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The study of 'molecular mimicry' or 'genetic piracy', with respect to the utilisation of cellular genes captured and modified during the course of virus evolution, has been an area of increasing research with the expansion in virus genome sequencing. Examples of cellular immunomodulatory genes which have been captured from hosts have been identified in a number of viruses. This review concentrates upon studies of murine cytomegalovirus (MCMV), investigating the functions of viral genes homologous to G protein-coupled receptors, MHC class I and chemokines. The study of recombinant MCMV engineered with specific disruptions of these genes has revealed their significance during virus replication and dissemination within the host. In the case of the latter two classes of genes, evidence suggests they interfere with cellular immune responses, although the detailed mechanisms underlying this interference have yet to be delineated., (Copyright 2000 S. Karger AG, Basel.)

High levels of natural cytotoxicity were detected in vitro in cells from the lung interstitium of the rat following collagenase digestion of lung tissue. In contrast, alveolar cells exhibited negligible levels of natural cytotoxicity and furthermore suppressed the natural cytotoxicity of interstitial lung leukocytes. This suppression was alleviated following in vivo administration of indomethacin. The natural cytotoxicity of cells from both the lung and spleen was transiently suppressed following exposure of normal rats to aerosols of Escherichia coli lipopolysaccharide or of ovalbumin-sensitized rats to an ovalbumin aerosol. Parenchymal lung leukocytes, like those from the spleen and peripheral blood, showed enhanced cytotoxicity when treated with interferon in vitro. In addition interstitial leukocytes were capable of producing interferon when cocultured with P815 cells and, as was the case with the spleen, low density cells produced the most interferon. However, alveolar cells did not produce interferon in this system. These studies suggest that the lung is capable of self-regulation of the high levels of natural cytotoxicity present in interstitial tissue; alveolar cells or their products may suppress interstitial natural killer cells whilst interstitial leukocytes have the capacity to stimulate natural killer cells by producing interferon.