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Retroviruses are ubiquitous agents present in wild mice as well as inbred laboratory mice. They occur as endogenous proviruses and are transmitted vertically through the germ line ceils (1, 2). Although they are present in the DNA of all the cells in the form of integrated provirus, their regulation is under strict control and they are strongly repressed in most tissues. These viruses, however, can be expressed naturally late in life in mice with certain genetic dispositions (3, 4). Their expression, though, is under genetic and developmental control and is often confined to the hemopoietic tissues, notably the cells in the bone marrow, spleen, and the thymus (2, 5-7). The expression of these viruses and their genes in these mice in some cases is associated with a variety of hemopoietic disorders such as autoimmune disease (8), lymphomas, and leukemias (3, 4). In some instances, infectious retroviruses have been recovered from these diseased animals, and these are capable of inducing hemopoietic aberrations similar to those in the diseased mice from which the viruses were isolated (5, 911). Viral induced modification of hemopoietic differentiation is thus well established. To understand the relationship between normal and virally induced hemopoietic differentiation and the genetic control of these processes, much effort has been devoted to the in vitro and in vivo studies of these events. The best-studied viral modified hemopoietic system is probably Friend erythroleukemia. Friend erythroleukemia virus (FLV), 1 isolated in 1957 by Charlotte Friend (9), is a complex of two viruses, a replication-defective, erythroleukemia-inducing, spleen focus-forming virus (SFFV) (12) and a replication-independent leukemia virus (F-MuLV) that provides the necessary function for SFFV to complete its replicative cycle (13, 14). Subsequent to infection with FLV, susceptible adult and newborn mice develop very rapid (1-3 wk) erythropoietic changes including splenomegaly (9, 15) and development of anemia or polycythemia, depending on whether the anemia strain (FV-A) (9) or the polycythemia strain (FV-P) (16) is used. This induction of early polycythemia by FV-P, however, has recently been shown to be mouse strain dependent (16), for whereas severe polycythemia is induced early in the mouse strains DBA/2, BALB/c, and AKR, rapid anemia is induced in mouse strains CBA and C3H (16).

Modulation of erythropoiesis by the helper-independent Friend leukemia virus F-MuLV.