Important note: Information in this article was accurate in 1987. The state of the art may have changed since the publication date.
PATHOGENESIS OF MURINE RETROVIRAL INFECTIONS
Animal Models of Retrovirus Infection and Their Relationship to AIDS. Salzman LA, ed. Orlando, Florida, Academic Press, p. 193-202, 1986.. Unique Identifier : AIDSLINE ICDB/87629276 Yetter RA; Hartley JW; Fredrickson TN; Morse HC III; Lab. of Immunopathology, Natl. Inst. of Allergy and Infectious; Diseases, NIH, Bethesda, MD
Abstract:
Abnormalities that are induced in mice by murine leukemia viruses (MuLVs) are the result of integrations of the viruses into the genomes of the mice. These integrations may take place in either the germ cell or the somatic cell. Pathogenic mechanisms in MuLV systems are briefly reviewed at the beginning of this chapter. Next, the authors turn to a system that they have been working with in their laboratory, involving a variant of the Duplan-Laterjet (DL) virus. This virus induces a polyclonal lymphoproliferative disease that is associated with hypergammaglobulinemia and profound immunosuppression. The DL virus differs from most other radiation leukemia viruses in that the latter require neonatal inoculation and result in thymic lymphomas, whereas DL virus can be transmitted by inoculation of both neonates and adults and has been associated with non-T cell lymphomas in C57BL/6 mice. The DL-induced disease in the susceptible B6 mouse presents as massive lymphadenopathy and splenomegaly. In studies by Haas, the tumors were passed several times through B6 mice by inoculation with cell-free filtrates, and a bone stromal cell line, called RCN-BM5, was derived. Lymphoproliferative disease is induced by injection of filtered culture supernatants of the RCN-BM5 cell line, which contain b-tropic viruses, MCF virus, ecotropic virus, and pseudotypes of both virions. Strain distribution of sensitivity to lymphoproliferative disease induced by the BM5 virus is shown in a table. Time course of the disease in three strains of mice (C57BL/6, BDP, and BALb/c) is shown in a figure. Observations have demonstrated that the disease is a non-neoplastic polyclonal proliferation of B immunoblasts. The susceptibility of various mouse strains to this disease indicates that Fv-1 and Rmcf are not playing the roles that would be expected of them in the modification of the disease. There is some other gene or genes that affects the outcome of the infection. This disease can be induced in both neonates and adults of susceptible strains, which makes the system amenable to studies of vaccine intervention in lymphoproliferative and immunosuppressive disease.
Keywords: Animal Disease Susceptibility Immune Tolerance Leukemia Viruses, Murine/GENETICS/*PATHOGENICITY Leukemia, Experimental/MICROBIOLOGY/PHYSIOPATHOLOGY Mice Mice, Inbred Strains Myeloproliferative Disorders/MICROBIOLOGY/*PHYSIOPATHOLOGY Oncogenes Recombination, Genetic Species Specificity Transduction, Genetic Virus Replication MONOGRAPH
AEGiS presents published material, reprinted with permission and neither endorses nor opposes any material. All information contained on this website, including information relating to health conditions, products, and treatments, is for informational purposes only. It is often presented in summary or aggregate form. It is not meant to be a substitute for the advice provided by your own physician or other medical professionals. Always discuss treatment options with a doctor who specializes in treating HIV.
Important note: Information in this article was accurate in 1987. The state of the art may have changed since the publication date.
