Cytomegalovirus (CMV) strain AD-169 replicated in smooth muscle cell (SMC) cultures derived from human umbilical arteries, producing enveloped infectious virions. However, unlike the effects of CMV on fully permissive human lung fibroblasts, the effects of strain AD-169 on SMC cultures were delayed and prolonged, resulting in extended survival of a fraction of the starting population. This period of survival did not exceed the lifespan of the control SMC cultures. Infectious CMV continued to be isolated from the surviving SMC cultures after extinction of the original inoculum by dilution and after treatment of the cultures with CMV neutralizing antibody. The implications of these findings for the pathogenesis of atherosclerosis are discussed.
The addition of tegument or matrix proteins and the outermost membrane to human cytomegalovirus (strain AD 169) replicating in human cells appeared to occur differently in the nucleus than in the cytoplasm. In the nucleus cytomegalovirus was completed structurally within intranuclear sacs, as envelopment at the end of tubular structures, containing an electron-dense material, included tegument and outer membrane simultaneously. In the cytoplasm structural completion occurred in separate steps. Tegument could be added by association with dense bodies; then, interaction with the membranes of vacuoles or vesicles provided the outermost covering. Tubes originating in intranuclear sacs have been described previously only in guinea pig cells infected with guinea pig cytomegalovirus.
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