4 Cellular Receptors for Type C Retroviruses

Abstract

HOST RANGE OF MAMMALIAN TYPE C RETROVIRUSES IS DETERMINED BY RECEPTOR EXPRESSION
Studies in mice have identified inbred strains that inherit proviruses encoding type C retroviruses which are expressed during fetal development, resulting in persistent viremia. These mice develop leukemia within 8–12 months after birth as a consequence of virus-induced changes in the expression of host genes that regulate cell growth. An important step in the pathogenesis of virus-induced leukemia is the appearance of recombinant retroviruses that carry alterations in envelope and long terminal repeat (LTR) sequences which enhance virus replication in hematopoietic cells (Elder et al. 1977; Cloyd et al. 1980). These viruses were initially identified because they infect mink fibroblasts (Chattopadhyay et al. 1981Chattopadhyay et al. 1982), a property that distinguishes them from the ecotropic parent virus, which infects only rodent cells (DeLarco and Todaro 1976). In addition, two other groups of type C viruses (amphotropic [Hartley et al. 1976; Rasheed et al. 1976]; xenotropic [Levy 1973]) have been identified in mice that also infect cells of other mammals. Comparison of mouse type C retroviral (murine leukemia virus [MuLV]) proteins identified differences in their envelope proteins that correlated with the pattern of infection of mammalian cells (Battini et al. 1992), a finding confirmed by pseudotyping experiments. In studies in mouse NIH-3T3 fibroblasts, Rein and Schultz (1984) correlated this property with the capacity of MuLVs to establish superinfection interference. Previous studies had suggested that the block to superinfection results from loss of sites for virus attachment caused by binding of...