Figure 1. Electron photomicrographs of replicating simian retroviruses in culture, showing the comparative structure of the following viruses; (a) simian immunodeficiency virus in CEMx174 cells; (b) simian T-cell lymphotropic virus in a cell line established from a seropositive baboon; (c) simian retrovirus in Raji cells; and (4) simian foamy virus growing in a human peripheral blood mononuclear cell culture. Courtesy of Eileen Breeding of the Yerkes Regional Primate Research Center (a–c) and Tom Folks and Cynthia Goldsmith of the Centers for Disease Control and Prevention (d).

Figure 2. Genomic structure of four simian retroviruses: simian retrovirus (SRV), simian T-cell lymphotropic virus (STLV), simian immunodeficiency virus (SIV), and simian foamy virus (SFV), showing the known coding regions in the three different ribosomal reading frames. The scale at the bottom illustrates the varying length (kilobases, kb) of the different retroviruses.

Figure 3. Replication strategy of simian immunodeficiency virus (SIV) as a model for simian retroviruses. Initial binding of SIV is through the CD4 receptor on the surface of the cell. This binding triggers the exposure of the chemokine receptor-binding domain which allows entry of virus into the cell. Reverse transcription occurs inside the uncoated capsid, which then proceeds to the nucleus to deliver the double-stranded viral DNA (proviral DNA) to the host chromosome for integration. Transcription of integrated DNA (provirus) produces RNA species for protein production and genomic RNA for capsid assembly. Nonstructural proteins play a role in regulating further transcription and translation to produce structural proteins for virion assembly. Courtesy of Terri Gibson.