Friend leukemia

About: Friend leukemia is a research topic. Over the lifetime, 319 publications have been published within this topic receiving 7463 citations.

Impeded progression of Friend disease in mice by an inhibitor of retroviral proteases.

Abstract: The protease of the human immunodeficiency virus type 1 (HIV-1) is essential for the processing of GAG and POL polyproteins and maturation of the virus particles. Using recombinant protease and a truncated GAG polyprotein as substrate, we developed a Western blot assay for the evaluation of inhibitors of the enzyme. Two statine-based inhibitors of the enzyme, KH161 and KH164, were effective in blocking the replication of HIV-1 in acutely infected human T4 lymphoid cells, with potency approaching that of zidovudine (ZDV) when tested in parallel. In chronically infected cells, the production of infectious virus was inhibited by KH161 and KH164, while ZDV was ineffective. Both KH161 and KH164 were also active as antivirals against the replication of murine leukemia virus (MLV) in cultured mouse cells. In an animal model of a murine retroviral disease, KH164 was shown to inhibit in a dose-dependent manner the progression of the disease induced by Friend virus complex (a mixture of Friend MLV and spleen focus-forming virus). The results suggest that the progression of the acquired immune deficiency syndrome (AIDS) may be impeded by inhibitors of HIV-1 protease.

Local and systemic response of mice to interferon-alpha 1-transfected Friend leukemia cells.

Abstract: DBA/2 mice were injected subcutaneously with an interferon (IFN)-alpha/beta-resistant line of Friend erythroleukemia cells (FLC) transfected with the mouse IFN-alpha 1 gene. These tumor cells produced IFN constitutively, and mice had persistently high levels of IFN in the circulation. We examined the IFN-induced host mechanisms responsible for the local inhibition of growth of these IFN-alpha-transfected FLC and some of the unusual systemic effects of constant interferonemia such as extramedullary hematopoiesis in the liver, an increase in myeloid cells in the spleen, and persistently elevated splenic natural killer (NK) cell activity. In addition, both DBA/2 +/bg and beige mice developed a rapid and specific resistance to intravenous challenge with parental FLC. In previous experiments DBA/2 beige mice could not be protected by exogenous IFN-alpha/beta. The differences in the response of mice to the constitutive production of IFN-alpha by IFN-alpha-transfected tumor cells and their response to exogenous IFN is discussed in terms of the effects of IFN on the host and of antitumor therapy.

Failure of peritoneal exudate macrophages to reverse immunologic impairment by Friend leukemia virus.

Abstract: SummaryTransfer experiments with peritoneal exudate macrophages from normal donor mice were performed to determine if a defect of normal macrophage function or activity was a major or contributing factor to the immunosuppression characterizing leukemia virus infection of mice. Challenge immunization of Friend leukemia virus-infected mice with sheep erythrocytes resulted in markedly depressed hemolytic antibody responses, as compared to responses of normal noninfected mice. When PE cell suspensions rich in macrophages were transferred from normal donor mice to leukemia virus infected recipients there was no affect on the FLV induced impairment of the immune response. Similar transfer of PE cells to normal uninfected mice generally resulted in a moderate depression of the expected immune response. In no case did the PE cells enhance the immune responses in normal or virus-infected mice.The capable technical assistance of Mr. Howard Gratizer and Ms. Kathy Katush is acknowledged.