The replication and spread of viral infections in the human host occurs by a variety of mechanisms. Replication of genetic sequences varies with the initial starting material (DNA or RNA). Proliferation in the host may be by direct cell-to-cell spread, cell lysis, or budding from the infected cell's membrane. Various viremic or localized stages have been demonstrated. Particular tropisms are thought to be due to the presence of particular receptors. Recent advances in molecular biology, which will be reviewed, have expanded our capacity to detect the genetic footprints of viruses, and our understanding of viral pathogenesis. The host immune system must be prepared for an array of mechanisms to prevent or ameliorate virus infection. These may take the form of specific and nonspecific antibody formation, or the generation of specific cytotoxic lymphocytes that are restricted by the HLA system. In addition, nonspecific mediators, such as the complement system, interferon, and other lymphokines, play a significant role in the pathogenesis of viral infections. While the greatest portion of these cellular efforts are aimed at the destruction or elimination of viral infection, the immune response may augment the pathogenic effect under some circumstances. The formation of immune complexes may also contribute to the pathogenesis of some infections.