By T. C. Pierson, R. W. Doms (auth.), John A. T. Young (eds.)
The articles during this quantity offer a accomplished evaluation of our present realizing of the jobs performed through mobile elements within the early steps of retroviral replication. a greater realizing of those services will supply severe new insights into retrovirus-host mobile interactions and is probably going to turn out important for the longer term improvement of potent antiretroviral therapies.
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Additional info for Cellular Factors Involved in Early Steps of Retroviral Replication
7 Host Range Control of g-Retrovirus Entry into Cells . . . Previous Hypotheses and Recent Alternative Interpretations. Mouse CAT1, the Receptor for Ecotropic MuLVs . . . . Pit 1 and Pit 2 Receptors . . . . . . . . . . . Xenotropic and Polytropic MuLVs . . . . . . . . The RD114 Superfamily of Retroviruses . . . . . . The FeLV-C Receptor. . . . . . . . . . . . A Pair of PERV-A Receptors . . . . . . . . . . . . . . 3 The Role(s) of Receptors in g-Retrovirus Infections.
E-MLV uses a cationic amino acid transporter of mice (mCAT-1) as a receptor, whereas FeLV-B, GALV, A-MLV and 10A1-MLV use the sodium-dependent phosphate symporters Pit1 and/or Pit2. The large group of retroviruses that include RD114, BaEV, HERV-W and type D simian retroviruses (SRVs) use the neutral amino acid transporter, ASCT2. Recent studies showed that BaEV and HERV-W can also use the related neutral amino acid transporter ASCT1 as a receptor. The normal cellular functions of the receptors for X-MLV/P-MLV (X-receptor) and for FeLV-C (FLVCR1) are unknown.
2000; Donahue et al. 1991; Herr and Gilbert 1984; Kristal et al. 1993; Lauring et al. 2001; Marin et al. 1999; Reinhart et al. 1993; Temin 1988; Yoshimura et al. 2001). We emphasize this because pathogenic variants of different animal viruses have often been associated with abilities to bind to apparently novel cell surface components and it has sometimes been inferred that the viruses have switched their receptor specificities. In these instances it has generally not been established that the cell surface binding components are receptors that directly mediate infections.