent IgG-containing immune complexes by mouse macrophages leads to the selective removal of Fc receptors (FcR) from the cell surface and to the rapid delivery of receptor and ligand to lysosomes, where both are degraded (I . Mellman and H. Plutner, 1984, journal of Cell Biology, 98:1170-1177. In this paper, we have studied the internalization of FcR tagged with a monovalent probe that, unlike IgG-complexes, cannot cross-link adjacent receptors . We have used an Fab fragment of high affinity anti-FcR monoclonal antibody whose binding was completely sensitive to low pH (4.0) at 4°C. Thus, surfacebound (acid-releasable) and intracellular (acid-resistant) '251-Fab could be readily distinguished . Incubation of )774 macrophages with 125 1-Fab at 37°C did not lead to the accumulation of large amounts of the antibody in the acid-resistant compartment . After 3 h, only 20% of the total cell-associated radiolabel was intracellular . The internalized '251-Fab was also shown by Percoll gradient centrifugation to be associated primarily with low density endosomes, as opposed to lysosomes. Significantly, most of the labeled antibody returned rapidly to the plasma membrane, still bound to FcR. This recycling was complete within 10 min, was unaffected by NH4CI, and was only slightly inhibited by the Na'-H' ionophore monensin .These results indicate that monovalent Fab-FcR complexes are internalized, delivered to endosomes, and rapidly returned to the cell surface . Since the internalization of polyvalent IgG-complexes removed the FcR from this recycling pathway and caused its transport to lysosomes, we suggest that the state of receptor aggregation in the endosome membrane helps determine its intracellular fate.Although endocytosis in animal cells isgenerally accompanied by the return (or recycling) ofinternalized plasma membrane to the cell surface, several plasma membrane receptors are known whose activities are largely if not irreversibly removed from the cell surface during ligand uptake (1). Classically, this phenomenon is illustrated by the "down regulation" ofreceptors for certain polypeptide hormones (e.g., insulin, epidermal growth factor) in cells exposed to hormone . In most cases, the mechanism of receptor loss is unknown. One well-studied example, however, is the mouse macrophage receptor for the Fc domain of immunoglobulin G (IgG). The Fc receptor

The spectrum of encephalitis in children has changed due to vaccination programs. The incidence, however, appears to be about the same due to increasing frequency of other associated old and new microbes.

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