Effect of the Gv-1 locus on Moloney ecotropic murine leukemia virus induced disease in inbred wild mice.

Abstract

The nonacute retroviruses induce neoplastic disease following a long latency period. During this latency period, the infectious ecotropic murine leukemia virus (MuLV) spreads throughout the mouse resulting in chronic viremia. As the virus spreads, it recombines with germline copies, or proviruses, of nonecotropic MuLVs to produce infectious mink cell focus-forming (MCF) viruses. These MCF viruses resemble their ecotropic MuLV progenitors but contain novel sequences in their envelope (env) genes which encode the major virion glycoprotein, and in the long terminal repeats (LTRs) which contain transcriptional control signals. These recombinant viruses have an expanded host range and are themselves leukemogenic. The mechanisms involved in the production of MCF viruses are unknown, although it has been established that multiple recombinations occur, and novel viruses have been isolated from preleukemic tissues which may represent intermediate recombinants in this process (Cloyd and Chattopadhyay 1986) . Proviral sequences related to both the xenotropic and MCF host range classes of infectious MuLVs ultimately contribute to the altered env and LTR regions of the MCF virus (Holland et al. 1985; Quint et al. 1984) . Although the specific proviruses involved in this process have not been identified, it has been suggested that the xenotropic provirus Bxv-1 contributes LTR sequences to the leukemogenic MCF MuLV (Hoggan et al. 1986) .KeywordsMurine Leukemia VirusWild MouseProviral SequenceExpand Host RangeGermline CopyThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.