[The sinusoid wall of the liver in viral infections].
The elements of the "peri-sinusoidal functional complex" (i.e. non-hepatocytes, space of Disse, vascular pole of hepatocytes) can react to the presence of virus in the sinusoidal blood stream by retaining viruses, sometimes followed by viral proliferation, by reactive proliferation, or by degenerative changes in the cells which may culminate in cell death. Immune processes may be also activated or alternatively, there may be no response whatever to the viremia. In hepatitis B infection the principal changes are in the Kupffer cells and in the vascular pole of the hepatocytes. Along with immunologic responses there are proliferative and degenerative events in the Kupffer cells, which may deleteriously affect the sinusoidal cell membrane of the hepatocytes. These factors, as well as the receptor structure of these cell membranes, are regarded as responsible for the uptake of virus in the hepatocyte. Cytotoxic T-cells which have migrated to the region also play a role in the overall process. The point should be made, however, that these concepts are largely hypothetical and that hepatitis B virus particles have yet to be demonstrated in the peri-sinusoidal complex.
D000818:Animals; D006003:Glycogen / Q000032:analysis; D006509:Hepatitis B / Q000276:immunology / Q000473:pathology / Q000503:physiopathology*; D006801:Humans; D002479:Inclusion Bodies; D007425:Intracellular Membranes / Q000648:ultrastructure; D007728:Kupffer Cells / Q000648:ultrastructure; D008099:Liver / Q000098:blood supply / Q000166:cytology / Q000648:ultrastructure*; D051379:Mice; D008854:Microscopy, Electron; D008871:Microvilli / Q000648:ultrastructure; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology
D006003:Glycogen
Die Sinusoidwand der Leber bei Virusinfektionen.